共查询到20条相似文献，搜索用时 31 毫秒
1.
AIM: To investigate the influence of hepatic portal interdicting on gastric mucosa of the liver cirrhosis rats and the protective effect of famotidine on gastric mucosa. METHODS: Fifty Wistar rats were randomly divided into 5 groups; group A (healthy rats), group B (healthy rats with interdicted hepatic portal), group C (liver cirrhosis rats without interdicted hepatic portal), group D (liver cirrhosis rats with interdicted hepatic portal) and group E (liver cirrhosis rats without interdicted hepatic portal and use of famotidine); The gastricfluid pH, gastric mucous content (GMC), gastric mucosa blood flow (GMBF) and the damage index of gastric mucosa (DIGM) of the every group were observed. RESULTS: There is no significant difference in the above parameters between group A and group B (P>0.05). Compared with group A, GMBF of group C, D, and E were reduced (P<0.01), pH, GMC of group C, D and E were also reduced (P<0.05); DIGM of group C, D and E were increased (P<0.01). All the changes of group D were more obvious than those of group C (P<0.01); While there was no significant difference in all the parameters between group E and group C (P>0.05). CONCLUSION: Hepatic portal interdicting can aggravate the gastric mucosa damage of the liver cirrhosis rat, and famotidine can protect against such gastric mucosa injury through improving the microcirculation of gastric mucosa. 相似文献
2.
AIM: To study the relationship between nitric oxide (NO) and gastric mucosal injury induced by reserpine in rats. METHODS: Sixteen healthy male Wistar rats were randomly divided into control group and experimental group (n=8). NO contents and malondialdehyde(MDA) contents in plasma, gastric mucosa of the rats were respectively determined with Cadmium-reduct plus Greiss and TBA; nitric oxide synthase in gastric walls of the rats were observed using NADPH-diaphorase histochemistry and quantitatively measured with image analyzer. RESULTS: The NO contents in both plasma and gastric mucosa of experimental group were significantly lower than that in control group (P＜0.01),but their MDA contents were both higher than that in control group(P＜0.05,P＜0.01);the densities and A values of nitric oxide synthase (NOS)-positive nerve-cells and nerve fibers in gastric walls of experimental group were all obviously lower than that in control group (P＜0.05,P＜0.01). CONCLUSION: The mechanism of the reserpine-induced gastric mucosal injury in rats might be related to NO insufficiency arisen from the inhibition of NOS activity in NANC nerves in gastric wall,which might weaken the protection to gastric mucosa. 相似文献
3.
WANG Jin-dan QIAO Wan-ning ZHU Jing FU Yao-yang HU Wan-li DONG Ren-jie HONG Kai-rui ZHANG Jia-li WANG Fang-yan 《园艺学报》2017,33(10):1906-1911
AIM: To observe the antiulcer effect of butyric acid and hydrogen, the main metabolites of Clostridium butyricum (C. butyricum), and to explore the underlying mechanism. METHODS: The mouse model of acute gastric mucosal lesion was prepared by gavage with ethanol. The mice were randomly divided into 4 groups: normal group, model group, butyric acid group and hydrogen group. The mice in butyric acid group and hydrogen group were given butyrate and hydrogen prior to model establishment, respectively. Macroscopic observation of the pathological changes in gastric tissues was performed to evaluate the effect of the 2 metabolites of C. butyricum. Meanwhile, the mRNA expression levels of inflammatory factors, such as IL-12, RAN1 and MCP-1, were determined by RT-qPCR. The expression levels of apoptosis-related proteins Bcl-2 and Bax were detected by immunohistochemical staining. RESULTS: The macroscopic observation found that butyrate, not hydrogen, protected gastric mucosa. HE staining also showed that butyrate significantly attenuated the pathological damage of the gastric mucosa induced by ethanol. Compared with model group, the mRNA levels of inflammatory factors IL-12, RAN1 and MCP-1 in butyrate group significantly decreased (P<0.01). In butyrate group, the protein level of Bax was obviously decreased compared with model group (P<0.01), while the protein level of Bcl-2 was significantly increased (P<0.01). CONCLUSION: The gastric mucosa protective metabolite of C. butyricum may be butyric acid, not hydrogen. Butyric acid protects the gastric mucosa against ethanol-induced lesion by inhibiting the inflammation and reducing the expression ratio of Bax/Bcl-2. 相似文献
4.
AIM: To investigate the protective role of heat-shock protein 70 (HSP70) in the pathogenesis of gastric mucosal damage in cirrhotic rats with portal hypertensive gastropathy (PHG).METHODS: The rat model of liver cirrhosis with PHG was established by injection with tetrachloride.The animals were divided into normal control group, PHG group, PHG+heat treatment group, PHG+BPI21 group and PHG+endotoxin groups.The endotoxin used in the experiment was at the dose of 3 mg/kg and endotoxin antagonist BPI21 was at the dose of 2 mg/kg.HSP70 was induced by pre-treating the animals with mild whole-body heating.The levels of HSP70 and tumor necrosis factor alpha (TNF-α) in the gastric mucosa were measured by ELISA.Furthermore, the pathological changes of the gastric mucosa were observed under microscope with HE staining.RESULTS: Compared with the normal control rats, the rats in PHG group showed obvious gastric pathological lesion, decrease in HSP70 production and increase in TNF-α level in the gastric mucosa, and increased endotoxin concentration in the plasma.Compared with PHG+endotoxin group, the gastric mucosal lesion in PHG+BPI21 group was significantly attenuated, accompanied by the increase in HSP70 production and decrease in TNF-α level in the gastric mucosa.Heat treatment increased HSP70 production and decreased TNF-α concentration in the PHG rats, thus attenuating the gastric mucosal damage.CONCLUSION: HSP70 alleviates the gastric mucosal lesion induced by endotoxin in cirrhotic rats with PHG and decreases the concentration of TNF-α in gastric mucosa, indicating a protective role of HSP70 in the pathogenesis of gastric mucosal damage in PHG. 相似文献
5.
AIM: To evaluate the changes of somatotropin axis in pre-pubertal rats with catch-up growth born small for gestational age (CUG-SGA). METHODS: The SGA rat model was prepared by diet restriction in pregnant rats.Growth hormone (GH) excretion in 24-h urine, serum level of insulin-like growth factor-1 (IGF-1), the expression of IGF-l and insulin-like growth factor-1 receptor (IGF-1R) in the tibial growth plate and the mRNA expression of IGF-1 in liver were measured in infant rats at the end of week 4. RESULTS: The level of 24-h urinary GH excretion in CUG-SGA group were significantly higher than that in the rats of non-catch-up growth born small for gestational age (NCUG-SGA) group and appropriate for gestational age (AGA) group (both P<0.01). The serum level of IGF-1 and the mRNA expression of IGF-1 in liver in CUG-SGA group were similar to those in AGA group, but significantly higher than those in NCUG-SGA group. The thickness of the tibial growth plate in NCUG-SGA group was significantly lower than that in CUG-SGA group and AGA group. No difference of the growth plate thickness between CUG-SGA group and AGA group was observed, but the thickness of hypertrophy zone of the growth plate in CUG-SGA group were significantly higher than that in NCUG-SGA group and AGA group (both P<0.01). The expression of IGF-1 in the growth plate in CUG-SGA group was similar to that in AGA group but significantly higher than that in NCUG-SGA group (P<0.01). No difference of the IGF-1R expression in the growth plate among these 3 groups was found (P>0.05). CONCLUSION: GH/IGF-1 resistance exists in SGA rats with and without catch-up growth. 相似文献
6.
AIM: To investigate the protective effect of Zhenrenyangzang decoction (ZRYZ) on the intestinal mucosal barrier function and the expression of tight junction proteins, zonula occludens-1 (ZO-1) and occludin, in the colon of rats with trinitrobenzenesulfonic acid (TNBS)-induced ulcerative colitis in order to explore the possible mechanism involved. METHODS: Male Wistar rats were randomly divided into normal group, model group, salazosulfapyridine (SASP) positive control group, high-dose ZRYZ (ZRYZ-H) group and low-dose ZRYZ (ZRYZ-L) group. Except the normal group, the rats in other groups were given the TNBS/50% ethanol mixed solution by enema to make the ulcerative colitis model. The rats in positive control group were given SASP suspension liquid. The rats in ZRYZ-H group and ZRYZ-L group were orally administered with ZRYZ at doses of 30.4 g/kg and 15.2 g/kg, respectively, while the rats in normal group and model group were orally administered with saline. All the drugs were administered to the rats for consecutive 21 d. Disease activity index (DAI) was investigated during the drug treatment, and colon samples were collected after drug administration for evaluating morphological damage score. Intestinal mucosal permeability was measured by detection of lactulose/mannitol (L/M) in urine. Colonic myeloperoxidase (MPO) activity and goblet cell number, serum diamine oxidase (DAO) and D-lactic acid (D-LA) levels, and the colonic expression of ZO-1 and occludin were also measured. RESULTS: Compared with normal group, DAI, morphological damage score, L/M value, colonic MPO activity as well as serum D-LA and DAO levels in model group significantly increased (P<0.05), while goblet cell number as well as the expression levels of ZO-1 and occludin in model group were significantly reduced (P<0.05). Compared with model group, DAI, morphological damage score, L/M value, colonic MPO activity as well as serum DAO and D-LA levels in ZRYZ-H group and ZRYZ-L group were reduced significantly (P<0.05), while goblet cell number as well as the expression of ZO-1 and occludin in ZRYZ-H group and ZRYZ-L group increased significantly (P<0.05). CONCLUSION: ZRYZ protects the intestinal mucosal barrier function in ulcerative colitis rats by reducing intestinal mucosal permeability, and its mechanisms may be related to increasing the expression of ZO-1 and occludin. 相似文献
7.
AIM: To demonstrate the changes of activity and electron microscopic enzyme cytochemistry staining of H+-K+-ATPase of gastric parietal cells under stress in rats. METHODS: Twenty-four male SD rats were randomly divided into normal group, stress group and stress+omeprazole (OM) group. Water immersion-restraint stress (WRS) model in SD rats was performed. The ulcer index (UI) of gastric mucosa and H+-K+-ATPase activity of gastric parietal cells were measured. The changes of ultrastructure and electron microscopic enzyme cytochemistry staining of parietal cells were observed under transmission electron microscope (TEM). RESULTS: Compared with control group, the UI of gastric mucosa and H+-K+-ATPase activity of gastric parietal cells increased (P<0.01 and P<0.05) in stress group. In stress+OM group, both UI and H+-K+-ATPase activity decreased (P<0.01) compared with stress group. Parietal cells were in a resting state in control group, and became active in stress group, where plenty of intracellular canaliculi were observed under the TEM. In stress+OM group, the dilated intracellular canaliculi lined with rare microvilli were founded. Enzyme cytochemistry staining showed that there was little black punctate enzyme reactive product scatted in intracellular canaliculi and the apical plasma membrane of parietal cells in control group, and there were large amounts of black enzyme reactive product accumulated at the intracellular canaliculi in stress group. Scarcely deposition of enzyme reactive product in intracellular canaliculi was observed in stress+OM group. CONCLUSION: The results indicate that the H+-K+-ATPase activity of gastric parietal cells increases under WRS, and is in accordance with ultrastructure changes. These findings suggeste that gastric acid might be one of the most important factors that result in stress ulcer. 相似文献
8.
SUN Wei-hao OU Xi-long YU Qian CAO Da-zhong CHEN Hong YU Ting SHAO Hua ZHU Feng SUN Yun-liang 《园艺学报》2003,19(11):1508-1512
AIM: To clarify the effects of specific and non-specific cyclooxygenase-2 (COX-2) inhibitors on gastric epithelial cell proliferating and gastric healing following acid-induced damage. METHODS: Male Sprague-Dawley rats were given 1 mL of 0.6 mol/L hydrochloric acid (HCl) into the stomach. Ten minutes after the administration of the acid, the animals were given NS-398 (COX-2 inhibitor) or indomethacin. Levels of COX-1 and COX-2 in the gastric mucosa before and after HCl-administration were analyzed using western blotting and immunohistochemical staining. Proliferating cell nuclear antigen (PCNA) was detected using immunohistochemistry for epithelial cell proliferation. Gastric lesion index (LI) was assessed using planimetry. RESULTS: Expression of COX-2 was enhanced mainly in surface epithelial cells and neck cells following HCl-administration. At 24 h following acid administration, PCNA labeling index (PCNA-LI) was (22.72±4.33) % and (21.98±5.18) % in the groups treated with 40 mg/kg of NS-398 and indomethacin respectively, which was significantly lower than that in the control group [ (34.46±3.61) %, P< 0.05 ]; LI was (1.28±0.58) % and (1.16±0.56) % in the groups treated with 4 mg/kg and 40 mg/kg of NS-398, respectively, which was significantly higher than that in the control group [ (0.58±0.24) %, P< 0.05 ]. CONCLUSIONS: The present study demonstrated that cyclooxygenase-2 inhibitors delayed gastric mucosal healing by suppressing expansion of the mucosal proliferative zone. These results provide evidence that cyclooxygenase-2 plays an important role in gastric mucosal regeneration. 相似文献
9.
AIM: To observe the dynamic changes of neurokinin A (NKA) and calcitonin gene-related peptide (CGRP) levels in gastric mucosal and plasma in rats after abdominal seawater-immersing trauma, and to investigate the influence of these two sensory neuropeptides on acute gastric mucosal lesion. METHODS: Thirty-two SD rats were randomly divided into four groups (normal group, celiac seawater-immersing trauma 1, 2 and 3 h groups). With emzyoimmunoassay and radioimmunoassay respectively, gastric mucosal and plasma NKA and CGRP levels in rats were measured.RESULTS: Compared with normal rats, with the seawater-immersing time prolonged, gastric mucosal NKA and CGRP levels in rats were progressively decreased (P<0.05), while plasma NKA and CGRP levels significantly elevated. CONCLUSION: Seawater-immersion is a harmful factor, it can lead to elevated plasma NKA and CGRP levels and decrease gastric mucosal NKA and CGRP levels. 相似文献
10.
AIM: To evaluate the significance of serum soluble CD40 ligand (sCD40L) in the vulnerability of coronary atherosclerotic plaque, the relationship between the level of sCD40L and the stenosis degree of the coronary artery by the coronary angiography (CAG), and other inflammatory factors. METHODS: According to WHO diagnostic criterior of coronary heart disease (CHD) and the results of CAG, 84 cases of CHD and 20 cases of non-CHD (NCHD) were included in this study. 84 cases of CHD were divided into three groups: 30 cases in acute myocardial infarction (AMI) group, 30 cases in unstable angina (UA), 24 cases in stable angina (SA). The sera levels of sCD40L in four groups were detected by the enzyme-linked immunosorbent assay (ELISA) and the results were expressed with μg/L. CAG were all conducted in four cases and the results were further evaluated by Jenkins score. ESR and CRP were detected at the same time. RESULTS: The sera levels of sCD40L in four groups were significantly different (P<0.01). The level of sCD40L in AMI group (8.48±4.13) μg/L was higher than that in SA group (4.36±2.68) μg/L, P<0.01 and NCHD group (4.12±1.96) μg/L, P<0.01. The level of sCD40L in UA group (8.72±4.26) μg/L was higher than that in SA group and NCHD group (P<0.01). The level of sCD40L in UA group was slightly higher than that in AMI group, but the difference of two group is not significant (P>0.05). The level of sCD40L in SA group was slightly higher than that in NCHD group, but the difference of two group is not significant (P>0.05). The sera levels of sCD40L in CHD were significantly and positively correlated with Jenkins score (r=0.524, P<0.01). The sera level of sCD40L was positively correlated with the levels of CRP and ESR. CONCLUSION: The sera levels of sCD40L in the patients with various types of CHD are significantly different. The level of sCD40L in the patients with AMI and UA are significantly higher than those in SA and NCHD groups, which may reflect the vulnerability of coronary atherosclerotic plaque. The sera levels of sCD40L is increased with the increasing number of diseased coronary branches and Jenkins score, suggesting that sCD40L promotes atherosclerosis and also can be used as a parameter to predict pathological severity of coronary atherosclerosis. The level of sCD40L is obviously correlated with the levels of CRP and ESR. 相似文献
11.
AIM: To explore the protective effects of riboflavin on the kidney in streptozotocin (STZ)-induced diabetic rats. METHODS: Male Sprague-Dawley rats were randomly divided into 3 groups: normal control group, diabetic model group and riboflavin-treated group. Diabetes was induced by a single injection of STZ (dissolved in 0.01 mol/L citrate buffer, pH 4.5, 65 mg/kg, ip) in rats. The biochemical methods were used to measure the contents of urine protein and malondialdehyde in the kidney, and the activities of superoxide dismutase (SOD) and catalase (CAT) in serum and renal tissues. Furthermore, the protein expression of TGF-β1 and plasminogen activator inhibitor-1(PAI-1) in renal cortex was detected by Western blotting. The morphological changes of renal tissue were observed under microscope.RESULTS: Compared to the diabetic model group, riboflavin significantly increased the activities of SOD and CAT (P<0.01) in the serum and renal tissues, and decreased the contents of urine protein and MDA (P<0.01) in the renal tissues in riboflavin-treated group. The levels of TGF-β1 and PAI-1 in the renal cortex were dramatically decreased in the treated diabetic rats compared to the diabetic model rats (P<0.01).CONCLUSION: Riboflavin inhibits the protein expression of TGF-β1 and PAI-1 in renal tissue of STZ-induced diabetic rats. Riboflavin may alleviate the pathologic changes and play an important protective role in diabetic kidneys. 相似文献
12.
WANG Xiang-hong LIU Sheng-yuan ZHANG Zhong-le YU Shang-bin YE Shi-qiao CHEN Qi-ling WANG Di-xun 《园艺学报》2007,23(3):488-491
AIM:To investigate the effect of histamine receptor antagonist on airway remodeling and acid-base imbalance in asthma of guinea pig. METHODS:Guinea pigs were divided into 5 groups: the normal control group, the asthma model group, the continued asthma model group, histamine group and histamine receptor antagonist group. For each group, the content of histamine, Na+, Cl-, PaO2, PaCO2, pH, AB, SB in serum, and thickness of airway mucosa and smooth muscle cell layer were measured and compared with each other. RESULTS:(1) According to the content of histamine in serum and thickness of airway mucosa and smooth muscle, the order was: the histamine group>continued asthma model group>the asthma model group>the normal control group (P<0.01), and the histamine receptor antagonist groupthe continued asthma model group (P<0.01), but for PaCO2, the order was conversed. Airway remodeling, increase in histamine in serum, respiratory acidosis and metabolic acidosis in asthmatic guinea pig were observed. Exogenous histamine accentuated the change, however, histamine receptor antagonist attenuated it. CONCLUSION:Histamine may take part in the airway remodeling of asthma. Histamine receptor antagonist can prevent and ameliorate airway remodeling and acid-base imbalance in asthma of guinea pig. 相似文献
13.
XIE Yong GONG Yan-feng ZHOU Nan-jin CHEN Jiang ZHOU Xiao-jiang L Nong-hua WANG Chong-wen 《园艺学报》2007,23(3):438-443
AIM:To study the immunological protection of H. pylori vaccine with chitosa as adjuvant. METHODS:One-grade female BALB/c mice were randomly divided into nine groups and immunized by ①PBS alone; ②chitosan solution alone; ③chitosan particles alone; ④H. pylori antigen alone; ⑤H. pylori antigen plus chitosan solution; ⑥H. pylori antigen plus chitosan particles; ⑦H. pylori antigen plus CT; ⑧H. pylori antigen plus chitosan solution and CT; ⑨H. pylori antigen plus chitosan particles and CT. At 4 weeks after the last immunization, these mice were challenged by alive H. pylori（1×1012CFU/L） twice at two-day intervals. At 4 weeks after the last challenge, these mice were all killed and gastric mucosa were embedded in paraffin, sectioned and assayed with Giemsa staining. The other gastric mucosa were used to quantitatively culture with H. pylori. ELISA was used to detect H.pylori IgA in saliva and gastric mucosa and anti-H.pylori IgG, IgG1, IgG2a in serum, and immunohistochemical method was used to examine sIgA in gastric mucosa. RESULTS:①In the groups with chitosan as adjuvant, 60% mice achieved immunological protection, which was according to that with CT as adjuvant (58.33%), and was significantly higher than H. pylori antigen alone and other groups without H. pylori antigen（P<0.01 or P<0.05）. While the rates of protection in the groups with chitosan plus CT as adjuvant were 84.62%,85.71% and the H. pylori colonization score in it was significantly lower than that in the groups with CT as an adjuvant and without adjuvants（P<0.01 or P<0.05）. ②The each isotype IgG levels induced by H. pylori vaccine with adjuvants were significantly higher than those in control group and non-adjuvant groups（P<0.01 or P<0.05），while the anti-H. pylori IgG levels in the groups with CT plus chitosan as adjuvant were significantly higher than those in the groups with CT or chitosan as an adjuvant alone（P<0.05）. ③ The labeling index for sIgA-positive lumen of glands and special anti-H. pylori IgA levels in gastric mucosa in the groups with chitosan as an adjuvant had no difference with those in the group with CT as an adjuvant（P>0.05）and were significantly higher than those in non-adjuvant groups, while those in the groups with chitosan plus CT were significantly higher than those in the group with CT as an adjuvant（P<0.01 or P<0.05）. CONCLUSION:H. pylori vaccine with chitosan as adjuvant could protect against H. pylori infection, suggested that chitosan is a mucosa adjuvant of H. pylori vaccine. 相似文献
14.
AIM: To investigate the effect of rosiglitazone, a peroxisome proliferators-activated receptor γ(PPARγ) agonist, on the expression of PPARγ, the activation of NF-κB and intestine injury in the rats undergoing orthotopic autologous liver transplantation(OALT).METHODS: Sprague-Dawley male rats were randomly divided into 4 groups:control group, sham group, OALT group and rosiglitazone(0.3 mg/kg, iv) pretreatment(ROS+OALT) group. The OALT model was established, and the intestinal tissues were collected 8 h after the liver reperfusion. The intestinal tissue sections were stained to visualize the damage. The expression of PPARγ and NF-κB in the tissues, the concentrations of diamine oxidase(DAO) and fatty acid-binding protein 2(FABP2) in the serum and the concentration of TNF-α and IL-6 in the tissues were measured.RESULTS: Compared with sham group, the intestinal mucosa of the rats showed obvious pathological injury after liver reperfusion in OALT group and ROS group, the Chiu,s scores of intestinal mucosa was significantly higher, and the serum concentrations of DAO and FABP2 increased(P<0.05). After rosiglitazone pretreatment, the injury of intestinal mucosa of the rats was alleviated, the Chiu,s scores was lower and the serum concentrations of DAO and FABP2 decreased(P<0.05), the PPARγ expression was obviously up-regulated in the intestinal tissues, the nuclear translocation of NF-κB was reduced and the concentrations of IL-6 and TNF-α were decreased.CONCLUSION: During perioperative period of OALT in rats, the inflammatory responses are obvious. Furthermore, obvious intestinal injury occurs. PPARγ agonist rosiglitazone obviously up-regulates PPARγ expression and inhibits the inflammation in the intestines, thus protecting against intestinal injury in rats undergoing OALT. 相似文献
15.
AIM To investigate the expression of Wnt1 and LGR5 in gastric mucosa with stress ulcer after traumatic brain injury （TBI） in rats, and to study the relationship between Wnt1/LGR5 expression and stress ulcer after TBI. METHODS Healthy 7-week-old male SD rats （n =30） were randomly divided into 3 groups： sham operation （sham） group, mild TBI （mTBI） group, and severe TBI （sTBI） group. The mTBI and sTBI were induced by electronic cortical contusion impactor. Neurological severity score （NSS） was calculated 24 and 48 h after modeling. Mucosal blood flow in gastric fundus, greater curvature, pylorus and cardia of anesthetized rats 48 h after injury was measured by Doppler flowmeter. All rats were sacrificed, and their gastric tissues were harvested after 48 h and then stained with hematoxylin and eosin. The protein expression of Wnt1 and LGR5 was analyzed by Western blot and immunohistochemistry. RESULTS Compared with sham group, the NSS in mTBI group and sTBI group was significantly increased （P <0.01）. Compared with sham group, the gastric mucosal blood flow of the rats after TBI was significantly decreased （P <0.01）, and the decrease in sTBI group was more significant than that in mTBI group （P <0.05）. The protein expression of Wnt1 and LGR5 in mTBI group was significantly higher than that in sham group （P <0.05）, and that in sTBI group was significantly higher than that in mTBI group （P <0.05）. Normal glandular gastric tissue was observed, and no abnormal change was found in sham group, while the infiltration of inflammatory cells in gastric lamina propria, mucosa and submucosa was obvious in mTBI group and sTBI group. CONCLUSION Traumatic brain injury activates Wnt1 and LGR5 expression to induce inflammatory changes in gastric mucosa, and then induces stress ulcer. This results provides experimental basis for the pathogenesis and treatment of stress ulcer after trauma. 相似文献
16.
Effect of ginsenoside Rb1 on liver cell pyroptosis in hyperlipidemia rats and its possible mechanism
AIM:To discuss the mechanism of ginsenoside Rb1 against liver lipid deposition by observing the effect of ginsenoside Rb1 on liver cell pyroptosis in hyperlipidemia rats. METHODS:Totally 32 healthy SPF rats were randomly divided into control group, model group, ginsenoside Rb1 group and simvastatin group. The rats in control group was given the basic feed, while the others were given high-fat diet. The rats in ginsenoside Rb1 group and simvastatin group were given corresponding drugs. The rats in control group and model group were intraperitoneal injected with equal volume of saline. Eight weeks later, the serum levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) were tested by the automatic biochemistry analyzer. The pathological changes of the liver tissues were observed with HE staining. The protein and mRNA expression levels of pyroptosis-related factors NLRP3, caspase-1, IL-1β, IL-18 and GSDMD were detected by Western blot and RT-qPCR. RESULTS:Compared with control group, the serum levels of TC, TG and LDL-C in model group were increased significantly (P<0.01), and the HDL-C content was decreased significantly (P<0.05). The steatotic liver cells covered the visual field. The mRNA and protein expression levels of NLRP3, caspase-1, IL-1β, IL-18 and GSDMD were increased significantly (P<0.01). Ginsenoside Rb1 significantly decreased the serum levels of TC, TG and LDL-C (P<0.05), and significantly increased the content of HDL-C (P<0.01). Ginsenoside Rb1 also significantly decreased the degree of steatosis, and the number and size of lipid droplets. The mRNA and protein expression levels of NLRP3, caspase-1, IL-1β, IL-18 and GSDMD were decreased significantly (P<0.05 or P<0.01). CONCLUSION:Ginsenoside Rb1 atte-nuates liver injury and inhibits liver lipid deposition in hyperlipidemia rats by reducing the expression of hepatic pyroptosis-related factors. 相似文献
17.
YIN Ming-jing WEN Han-chun YE Yong-wei GUAN Qing-lin HUANG Hao-zhang HUANG Lu-shuang ZHU Ji-jin 《园艺学报》2012,28(2):228-233
AIM: To investigate the effect of simvastatin intervention on the changes of blood pressure, serum lipid fluctuation and aortic configuration induced by high-sodium and high-fat diet in rats. METHODS: Sixty adult male SD rats were randomly divided into 5 groups (n=12): control (N)group, high salt (S)group, high fat (F) group, high salt+ high fat (SF) group and high salt+high fat + simvastatin (T) group. After fed for 16 weeks, the rats were subject to determine blood pressures and serum concentrations of triglycerides (TG),total cholesterol(TC) and soluble CD40 ligand (sCD40L). The expression of CD40/CD40L in the root of ascending aorta was detected by immunohistochemical method. The thickness of intima media in the ascending aorta as well as the ratio of lumen area/total vascular area were measured and calculated after HE staining. RESULTS: In S group, F group and SF group, systolic blood pressure was significantly higher than that in N group (P<0.01). Systolic blood pressure in T group were slightly higher than that in N group with statistical significance and significantly lower than that in SF group. The serum concentrations of TG and TC in F group and SF group were significantly higher than those in N group and T group (P<0.01), and no significant difference among S group, N group and T group was observed. In S group, F group and SF group, the serum concentrations of sCD40L were higher than that in N group and T group (P<0.05), meanwhile that in SF group was also higher than that in S group and F group (P<0.05). However, no significant difference of sCD40L concentration between S group and F group as well as N group and T group was observed. The expression of CD40/CD40L in the ascending aorta in S group, F group and SF group was higher than that in N group and T group (P<0.05), and that in SF group was also higher than that in S group and F group (P<0.05).No significant difference of CD40/CD40L expression between S group and F group as well as N group and T group was observed. The thickness of intima media in S group, F group and SF group was significantly thicker than that in N group (P<0.01), and no significant difference of the intima media thickness between T group and N group was observed. The ratio of lumen area/total vascular area in S group, F group and SF group was smaller than that in N group (P<0.05), and no significant difference of the ratio between T group and N group was found. CONCLUSION: Feeding high-fat and high-salt diet leads to blood pressure elevation, induces atherosclerosis, increases serum concentration of sCD40L and enhances the expression of CD40/CD40L in arterial tissues. The combination of the stimuli has stronger effect than a single factor. Statins protect the arterial tissues against atherosclerosis by decreasing the level of serum sCD40L and inhibiting the arterial expression of CD40/CD40L. 相似文献
18.
AIM: To explore the protective effects of luteolin on the diabetic kidneys. METHODS: Male Sprague-Dawley rats were randomly divided into 5 groups: normal control group, diabetic model group and the groups of diabetic rats treated with luteolin at a low dose, a middle dose and a high dose. The diabetic model was induced by a single intraperitoneal injection of streptozotocin (STZ,65 mg/kg). Blood glucose, urine protein, the activity of superoxide dismutase and catalase in serum and kidney, and the content of malonaldehyde(MDA) in kidney were analyzed by biochemical methods. Western blotting was used to detect the protein expression of transforming growth factor-β1(TGF-β1) and plasminogen activator inhibitor-1(PAI-1) in the renal cortex. The morphological changes of the renal tissues were observed under microscope. RESULTS: Compared with diabetic model group, luteolin significantly reduced the level of blood glucose (P<0.01), the content of urine protein (P<0.01) and MDA (P<0.01) in the kidneys, and increased the activity of superoxide dismutase and catalase (P<0.01) in serum and kidneys in the diabetic rats. The protein levels of TGF-β1 and PAI-1 in the renal cortex were dramatically decreased as the rats were treated with luteolin. CONCLUSION: Luteolin may exert an important protective effect on diabetic kidneys by relieving oxidative stress and inhibiting the protein expression of TGF-β1 and PAI-1 in the renal tissues of STZ-induced diabetic rats. 相似文献
19.
AIM: To investigate the protective mechanism of extract of Ginkgo biloba (EGB) on apoptosis of hippocampus neuronal cells in type 1 diabetic encephalopathic rats. METHODS: Thirty-six male Sprague-Dauley rats were divided into 3 groups: control group, diabetic group and EGB-treated group. Streptozotocin was injected intraperitoneally to the animals in later two groups to induce diabetes. The rats in EGB-treated group were injected intraperitoneally with EGB, and the same volume of normal saline was injected to the rats in other groups. At the end of the 12th week, the spatial learning and memory abilities of rats in each group were examined by Morris water maze test. Blood glucose and serum insulin concentration were measured. The neuron densities in hippocampus were measured by Image-Pro Plus 6.0 software. The expressions of Bax, Bcl-2, caspase-3 were assayed by Western blotting and immunohistochemistry. RESULTS: Compared to control group, the level of blood glucose (P<0.01), the protein expression of Bax (P<0.01) and caspase-3 (P<0.01) in hippocampus neuronal cells, and the ratio of Bax/Bcl-2 (P<0.01) and the escape latency (P<0.01) in diabetic group, were significantly increased, while the serum insulin concentration (P<0.01), the neuronal density (P<0.05) in CA1,CA2 hippocampal regions and the platform searching score (P<0.01) were significantly deceased. After treated with EGB, the serum insulin concentration (P<0.05), the neuronal density (P<0.05) in CA1,CA2 hippocampal regions and the platform searching score (P<0.01) were significantly increased, while the level of blood glucose (P<0.01), the protein expression of Bax (P<0.05), caspase-3 (P<0.05) in hippocampus neuronal cells, the ratio of Bax/Bcl-2 (P<0.01) and the escape latency (P<0.05) were significantly deceased than those in diabetic group. The protein expression of Bcl-2 in hippocampus neuronal cells did not alter in any experimental rats. CONCLUSION: EGB improves the spatial learning and memory capacity in diabetic rats by decreasing the expression of Bax, Bax/Bcl-2 ratio and down-regulating caspase-3 to reduce neurocyte apoptosis and increase the neuron density in CA1, CA2 hippocampal regions, suggesting that effective regulation of neuron apoptosis associated genes may be one of the mechanisms for EGB to treat diabetic encephalopathy. 相似文献
20.
AIM:To investigate the post-receptor mechanism of growth hormone (GH) resistance and insulin (INS) resistance and their relationship in non-catch-up growth rats born small for gestational age (NCU-SGA), based on the post-receptor signalling cross-talk between GH and INS at PI3K signaling pathway. METHODS:NCU-SGA rat model was developed by food restriction to pregnant dams. 4 weeks old male NCU-SGA rats were studied. Total and phosphate insulin receptor substrate-1(IRS-1) and its downstream signal Akt levels in liver tissue were measured by Western blotting or immunoprecipitation at baseline, post-stimulating of insulin, and pre-treatment with JAK2 (post-receptor signaling protein of GH) inhibitor AG490 then given insulin stimulation, respectively. RESULTS:(1) Expression levels of total and phosphate IRS-1: No difference between NCU-SGA rats and normal control was observed (P>0.05). (2) Expression levels of Akt : At baseline, Akt was already activated in NCU-SGA rats compared to no Akt activation in normal control rats. However, post- stimulating of insulin, the increase level of phosphate Akt in NCU- SGA rats was remarkably lower than that in control rats (P<0.01). When pre-treatment with JAK2 inhibitor to block GH signaling pathway, the impaired Akt activity was significantly restored (P<0.01), which suggested that the signaling of GH uncouples signal transduction from IRS-1 to Akt in NCU-SGA rats.CONCLUSION:Insulin resistance is related to impaired IRS-1-Akt signaling pathway in NCU-SGA rats. GH resistance mediates and aggrevates INS resistance by uncoupling signal transduction from IRS-1 to Akt via signaling cross-talk at post-receptor level between GH and INS. PI3K/Akt may be the major site for this uncoupling. 相似文献