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1.
AIM：To study the effect of ghrelin in septal nucleus on the gastric motility of the rats with diabetes mellitus (DM) and to investigate the regulation of ghrelin pathway between arcuate and septal nucleus nuclei on gastric motility. METHODS：Streptozotocin was injected intraperitoneally to establish a DM rat model. Fluorescence immunohistochemistry and real-time PCR were used to detect the expression of ghrelin receptor GHS-R1a. The gastric motility was evaluated by implantation of a force transducer on the surface of rats stomachs and the motility index was also calculated. The neural connections between arcuate and septal nuclei were analyzed by the technique of fluorogold tracing. The neural control pathway of gastric motility was determined by central drug injection, nucleus lesion or nucleus electrical stimulation. RESULTS：The expression of GHS-R1a in the septal nucleus of DM rats was lower than that in normal rats (P<0.05). The amplitude and frequency of gastric motility in the DM rats were lower than those in the normal rats (P<0.05). The gastric motility of normal and DM rats were increased by injection of ghrelin into the septal nucleus in a dose-dependent manner. Seven days after injection of fluorogold into the septal nucleus, some neurons in arcuate nucleus were labeled by fluorogold and part of the labeled neurons were ghrelin immunopositive. No effect of nucleus lesion or nucleus electrical stimulation on the gastric motility in the normal rats was observed. In DM rats, the lesion of septal nucleus decreased the gastric motility (P<0.05). In the normal rats, the change of gastric motility caused by electrical stimulation in arcuate nucleus was not affected by the lesion of septal nucleus (P>0.05), while the change was attenuated in DM rats (P<0.05). The ghrelin receptor antagonist ［D-Lys-3］-GHRP-6 had no significant effect on the gastric motility induced by electrical stimulation in arcuate nucleus of the normal rats (P>0.05), but it reduced the change in the DM rats (P<0.05). CONCLUSION:Ghrelin in septal nucleus and the ghrelinergic pathway between arcuate and septal nuclei play an important role in the modulation of gastric motility in DM rats.  相似文献   

2.
无 《园艺学报》2007,34(3):574-578
由《园艺学报》编辑部和中国农业科学院蔬菜花卉研究所生物技术研究室共同发起和主办的“信息园艺学论坛”于2007年5月28～29日在成都举行。  相似文献   

3.
AIM:To investigate whether glucagon-like peptide 1 (GLP-1) receptor (GLP-1R) signaling pathway is involved in regulating the effects of exogenous γ-aminobutyric acid (GABA) in hypothalamic nucleus accumbens (NAc) on discharge activity of gastric distension (GD) sensitive neurons, gastric motility and gastric acid secretion in rats. METHODS:Fluorescence immunohistochemistry was used to observe the expression of GABA-A receptor (GABA-AR) and GLP-1R in rat NAc. The single-cell discharge recording experiment was used to observe the effects of GABA, GLP-1 and their receptor antagonists on the excitability of GD neurons in rat NAc. Implantation of cannula in rat NAc and injection of GLP-1, GLP-1R antagonist exendin 9-39 (Ex9) and GABA-AR antagonist bicuculline (BIC) were performed to investigate the changes of gastric motility and gastric acid secretion in the rats. RESULTS:GABA-AR and GLP-1R immunoreactive positive neurons coexisted in rat NAc. GABA inhibited the discharge activity of GD neurons in NAc, but this inhibitory effect was antagonized by BIC and partially blocked by Ex9. Microinjection of GABA into rat NAc promoted gastric motility and gastric acid secretion, which was antagonized by BIC and partially blocked by Ex9. CONCLUSION:Exogenous GABA in NAc may be involved in the regulation of gastric motility, gastric acid secretion and GD neuron excitability in the rats through GABA-AR signaling pathway. The promotion of GABA-AR signaling pathway is partially inhibited by GLP-1R signaling pathway.  相似文献   

4.
AIM: To investigate the changes of oxidative stress in the stomach tissues and their roles in gastric motility and interstitial cells of Cajal (ICC) in diabetic rats. METHODS: Thirty-eight SD rats (8-week-old, male) were intraperitoneally injected with streptozotocin (STZ). Diabetes was successfully induced in 36 of them. The diabetes rats were randomly divided into untreated diabetes group and treated diabetes group. Eighteen healthy SD rats (8-week-old, male) served as controls. The body weight and the levels of blood glucose and glycosylated hemoglobin were measured. At the end of week 1 and week 10, 9 rats were sacrificed in each group. The gastric emptying rate and the levels of malondialdehyde (MDA),superoxide dismutase (SOD), tumor necrosis factor α (TNF-α), tyrosine kinase receptor c-Kit and stem cell factor (SCF) in gastric smooth muscle were analyzed. The apoptosis of ICC in gastric tissues was detected by the methods of immunocytochemistry and TUNEL. RESULTS: Compared with control group, gastric motility and SOD activity in untreated diabetes group were significantly weakened, the levels of MDA and TNF-α increased, the levels of c-Kit and SCF decreased, and apoptosis of ICC enhanced. In treated diabetes group, the oxidative stress level was attenuated, antioxidant capacity was enhanced, the levels of c-Kit and SCF were significantly increased, and the ICC apoptosis was reduced. Gastric motility was significantly improved after antioxidant therapy. CONCLUSION: Hyperglycemia affects the expression of antioxidant enzymes in the stomachs of diabetic rats. Oxidative stress is caused by hyperglycemia and is an important factor in the etiology of gastric motility dysfunction in diabetic rats, which may be correlated with the augmentation of ICC apoptosis resulting from oxidative stress-induced c-Kit/SCF damage.  相似文献   

5.
WAN Jun-li 《园艺学报》2000,16(3):237-242
AIM: To determine the effects of anisodamine (Ani) administered intraperitoneally on the gastric mucosal lesion induced by reserpine.METHODS:In reserpine-treated rats, gastric mucosal lesion, gastric acid secretion, gastric barrier mucus secretion, gastric contraction, gastric mucosal blood flow (GMBF), gastric mucosal nitric oxide synthase (NOS) activity and nitric oxide (NO) content were examined.RESULTS:Ani in doses of 1,5 and 10 mg/kg significantly inhibited the formation of gastric lesions induced by reserpine, with the suppressive rate of 60.0%, 66.7% and 76.6%, respectively. Ani (10 mg/kg) significantly inhibited the secretion of gastric acid, but had no effect on the volume of gastric juice. Ani (10 mg/kg) significantly prompted the secretion of gastric barrier mucus. Our findings also showed that Ani (10 mg/kg) significantly suppressed the frequency and amplitude of gastric contraction. Ani (10 mg/kg) significantly prompted GMBF. In reserpine treated rats, gastric mucosal NOS activity and NO content were decreased and Ani (10 mg/kg) could inhibit the decrease in NOS activity and NO content.CONCLUSIONS:The protective effect of Ani may results in part from inhibiting gastric acid secretion, prompting gastric barrier mucus secretion, suppressing gastric contraction and improving GMBF. NO seems to play an important mediator role in the Ani protective mechanisms.  相似文献   

6.
AIM: To explore the effects of ghrelin on the brain edema, the permeability of blood-brain barrier (BBB) and the expression of aquaporin 4 (AQP4) after cerebral ischemia/reperfusion in rats. METHODS: Adult male Sprague-Dawley rats were randomly divided into sham operation group, middle cerebral artery occlusion (MCAO) group and ghrelin treatment group. The MCAO model was made with nylon thread for 2 h of occlusion following 22 h of reperfusion. Ghrelin at a dose of 10 nmol/kg was injected via femoral vein at the beginning of reperfusion. The cerebral infarct volume was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Brain functional deficits were evaluated by determining the neurological scores. The changes of brain swelling and water content were analyzed through volume calculation and dry/wet weight measurement. The permeability of BBB was detected by collecting extravascular Evans blue (EB) in the brain cortex. The changes of AQP4 expression were assessed by the methods of immunohistochemistry and Western blotting. RESULTS: Compared with MCAO group, the rats in ghrelin treatment group had smaller brain infarct volume, lower EB exudation content and neurological scores. The percentage of brain swelling, water content and AQP4 expression were lower in ghrelin treatment group than those in MCAO group. CONCLUSION: Ghrelin reduces the injury of cerebral ischemia/reperfusion, and lightens the brain edema and BBB damage in rats. Ghrelin also inhibits the expression of AQP4 in brain tissue.  相似文献   

7.
AIM: To investigate the effect of ghrelin on inducible nitric oxide synthase (iNOS) expression in alveolar macrophages and lung tissues in sepsis-induced acute lung injury (ALI) rats. METHODS: The septic rat model was established by cecal ligation and puncture (CLP). Male SD rats were divided into sham group, CLP group and CLP+ghrelin group. The rats in the former 2 groups were further divided into 3 subgroups, which were 6 h, 12 h and 20 h post-operation groups. Ghrelin was administered by intraperitoneal injection at 3 h and 15 h after operation in ghrelin group. The samples were harvested 20 h after operation. The mRNA expression of iNOS in alveolar macrophages collected from bronchoalveolar lavage was detected by RT-PCR. The protein levels of lung iNOS were measured by Western blotting. The lung pathological examination was performed 20 h after operation. RESULTS: In CLP group, the mRNA expression levels of iNOS in the alveolar macrophages were 1.33±0.05, 1.44±0.08, 1.57±0.11 at 6 h, 12 h and 20 h after CLP, respectively, which were higher than that in sham group, but did not show time correlation. However, it was lower in CLP group than that in CLP+ghrelin group at 20 h after CLP (2.27±0.37, P<0.05). At 20 h after CLP, the protein level of lung iNOS was decreased in CLP+ghrelin group (0.87± 0.03) as compared with CLP group (1.08±0.05). Compared with sham group, the histopathological score was increased in both CLP group and CLP+ghrelin group, but it was lower in CLP+ghrelin group (5.83±0.477) than that in CLP group (7.83±0.75). CONCLUSION: Ghrelin treatment improves the degree of ALI. During 6 h to 20 h after CLP, the mRNA expression of iNOS in alveolar macrophages was elevated, but the difference was not seen as the time went on. Ghrelin up-regulates the mRNA expression of iNOS in alveolar macrophages and inhibits iNOS expression in lungs of septic rats.  相似文献   

8.
AIM: To investigate the role of the nucleus tractus solitarius (NTS) in the regulation of paraventricular nucleus (PVN) AVP-ergic neurons on gastric ischemia- reperfusion injury (GI-RI). METHODS: Male SD rats were used in experiments. The celiac artery were clamped for 30 min and reperfused 1 h by removal of the clamp to obtain the ischemia-reperfusion state. The mechanism was analysed with nucleus electrical stimulation, electrolytic lesion and nucleus microinjection technique. RESULTS: Microinjection of arginine-vasopressin (AVP) into PVN obviously attenuated the GI-RI and dose-dependent effects were observed (r=-0.477, P<0.05) ; NTS lesion or microinjection of AVP antagonist into NTS both eliminated the attenuate effect of electrical stimulation of PVN on GI-RI. The effect of microinjection of AVP into NTS was similar to microinjection of AVP into PVN. CONCLUSION: The NTS participates in regulation of PVN AVP-ergic on GI-RI, which is mediated by the AVP receptor in the NTS.  相似文献   

9.
AIM:To study the role of ghrelin in cell protection by up-regulating heat shock protein 70 (HSP70) and inhibiting apoptosis induced by oxidative stress through extracellular regulated protein kinases 1/2 (ERK1/2) signaling pathway in the PC12 cells. METHODS:Sodium nitoprusside (SNP) was used to induce oxidative stress injury in the PC12 cells. The cultured PC12 cells were divided into SNP-injured group (incubated with SNP at 0.5 mmol/L for 6, 12, 18 and 24 h), ghrelin pretreatment group (ghrelin at 100 nmol/L was given 30 min before adding SNP); HSP70 inhibitor group (quercetin at 10 μmol/L was added 60 min before ghrelin treatment), ERK inhibitor group (ERK 1/2 inhibitor PD98059 was added 60 min before ghrelin treatment) and control group (added same amount of culture medium only). The apoptotic rate was detected by flow cytometry. The protein expression was determined by Western blot and immunocytochemistry. RESULTS:Compared with control group, the apoptotic rate of PC12 cells in SNP-injured group was significantly increased (P<0.05). Compared with SNP-injured group, ghrelin (100 nmol/L) pretreatment significantly inhibited SNP-induced apoptosis of PC12 cells (P<0.05), and significantly up-regulated the protein expression of HSP70 (P<0.05). Time-effect analysis showed that ghrelin had the most significant effect at 18 h after SNP injury. Quercetin, an inhibitor of HSP 70, significantly reduced the anti-apoptotic effect of ghrelin (P<0.05). Ghrelin pretreatment promoted the phosphorylation of ERK1/2. ERK1/2 inhibitor PD98059 significantly inhibited the effects of ghrelin on up-regulation of HSP70 expression (P<0.05). CONCLUSION:Ghrelin upregulates the expression of HSP70 and inhibits the apoptosis in the PC12 cells induced by oxidative stress by promoting the phosphorylation of ERK1/2.  相似文献   

10.
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   

11.
AIM: To discuss the relevance between the pathogenesis of diabetic gastroparesis and the large-conductance calcium-activated potassium channels (BKCa) in gastric smooth muscle cells. METHODS: The SD rats were randomly divided into control group and model group. The gastric smooth muscle cells of the SD rats were enzymatically isolated in a low calcium solution containing papain. The current was recorded by patch clamp single channel recording technique. The expression of KCNMA and KCNMB1 were observed by the method of immunohistochemistry. RESULTS: The value of BKCa single channel conductance was (220.10±10.90) pS; the channels had distinct voltage dependent and calcium dependent characteristics. In outside-out patch (Vm =+30 mV), the activation of BKCa was blocked by 200 nmol/L IbTX completely. Compared with control group, the open probability and amplitude of current in model group significantly increased, while the mean open time and mean close time significantly decreased. Compared with control group, the expression of KCNMB1 in model group was significantly increased. CONCLUSION: Up-regulation of β1-subunit and increase in BKCa functional activities may be associated with diabetes gastroparesis in rats.  相似文献   

12.
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   

13.
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   

14.
WANG Yue-hui  ZHU Shi-gong 《园艺学报》2001,17(12):1256-1259
Ghrelin is a novel growth hormone-releasing acylated brain-gut peptide, consisting of 28 amino acids, discovered and isolated from stomach.Ghrelin stimulates the release of growth hormone (GH) through the binding with growth hormone secretagogue receptor (GHSR) in the hypothalamus and anterior pituitary. The intensive results imply that ghrelin exists in brain and gastrointestinal tract, and that many other cells can secret ghrelin. Functionaly, ghrelin not only increase the GH release, but also is related to body growth energy metabolism, endocrine, blood circulation and some diseases.  相似文献   

15.
AIM: To investigate the regulation of ghrelin on the expression of ATP-binding cassette transporter A1 and G1 (ABCA1/ABCG1)during the foam cell formation. METHODS: The human monocytic leukemia cell line (THP-1)was chosen in our study. The differentiation of THP-1 cells into macrophages was induced by using phorbol myristate acetate (PMA). Macrophages were then incubated with oxidized LDL (ox-LDL)to generate foam cells. Ghrelin of different concentrations were treated at different time points during foam cell formation. The ABCA1/ABCG1 protein and mRNA levels were detected by Western blotting and RT-PCR. The effect of variance of cholesterol content was measured by zymochemistry via-fluorospectrophotometer. RESULTS: Ghrelin reduced the content of lipid droplet in foam cells, and increased the efflux of intracellular cholesterol significantly. Ghrelin increased ABCA1 protein mass and mRNA level in dose-dependent manner. The changes of ABCG1 protein and mRNA level were the same as ABCA1. CONCLUSION: Ghrelin interfere atherosclerosis by up-regulating the expression of ABCA1 and ABCG1.  相似文献   

16.
AIM:To investigate the effect of lansoprazole on gastric ulceration in rats. METHODS:Using the gastric ulcer model induced by hemorrhagic shock, restraint water-immersion stress and pylorus-ligature, the protective effect of lansoprazole (iv) on gastric ulceration was observed. RESULTS:Pretreatment with lansoprazole (7.5-60 mg/kg) significantly inhibited the formation of gastric ulcer in the three models in a dose-dependent manner. The autiulcer efficacy of lansoprazole was similar to that of omeprazole in the equal dose, but stronger than that of omeprazole for ulcer induced by water-immersion stress.CONCLUSION:The intravenously administered lansoprazole inhibited formation of experimental gastric ulcer in rats.  相似文献   

17.
AIM: To observe the effect of ginkgolide B (GB) on the intracellular calcium ion concentration (［Ca2+］i) and mitochondrial function of cultured rat retinal neurons in vitro.METHODS: in vitro primary culture of rat retinal neurons was used in the experiment. The apoptosis model of glutamate-induced retinal neurons was established and co-cultured with ginkgolide B. The ［Ca2+］i and mitochondrial membrane potential of the retinal neurons were detected by laser scanning confocal microscope.RESULTS: Glutamate decreased the survival rate of retinal neurons, increased the apoptosis and the ［Ca2+］i, lowered the mitochondrial membrane potential. The ［Ca2+］i was clearly diminished and the mitochondrial membrane potential was significantly increased with the GB intervention, and the apoptosis decreased significantly.CONCLUSION: GB protects retinal neurons from glutamate induced neurotoxicity. The effect of GB on retinal neurons might be due to its ability to decrease the ［Ca2+］i and increase mitochondrial membrane potential.  相似文献   

18.
AIM: To investigate the expression of E-cadherin and forkhead box protein O3a (FOXO3a) in gastric cancer tissues and cells, and its correlation with cell viability. METHODS: The expression of E-cadherin and FOXO3a was detected by immunohistochemical staining in 53 specimens of gastric cancer tissues and their adjacent tissues, and the relationship between their expression and clinicopathological characteristics were analyzed. E-cadherin-over-expressing gastric cancer AGS cells were constructed by lentivirus-mediated cell transfection, and the protein expression of E-cadherin and FOXO3a was detected by immunocytochemistry method. The expression of E-cadherin, FOXO3a, Akt, Bcl-2 and Bax was determined by Western blot. The cell viability was detected by CCK-8 assay. RESULTS: The positive expression rates of E-cadherin and FOXO3a proteins in gastric cancer tissues were both significantly lower than those in their adjacent tissues (P<0.05). E-cadherin positive expression in gastric cancer tissues was significantly related to tumor grade and TNM stage (P<0.05), but not related to age, sex, location, T stage or lymph node metastasis. FOXO3a positive expression was significantly related to tumor grade (P<0.05), but not related to age, sex, location, TNM stage, T stage or lymph node metastasis. The expression of E-cadherin was positively correlated with FOXO3a expression in gastric cancer tissues (r=0.376, P=0.003). After over-expression of E-cadherin, the viability of gastric cancer AGS cells was significantly inhibited, the expression of FOXO3a, Bcl-2 and Bax was significantly increased, and the expression of Akt was significantly decreased. CONCLUSION: E-cadherin and FOXO3a are involved in the development of gastric cancer, and E-cadherin may affect the viability of gastric cancer cells by regulating Akt/FOXO3a signaling pathway.  相似文献   

19.
AIM: To investigate the clinical significance of microRNA-326 (miRNA-326) expression in gastric carcinoma and the effect of up-regulation of its expression on the viability and apoptosis of gastric cancer cells. METHODS: The expression of miRNA-326 in 55 tissue samples of gastric cancer was detected by RT-qPCR, and the relationship between the expression and the clinicopathological features was analyzed. The expression of miRNA-326 in gastric cancer BGC-823 cells was detected by RT-qPCR. The BGC-823 cells were transfected by liposome method, and randomly divided into normal control group (untransfected), mimic-NC group (transfected with negative control mimic) and miRNA-326 mimic group (transfected with miRNA-326 mimic). After up-regulation of miRNA-326 expression, the cell viability was measured by CCK-8 assay, and the apoptosis of the cells was analyzed by flow cytometry. The protein levels of matrix metalloprotein 9 (MMP-9), p21, cyclin D1, Bcl-2 and cleaved caspase-3 were determined by Western blot, and the mRNA expression of cyclin D1 was detected by RT-qPCR. Whether CCND1 (the gene of cyclin D1) was the target gene of miRNA-326 was evaluated by dual-luciferase reporter assay. RESULTS: The expression of miRNA-326 in the gastric cancer tissues was significantly lower than that in the adjacent tissues (P<0.05). The miRNA-326 expression had a significant correlation with the tumor size, lymph node metastasis, differentiation, and clinical stages (P<0.05), but it had no correlation with the age and sex of the patients. Moreover, the expression of miRNA-326 was also closely related to the survival rate of the patients (P<0.05). The expression of miRNA-326 in the BGC-823 cells was significantly lower than that in the normal gastric mucosa GES-1 cells (P<0.05). Compared with normal control group, the expression of miRNA-326 in mimic-NC group did not change significantly, while that in miRNA-326 mimic group was increased significantly (P<0.05). Compared with normal control group, the cell viability in miRNA-326 mimic group was significantly decreased, and the apoptosis was increased (P<0.05). In addition, compared with normal control group, the protein levels of MMP-9, cyclin D1 and Bcl-2, and the mRNA expression of cyclin D1 in miRNA-326 mimic group were decreased, while the protein levels of p21 and cleaved caspase-3 were increased (P<0.05). However, no significant difference of above protein and mRNA levels between mimic-NC group and normal control group was observed. Compared with mimic-NC+miR-326 mimic group, the activity of luciferase in the cells transfected with pmiR-CCND1-WT plasmid was significantly decreased (P<0.05), but that in the cells transfected with pmiR-CCND1-Mut plasmid did not change significantly. CONCLUSION: The expression level of miRNA-326 in gastric cancer tissues is low, and it may promote cell viability and inhibit cell apoptosis by targeting CCND1.  相似文献   

20.
AIM: To study the relationship between IL-1B-511 single nucleotide polymorphism,H.pylori infection,and gastric atrophy in high prevalent (Shanxi) region in China.METHODS: Five hundred healthy volunteers from Shanxi Province of China were recruited in this study,which were divided into five subgroups according to age,namely age 20-29,30-39,40-49,50-59 and >60 years,respectively.Genomic DNA was extracted from peripheral blood.IL-1B-511 single nucleotide polymorphism was analyzed by PCR-RFLP.Serum pepsinogen was used as a biomarker of gastric atrophy.Serum pepsinogen Ⅰ (PGⅠ),pepsinogen Ⅱ (PGⅡ) and anti-H.pylori IgG were determined by an ELISA assay.RESULTS: The mean serum PGⅠ concentration and ratio of PGⅠ /PGⅡ decreased gradually with increasing age,and were lower in subjects with IL-1B-511 T/T genotype and H.pylori infection than those without H.pylori infection in each subgroup,respectively (All P<0.05).Multiple linear regression showed that IL-1B-511 T/T genotype,age and Hp infection were significantly associated with gastric atrophy (P<0.05,P<0.05 and P<0.01,respectively).CONCLUSION: Gastric atrophy is closely correlated with IL-1B-511 T/T genotype,age,H.pylori infection in high prevalence region of gastric cancer in China.The risk of gastric atrophy is significantly increased for the IL-1B-511 T/T genotype with Hp infection.  相似文献   

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