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ZHAO Min  MENG Xing 《园艺学报》2005,21(8):1587-1589
AIM: To study the protective effect of glutamine (Gln) against endotoxemia by observing the effect of glutamine on heat shock proteins (HSPs) and tumor necrosis factor-α (TNF-α) in endotoxemic rats. METHODS: The rats were randomly divided into 3 groups, lipopolysaccharide group (LPS), glutamine-treated group (Gln) and control group (C). The blood was drawn from lateral tail vein for analysis of cytokine levels at 0, 2, 4 and 6 h post-lipopolysaccharide (LPS) challenge. TNF-α was measured by radioimmunity assay. Multiple tissues were harvested from the rats, and HSP70 was detected by immunohistochemistry. At the same time, lung, liver, and ileum tissue section were stained with hematoxylin and eosin. RESULTS: Gln treatment resulted in marked attenuation of TNF-α expression at 2 h post-LPS injection (P<0.01). Gray gradients of HSP70 in lungs, liver and ileum tissue in group Gln were much lower than those of group LPS (P<0.05), This suggested that HSP70 content in these tissues of group Gln was higher than that of group LPS. Tissue sample from lung, liver and ileum revealed significantly less evidence of endotoxin-induced tissue damage in Gln-treated animals. CONCLUSION: Gln can significantly enhance HSP70 expression in multiple tissues of endotoxin-treated rats. A single dose of intravenous Gln given concomitantly with an endotoxin injury can markedly reduce organ histological damage, and attenuate pro-inflammatory cytokine release.  相似文献   

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AIM:To approach the relationship between the expression of intercellular adhesion (ICAM-1 mRNA) and acute lung injury (ALI) as well as the mechanisms of rhubarb in the prevention and treatment of the lung injury. METHODS:ALI animal model was performed by Lipopolysaccharide (LPS). The rats were divided into 4 groups: LPS group, control group, rhubarb+LPS group and dexamethasone+LPS group. Histopathological examination and biological markers were measured for the lung specimens. Molecular hybridization method was used to determine the expression of ICAM-1 mRNA. RESULTS:The ICAM-1 mRNA expression in the lung tissues of LPS group significantly increased compared with control group (P<0.01), rhubarb and dexamethasone had the action of decreasing the ICAM-1 mRNA expression (P<0.05, P<0.01); pathologic changes and the biological markers of ALI significantly decreased or ameliorated. CONCLUSION:The increase in the expression of ICAM-1 mRNA in the lung tissues of ALI is involved in the formation of ALI. Rhubarb and dexamethasone can ameliorate the lung damage, mechanism of which may be related to the inhibition of ICAM-1 mRNA expression.  相似文献   

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AIM: To investigate the dynamic expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN) in liver tissue in the process of hepatic fibrosis in rats. METHODS: The rat model of hepatic fibrosis used in this study was induced by common bile duct ligation (BDL). Hematoxylin and eosin (HE) and Masson’s trichrome staining were used for observing the histological changes in hepatic fibrosis tissue. At 4 time points, the expressions of PTEN protein and mRNA in hepatic tissues of rats were detected by immunohistochemical staining, Western blotting and real-time fluorescent quantitative PCR assay, respectively. RESULTS: The rat model of hepatic fibrosis was established successfully. With each consecutive week after BDL, increased fibrosis, degeneration and necrosis were found in rat liver cells. Not surprisingly, a disruption of normal architecture and a decrease in normal hepatic cells was concomitantly observed. The immunohistochemical staining indicated that there was extensive expression of PTEN in liver tissues of normal rats, it expressed mainly in the cytoplasm, and with the aggravation of hepatic fibrosis, the expression of PTEN in liver tissues decreased gradually (P<0.01). Western blotting and real-time fluorescent quantitative PCR at weekly time points (1, 2, 3, and 4 weeks) after BDL showed that, the expression of PTEN protein and mRNA in fibrotic rat liver tissue decreased gradually with increasing severity of hepatic fibrosis (P<0.01). Furthermore, all values from BDL rats were significantly lower than those from the sham operation group (P<0.01). CONCLUSION: The expressions of PTEN protein and mRNA in fibrotic liver tissue of rat decrease gradually with the progression of hepatic fibrosis, and increasing severity of fibrosis correlated well with decreasing PTEN expression.  相似文献   

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AIM: To observe the level of metallothionein (MT) in liver, aorta and plasma of rabbit with atherosclerosis (AS) in order to recognize the alteration of oxidative defense system in body when AS occurred.METHODS:Preparation of AS model of rabbit induced by having high-fat diet for eight weeks; the levels of MT and malondialdehyde (MDA) were measured in the tissues of liver and aorta and plasma of rabbit.RESULTS:The MT levels in liver tissues and plasma in atherosclerotic group increased 318%(P<0.01) and 62% (P<0.01), compared with control group, but its level in aortic tissue in atherosclerotic group decreased 33% (P<0.01). The MDA levels in liver, aortic and plasma in atherosclerotic group increased 95%(P<0.01), 76%(P<0.01) and 42%(P<0.01), respectively, compared with control group. The changes of contents of MT in liver and plasma have relation with level of MDA in liver tissues and plasma.CONCLUSION:The alteration of MT in liver tissues and plasma in atherosclerotic rabbits may be related to lipid hyperoxidative injury.  相似文献   

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AIM:To study the effect of fructose-1, 6-diphosphate (FDP) on adriamycin(ADM)-induced cardiomyocyte apoptosis in rats. METHODS:Twenty-four Wistar rats were randomly divided into three groups: control group, ADM treated group and FDP intervention group. The contents of malondialdehyde (MDA) and NO2-/NO3-, the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD) were determined by colorimetric method in myocardial tissue, and the cardiomyocyte apoptosis was detected by TUNEL method in myocardial tissue, and the expression of inducible nitric oxide synthase (iNOS) mRNA, Bcl-2 mRNA and Bax mRNA in myocardial tissue were detected by in situ hybridization. RESULTS:The contents of NO2-/NO3- and MDA in myocardial tissue, the expressive levels of iNOS mRNA and Bax mRNA in cardiomyocyes and its apoptotic amounts in FDP intervention group were significantly lower than those in ADM treated group (P<0.01). However, the activities of SOD and GPx in myocardial tissue, the expressive level of Bcl-2 mRNA of cardiomyocytes in FDP intervention group were significantly higher than those in ADM treated group (P<0.01). CONCLUSION:FDP antagonized the reduced expression of Bcl-2 mRNA and increased expression of Bax mRNA in myocardial tissue induced by ADM, and in turn inhibited ADM-induced cardiomyocyte apoptosis.  相似文献   

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AIM:To study the effect of proliferating cell nuclear antigen (PCNA) expression on alveolar macrophages (AM) and Fas/FasL expression on alveolar type Ⅱ epithelial cells induced by lipopolysaccharide (LPS) in smoking rats. METHODS:Immunohistochemistry SABC and immunofluorescence techniques were used to examine PCNA expression on AM and Fas/FasL system expression on alveolar type Ⅱ epithelial cells in smoking rats of different stages induced by LPS. RESULTS:The AM PCNA expression in smoking rats reached the highest level after 3 or 4 months. The AM PCNA expression in every groups stimulated by LPS significantly increased ( P<0.01). The Fas/FasL system expression on alveolar type Ⅱepithelial induced by LPS were higher than control groups ( P<0.01). Both the AM PCNA expression and Fas/FasL system expression on alveolar type Ⅱ epithelial cells were parallel. CONCLUSION:Smoking caused the increase in proliferous rate of AM and it may play an important role in the regulation of the injury and repair of alveolar type Ⅱ epithelial cells.  相似文献   

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AIM: To explore the role of 78 kD glucose-regulated protein (GRP78) in the development of liver cirrhosis in rats promoted by intestinal endotoxemia (IETM). METHODS: Fifty-one male Wistar rats were randomly divided into liver cirrhosis groups of 4th-week, 6th-week and 8th-week, and normal control group at the corresponding time points. The rat model of hepatic cirrhosis was induced by employing multiple pathogenic factors to the animals. The liver injury and hepatic fibrosis were observed with the staining of HE and VG, respectively. The expression of GRP78 at the mRNA and protein levels was measured by the methods of RT-PCR and immnunohistochemistry, respectively. The concentrations of alanine aminotransferase(ALT), endotoxin, TNF-α and homocystine (HCY) in plasma, and the content of TNF-α, malondialdehyde(MDA) and PⅢP in liver tissues were detected. RESULTS: As liver cirrhosis developed, the levels of ALT, endotoxin, TNF-α and HCY in plasma, the expression of GRP78 at mRNA and protein, the content of TNF-α, MDA and PⅢP in liver tissues, and the index of liver fibrosis were gradually increased and were significantly higher than those in normal control group (P<0.05). Elevated endotoxin in plasma was correlated positively with the protein expression of GRP78, the content of MDA and HCY in plasma and the index of liver fibrosis (P<0.01). Elevated protein expression of GRP78 was correlated positively with the content of MDA and HCY in plasma and the index of liver fibrosis (P<0.01). CONCLUSION: GRP78 plays an important role in the development of liver cirrhosis. Endoplasmic reticulum stress is a possible mechanism in the development of liver cirrhosis promoted by IETM.  相似文献   

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AIM: To investigate the role of infiltration of macrophages and expression of intracellular adhesion molecule-1 in the pathogenesis of oleic-acid-induced acute lung injury rats. METHODS:The rats were subjected to injection of oleic acid (oleic acid group) or saline solution (control). After injecting oleic acid or saline for 4 hours, the PaO2 of the left heart, lung permeability index(LPI), the number of macrophage and the levels of soluble intercellular molecule-1 (sICAM-1) in the bronchial alveolar lavage fluid (BALF) were measured. The levels of expression of ICAM-1 mRNA were evaluated by in situ hybridization and the degree of macrophage infiltration and the expression of ICAM-1 were evaluated by double staining immunocytochemistry. RESULTS:The PaO2 of the oleic acid group was significantly lower than that of the control group (P<0.01) and the LPI of the oleic acid group was significantly higher than that of the control group (P<0.01). The cell number of macrophage and sICAM-1 level were significantly higher in the oleic acid group than those of the control group (P<0.01). There were marked upregulation of ICAM-1 mRNA expression in injuried lung tissue compared with the normal lung tissue. Furthermore, the infiltrated number of macrophage and the level of ICAM-1 expression showed strong positive correlation with the lung injury parameters, PaO2 and LPI.CONCLUSION:The infiltration of macrophage may play a pivotal role in the pathogenesis of progressive lung injuries induced by intravenous oleic acid injection,ICAM-1 may mediate the infiltrat ion and adhesion of macrophage in the injuried lung t issue and contribute to the development of acute lung injury.  相似文献   

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AIM:To investigate the correlation between the signal pathway of IKK/NF-κB and the anti-oxidant activity in asthmatic rats and the modulation of Ginkgo biloba extract (Egb). METHODS:Thirty-six male SD rats were randomly divided into three groups:control group (group C), asthmatic group (group A) and Egb group(group E). Asthma in rats was established by ovalbumin (OVA) challenge methods. The mRNA of IKKβ and the protein of NF-κB P65 in lung tissue were assessed by using in situ hybridization with oligonucleotide probe and immunohistochemisty, respectively. RESULTS:The expression of IKKβ mRNA and NF-κB P65 protein in group A were significantly increased when compared with group C (P<0.01, respectively), but those data in group E were significantly decreased when compared with group A (P<0.01, respectively). The concentrations of MDA in serum and BLAF in group A were significantly higher than those in control group (P<0.01,respectively), but the concentrations of MDA in group E were significantly lower than those in group A (P<0.01, respectively). The concentrations of GSH in group A were significantly lower than those in group C (P<0.01, respectively), but the concentrations of GSH in group E were significantly higher than those in group A (P<0.01, respectively). CONCLUSION:The expression of IKKβ mRNA and NF-κB P65 protein were increased significantly in asthmatic rats. This was possibly attributed to the decreased anti-oxidant activity. Egb increased the anti-oxidant activity and inhibited the activity of IKK/NF-κB.  相似文献   

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AIM: To investigate changes of the level of reactive oxygen species (ROS),malondialdehyde (MDA),transforming growth factor-β1 (TGF-β1) and platelet-derived growth factor (PDGF) expression in a rat hepatic fibrosis model and the effect of curcumin ,and discuss the mechanism of the prophylactic effect of curcumin on hepa tic fibrosis.METHODS: Rat models of hepatic fibrosis were established by intraperitoneally injection of carbon tetrachloride.Curcumin of 20 mg,10 mg,5mg per 100 gram weight of rat was given to these rats respectively at the same time.Normal,fibrosis model and positive groups were made as controls.After eight weeks,all rats were executed and the blood and liver were kept.Serum level of ROS was tested by chromatometry.Content of MDA in liver homogenate was tested by thiobarbituric acid (TBA) method.Expressions of TGF-β1 and PDGF in liver were detected by immunohistochemical method. RESULTS: Serum level of ROS in fibrotic group increased significantly compared with that of normal group,and which was depressed obviously in curcumin groups(P<0.05).Content of MDA in liver of curcumin group reduced significantly compared with that of fibrotic group (P<0.01).Expressions of TGF-β1 and PDGF in fibrotic group increased significantly compared with those of normal group,which were depressed obviously in curcumin groups (P<0.01).CONCLUSION: Curcumin could inhibit expression of TGF-β1,PDGF and lipid peroxidation in liver.These may be mechanisms of curcumin preventing hepatic fibrosis.  相似文献   

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AIM: To explore the molecular mechanism of panaxadiol saponin (PDS) by observing Toll like receptor (TLR) 2 and TLR9 mRNA expression induced by lipopolysaccharide (LPS).METHODS: Rats were divided into LPS, LPS+PDSL, LPS+PDSM and control group, respectively. Nitric oxide synthase (NOS) activity, nitric oxide (NO) content, LPO content, SOD activity and TLR2 and TLR9 mRNA expression were assayed 4 h after intravenous injection of LPS. RESULTS: NOS activity, NO content, LPO content of LPS+PDSL group and LPS+PDSM group were significantly lower than those in LPS group. TLR2 mRNA expression in the liver tissue of LPS+PDSL group and LPS+PDSM group was decreased compared with LPS group.CONCLUSION: PDS has a protective effect on liver tissues by triggering the down-regulation of TLR2 expression, reducing NOS activity, and NO content.  相似文献   

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AIM: To observe the changes of metallothionein (MT) in various tissues of mice during hyperhomocysteinemia. METHODS: Intraperitoneal injection of homocysteine into mice induced hyperhomocysteinemia. The contents of tissue MT and malondialdehyde (MDA) in liver, heart and kidney were determined. RESULTS: Compared with control group, tissue MT levels in Hcy-group animals were increased by 210% (P<0.01) for liver, by 133% (P<0.05) for heart and by 60% (P<0.01) for kidney. Tissue MDA contents were increased by 6%, 52%(P<0.05) and 69% (P<0.05), respectively. However, in treated animals with Hcy plus superoxide dismutase (SOD), the tissue MT contents in liver, heart and kidney were decreased by 22% (P<0.05), 33% (P<0.05) and 13% (P>0.05), respectively, compared with Hcy alone group. Tissue MDA contents were decreased by 24% (P<0.05), 21% (P<0.05) and 48% (P<0.01). There was a positive correlation between tissue MT content and MDA level. CONCLUSION: Hcy could induce tissue MT formation through oxidative stress.  相似文献   

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AIM:To investigate the effect of glycine on endotoxin and hypoxia-induced necrotizing exterocolitos (NEC) in rats. METHODS:In glycine+NEC group, twenty anesthetized and artificially ventilated rats received 1g/kg glycine (20%, iv). Five minutes later, the rats were treated with 2 mg/kg lipopolysaccharide (LPS). In control group (NS+NEC), twenty rats were treated with normal saline as a substitute for glycine. In all animals, FiO2 was reduced after 90 min from 21% to 5% and ventilation continued until 180 min or death. At the end of the experiment, the samples of blood and intestine were obtained immediately. Serum TNFα was measured with ELISA, serum NO was determined by nitrate reductase. The histopathology of the necrotic lesions were categoried: grade Ⅰ, focal mild injury confined to villous tips; grade Ⅱ, partial loss of villi; grade Ⅲ, necrosis extending to submucosa; grade Ⅳ, transmural necrosis. RESULTS:The survival time was shorter in the NS+NEC group (P<0.01). The intestinal injury of the rats in glycine+NEC group was markedly alleviated (P<0.01). The levels of TNF-α and NO2-/NO3- in serum decreased significantly in animals treated with glycine (P<0.01, P<0.05). CONCLUSION:Glycine alleviated LPS-induced NEC by inhibiting excessive production of TNFα and nitric oxide.  相似文献   

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AIM:To investigate the protective effect of ischemic preconditioning (IPC) on hepatic ischemia-reperfusion(I/R) injury in cirrhotic rats and its possible mechanism. METHODS:Hepatic I/R was induced by Pringle maneuver. The cirrhotic rats were randomized into three groups: Group A: before 30 min of ischemia, a short period of 5 min ischemia and 5 min reperfusion were given; Group B: before 30 min of ischemia, a short period of 10 min ischemia and 10 min of reperfusion were given; Group C: 30 min ischemia only. The serum alanine transferase (ALT), hepatic Fas-mRNA, caspase-3 activity and hepatocyte apoptosis were analyzed. RESULTS:The 7-day survival rate in the group A and B were 100%, respectively. However, it was only 62.5% in the group C. After 6 h of reperfusion, the ALT levels in both group A and B were significantly lower than that of in group C, P<0.01. The ALT level of group A was also lower than that of group B, P<0.01. The hepatic Fas-mRNA expression, caspase-3 activity and apoptotic hepatocyte in group A were significantly lower than those of in group C, P<0.01. CONCLUSIONS:IPC has significant protective effect against hepatic I/R injury. An IPC with 5 min of ischemia and 5 min of reperfusion has the maximal protective effect. The protective mechanism of IPC against hepatic I/R injury is via down-regulation of Fas-mRNA expression, inhibiting caspase-3 activity and subsequently inhibiting hepatocyte apoptosis.  相似文献   

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AIM: To investigate the role of hydrogen sulfide (H2S) in the cholecystokinin octapeptide (CCK-8) attenuating lipopolysaccharide (LPS)-induced lung injury. METHODS: A rat model of lung injury induced by intravenous injection of LPS was developed. Male Wistar rats were divided into normal control group, LPS group, LPS+CCK-8 group and CCK-8 group. Six hours after LPS injection, partial pressure of oxygen in the arterial blood (PaO2), H2S content and cystathionine-γ-lyase (CSE) activity in lung tissue were detected. The mRNA expression of CSE in lung tissue was determined by RT-PCR; the structure of lung tissues was observed under optical microscope. RESULTS: Compared to normal control rats, the LPS-treated rats had significantly decreased PaO2 level, increased index of quantitative assessment (IQA) score, while H2S content, CSE activity and the mRNA expression of CSE in lung tissue were significantly increased (all P<0.05). Administration of CCK-8 into LPS-treated rats increased the PaO2 level and alleviated the degree of lung injury (measured by IQA score). In addition, CCK-8 decreased H2S content, CSE activity, and the mRNA expression of CSE (all P<0.05). No significant difference of the above-mentioned parameters between CCK-8 group and normal control group was observed. CONCLUSION: CCK-8 reduces LPS-induced lung injury through inhibiting the generation of endogenous H2S.  相似文献   

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AIM:To observe the changes of interleukin-1 receptor associated kinase-4 (IRAK-4) in ischemia/reperfusion (I/R) liver pretreated with lipopolysaccharide (LPS) and to explore the protective mechanisms of LPS pretreatment against hepatic I/R injury. METHODS:Male Sprague-Dawley rats, weighing 240-280 g, were divided into three groups:control, ischemia/reperfusion group (I/R group) and LPS-pretreated group (LPS group). On the first day, LPS group received 0.1 mg/kg LPS via the tail vein, followed by 0.5 mg/kg on the 2nd, 3rd, 4th and 5th day. I/R group received the equivalent volumes (0.5 mL) of sterile PBS. Experiments of I/R injury was induced by temporary ischemia of the left lateral liver lobe for 90 min followed by 3 h reperfusion on 2 days after the last LPS treatment. At 0 min, 60 min and 180 min after reperfusion, the expression of IRAK-4 gene and protein level were determined by RT-PCR and Western blotting. The activity of NF-κB and the serum TNF-α level were also detected by ELISA. RESULTS:Although the level of IRAK-4 gene and protein were higher in the LPS group than that in I/R group and control group (P<0.01), no difference of the activities of NF-κB and the TNF-α level was observed between the LPS group and I/R group (P>0.05) at 0 min after reperfusion. However, all those indexes were evidently lower in the LPS group than those in I/R group (P<0.01) at 60 min and 180 min after reperfusion. CONCLUSION:This data suggests that the protective effects induced by LPS pretreatment against hepatic I/R injury may be via down-regulation of IRAK-4 expression.  相似文献   

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AIM: To investigate the effects of polysaccharides isolated from Aconiti tuber (Fuzi polysaccharides,FPS) on the prevention of hypercholesterolemia induced by high-cholesterol diet and the expression of hepatic cholesterol 7α-hydroxylase (cytochrome P450 7α-1, CYP7α-1) in rats.METHODS: Fifty male Wistar rats were randomly divided into 3 groups. The rats were fed with normal diet (control group), high-cholesterol diet (HC group) or high-cholesterol diet plus FPS (224, 448 or 896 mg·kg-1·d-1, FPS group) for 2 weeks. The serum lipid level, body weight, food-intake and fecal amount were measured at week 2. The pathological changes of the liver were observed with HE staining. The mRNA expression of hydroxy methylglutaryl coenzyme A (HMG-CoA) reductase and CYP7α-1, the protein level of CYP7α-1, and fecal bile acid were also detected at week 2.RESULTS: FPS significantly inhibited high-cholesterol diet-induced elevation of serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) (P<0.05). HE staining showed that FPS attenuated fatty degeneration in liver. Real-time PCR analysis showed that FPS significantly up-regulated the mRNA expression of CYP7α-1, but down-regulated the mRNA expression of HMG-CoA reductase (P<0.01). The protein level of CYP7α-1 was higher in FPS group than that in HC group (P<0.01). The level of fecal bile acid in HC-treated rats was higher than that in the control rats, and FPS stimulated the excretion of fecal bile acid (P<0.05).CONCLUSION: FPS significantly reduces serum cholesterol levels, which is associated with the up-regulation of hepatic CYP7α-1 expression and down-regulation of hepatic HMG-CoA reductase expression.  相似文献   

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