AIM: To investigate the effects of ketamine anesthesia on the motility alterations and tissue injury caused by ischemia/reperfusion in rats. METHODS: Thirty male Wistar rats weighing 200-250 g were used. Ischemia was ...AIM: To investigate the effects of ketamine anesthesia on the motility alterations and tissue injury caused by ischemia/reperfusion in rats. METHODS: Thirty male Wistar rats weighing 200-250 g were used. Ischemia was induced by ob-structing blood flow in 25% of the total small intesti-nal length (ileum) with a vascular clamp for 45 min, after which either 60 min or 24 h of reperfusion was allowed. Rats were either anesthetized with pento-barbital sodium (50 mg/kg) or ketamine (100 mg/kg). Control groups received sham surgery. After 60 min of reperfusion, the intestine was examined for mor-phological alterations, and after 24 h intestinal basic electrical rhythm (BER) frequency was calculated, and intestinal transit determined in all groups. RESULTS: The intestinal mucosa in rats that were anesthetized with ketamine showed moderate altera-tions such as epithelial lifting, while ulceration and hemorrhage was observed in rats that received pento-barbital sodium after 60 min of reperfusion. Quantita-tive analysis of structural damage using the Chiu scaleshowed significantly less injury in rats that received ketamine than in rats that did not (2.35 ± 1.14 vs 4.58 ± 0.50, P < 0.0001). The distance traveled by a mark-er, expressed as percentage of total intestinal length, in rats that received pentobarbital sodium was 20% ± 2% in comparison with 25.9% ± 1.64% in rats that re-ceived ketamine (P = 0.017). BER was not statistically different between groups. CONCLUSION: Our results show that ketamine anesthesia is associated with diminished intestinal injury and abolishes the intestinal transit delay induced by ischemia/reperfusion.展开更多
Objective: To observe the anti inflammatory effect of cerivastatin in a mouse model of vascular injury and its cholesterol lowering effect. Methods: We developed a mouse model of vascular remodeling induced by polyeth...Objective: To observe the anti inflammatory effect of cerivastatin in a mouse model of vascular injury and its cholesterol lowering effect. Methods: We developed a mouse model of vascular remodeling induced by polyethylene cuff placement and determined the anti inflammatory effects of cerivastatin in wild mice. Cerivastatin was given by Alzet micro osmotic minipumps implanted intraperitoneally at the same time as cuff placement at doses of 0.1 mg/kg, 0.5 mg/kg and 1 mg/kg per day, respectively for 2 weeks after cuff placement. The insufficient doses of Cerivastatin to lower serum cholesterol and systolic blood pressure through the neointimal formation and BrdU index were investigated in mouse femoral injury artery induced by cuff placement. Results: There was a little change in serum cholesterol by the treatment with cerivastatin, the cross sectional area of intima of injured femoral artery was significantly increased, the neointima formation was significantly increased by the cuff induced vascular injury at day 14. The neointimal formation and BrdU index were inhibited in the 1 mg/kg cerivastatin, but not in the 0.1 mg/kg and 0.5 mg/kg cerivastatin. Furthermore, 1 mg/kg of cerivastatin significantly inhibited the expression of tumor necrosis factor α (TNF α) and interleukin 1β (IL 1β) without lowering serum cholesterol. Conclusions: These results suggest that cerivastatin can inhibit vascular inflammation and the proliferation of vascular smooth muscle cells (VSMCs) through its lipid lowering independent action. Such effects of cerivastatin may be an important mechanism, by which it prevents the development of atherosclerotic lesions.展开更多
Alcohol consumption causes significant liver damage,including hepatitis,fibrosis,cirrhosis,and even primary liver carcinoma.Metadoxine(MTDX)is considered to be a beneficial treatment for alcoholic liver disease(ALD)be...Alcohol consumption causes significant liver damage,including hepatitis,fibrosis,cirrhosis,and even primary liver carcinoma.Metadoxine(MTDX)is considered to be a beneficial treatment for alcoholic liver disease(ALD)because it accelerates the metabolism and elimination of ethanol.However,the underlying mechanism is not well understood.Here,the rat model of ALD was developed by feeding with 50%ethanol at the dose of 5 g/kg,and samples of serum and liver tissue were collected to test the levels of liver injury and inflammation and evaluate the hepatoprotective function of MTDX in alcohol-induced liver injury.Further investigation on the infiltration of immune cells was performed to understand the potential hepatoprotective mechanism of MTDX in the ALD model.The results showed that MTDX attenuated liver injury,evidenced by decreased levels of alanine transaminase(ALT),aspartate aminotransferase(AST),and alkaline phosphatase(ALP).Meanwhile,the liver proinflammatory environment was improved after MTDX treatment,evidenced by decreased levels of TNF-α,IL-6,and NLRP3 in the liver tissue.Furthermore,inhibited infiltrations of macrophages and neutrophils were observed in MTDX-treated ALD rats compared with the untreated ALD rats.Our results indicated that MTDX played an important role in preventing the progression of ALD,and the underlying mechanisms might be related to its function of attenuating liver inflammation by inhibiting immune cell infiltration.展开更多
文摘AIM: To investigate the effects of ketamine anesthesia on the motility alterations and tissue injury caused by ischemia/reperfusion in rats. METHODS: Thirty male Wistar rats weighing 200-250 g were used. Ischemia was induced by ob-structing blood flow in 25% of the total small intesti-nal length (ileum) with a vascular clamp for 45 min, after which either 60 min or 24 h of reperfusion was allowed. Rats were either anesthetized with pento-barbital sodium (50 mg/kg) or ketamine (100 mg/kg). Control groups received sham surgery. After 60 min of reperfusion, the intestine was examined for mor-phological alterations, and after 24 h intestinal basic electrical rhythm (BER) frequency was calculated, and intestinal transit determined in all groups. RESULTS: The intestinal mucosa in rats that were anesthetized with ketamine showed moderate altera-tions such as epithelial lifting, while ulceration and hemorrhage was observed in rats that received pento-barbital sodium after 60 min of reperfusion. Quantita-tive analysis of structural damage using the Chiu scaleshowed significantly less injury in rats that received ketamine than in rats that did not (2.35 ± 1.14 vs 4.58 ± 0.50, P < 0.0001). The distance traveled by a mark-er, expressed as percentage of total intestinal length, in rats that received pentobarbital sodium was 20% ± 2% in comparison with 25.9% ± 1.64% in rats that re-ceived ketamine (P = 0.017). BER was not statistically different between groups. CONCLUSION: Our results show that ketamine anesthesia is associated with diminished intestinal injury and abolishes the intestinal transit delay induced by ischemia/reperfusion.
文摘Objective: To observe the anti inflammatory effect of cerivastatin in a mouse model of vascular injury and its cholesterol lowering effect. Methods: We developed a mouse model of vascular remodeling induced by polyethylene cuff placement and determined the anti inflammatory effects of cerivastatin in wild mice. Cerivastatin was given by Alzet micro osmotic minipumps implanted intraperitoneally at the same time as cuff placement at doses of 0.1 mg/kg, 0.5 mg/kg and 1 mg/kg per day, respectively for 2 weeks after cuff placement. The insufficient doses of Cerivastatin to lower serum cholesterol and systolic blood pressure through the neointimal formation and BrdU index were investigated in mouse femoral injury artery induced by cuff placement. Results: There was a little change in serum cholesterol by the treatment with cerivastatin, the cross sectional area of intima of injured femoral artery was significantly increased, the neointima formation was significantly increased by the cuff induced vascular injury at day 14. The neointimal formation and BrdU index were inhibited in the 1 mg/kg cerivastatin, but not in the 0.1 mg/kg and 0.5 mg/kg cerivastatin. Furthermore, 1 mg/kg of cerivastatin significantly inhibited the expression of tumor necrosis factor α (TNF α) and interleukin 1β (IL 1β) without lowering serum cholesterol. Conclusions: These results suggest that cerivastatin can inhibit vascular inflammation and the proliferation of vascular smooth muscle cells (VSMCs) through its lipid lowering independent action. Such effects of cerivastatin may be an important mechanism, by which it prevents the development of atherosclerotic lesions.
基金Jinan Technology Development Program(Grant No.201907035)。
文摘Alcohol consumption causes significant liver damage,including hepatitis,fibrosis,cirrhosis,and even primary liver carcinoma.Metadoxine(MTDX)is considered to be a beneficial treatment for alcoholic liver disease(ALD)because it accelerates the metabolism and elimination of ethanol.However,the underlying mechanism is not well understood.Here,the rat model of ALD was developed by feeding with 50%ethanol at the dose of 5 g/kg,and samples of serum and liver tissue were collected to test the levels of liver injury and inflammation and evaluate the hepatoprotective function of MTDX in alcohol-induced liver injury.Further investigation on the infiltration of immune cells was performed to understand the potential hepatoprotective mechanism of MTDX in the ALD model.The results showed that MTDX attenuated liver injury,evidenced by decreased levels of alanine transaminase(ALT),aspartate aminotransferase(AST),and alkaline phosphatase(ALP).Meanwhile,the liver proinflammatory environment was improved after MTDX treatment,evidenced by decreased levels of TNF-α,IL-6,and NLRP3 in the liver tissue.Furthermore,inhibited infiltrations of macrophages and neutrophils were observed in MTDX-treated ALD rats compared with the untreated ALD rats.Our results indicated that MTDX played an important role in preventing the progression of ALD,and the underlying mechanisms might be related to its function of attenuating liver inflammation by inhibiting immune cell infiltration.
