目的:探讨铁皮枫斗对高糖诱导人肾小球系膜细胞p-38MAPK表达的影响及其对糖尿病大鼠肾脏的保护作用。方法:以链脲佐菌素诱导建立糖尿病大鼠模型,给予不同剂量的铁皮枫斗混悬液,共8 w。观察各组大鼠的生化指标及肾脏组织病理学变化。体...目的:探讨铁皮枫斗对高糖诱导人肾小球系膜细胞p-38MAPK表达的影响及其对糖尿病大鼠肾脏的保护作用。方法:以链脲佐菌素诱导建立糖尿病大鼠模型,给予不同剂量的铁皮枫斗混悬液,共8 w。观察各组大鼠的生化指标及肾脏组织病理学变化。体外培养HMC细胞,分别加入正常浓度葡萄糖、甘露醇、高糖及不同浓度的铁皮枫斗,观察p-38MAPK的活性及下游TGF-β1、CTGF的表达。结果:动物实验发现,与模型组比较,铁皮枫斗各组大鼠的肾脏指数、Scr、BUN、24 h UP、肾皮质MDA等指标均显著降低(P<0.05或P<0.01),肾脏组织病理学改善明显,大鼠肾皮质中TGF-β1、CTGF的表达显著降低,SOD活性显著升高(P<0.05或P<0.01)。体外实验发现,与高糖组比较,铁皮枫斗各组p-38MAPK、TGF-β1、CTGF表达显著降低(P<0.05或P<0.01)。结论:铁皮枫斗可能通过p-38MAPK-TGF-β-CTGF通路抑制糖尿病肾病中肾纤维化,发挥保护肾脏的作用。展开更多
Objective: To study the molecular mechanisms of TNF--a expression induced by lipopolysaccharide (LPS) for exploring novel methods to prevent or treat clinical patients with endotoxic shock. Methods:Protein kinase assa...Objective: To study the molecular mechanisms of TNF--a expression induced by lipopolysaccharide (LPS) for exploring novel methods to prevent or treat clinical patients with endotoxic shock. Methods:Protein kinase assay was used to detect the kinase activity stimulated by LPS; Con focal laser scan technique was used to show the translocation of p38 on the activation; RT PCR and reporter gene system were used to study the molecular mechanism of TNF -a gene transcription. Results: In RAW cells it was found that p38 was activated on the stimulation of LPS. and activated p38 moved into nucleus from cytosol; TNF--a mRNA increased on the stimulation of LPS and the increased promoter transactivity induced by LPS could be inhibited significantly by specific inhibitor for p38. Conclusion: p38 mitogen activated protein kinase (MAPK ) was activated by the stimulation of LPS,which brought about its entry to the nucleus to act on transcription factors to regulate cellular processes. p38 MAPK Is an important regulator of TNF--a gene expression induced by LPS.展开更多
目的探讨人参二醇组皂苷(PDS)20(s)对大脑中动脉梗塞(MCAO)老年小鼠p-erk1/2、p-JNK2、P-38蛋白表达的影响及其机制。方法 C57BL/6老年小鼠40只,制备老年小鼠MCAO模型,随机分为4组:90 min MCAO组、PDS小剂量组、PDS中剂量组、PDS大剂量...目的探讨人参二醇组皂苷(PDS)20(s)对大脑中动脉梗塞(MCAO)老年小鼠p-erk1/2、p-JNK2、P-38蛋白表达的影响及其机制。方法 C57BL/6老年小鼠40只,制备老年小鼠MCAO模型,随机分为4组:90 min MCAO组、PDS小剂量组、PDS中剂量组、PDS大剂量组,应用激光多普勒血流仪进行术中脑血流监测,应用Western印迹方法观察各组p-erk1/2、p-JNK2、P-38蛋白表达的变化。结果与90 min MCAO组比较,中、大剂量PDS组p-erk1/2、p-JNK2蛋白表达明显增高,P-38蛋白表达无变化。结论 PDS促进MCAO老年小鼠脑p-erk1/2、p-JNK2蛋白表达早期明显升高。展开更多
文摘目的:探讨铁皮枫斗对高糖诱导人肾小球系膜细胞p-38MAPK表达的影响及其对糖尿病大鼠肾脏的保护作用。方法:以链脲佐菌素诱导建立糖尿病大鼠模型,给予不同剂量的铁皮枫斗混悬液,共8 w。观察各组大鼠的生化指标及肾脏组织病理学变化。体外培养HMC细胞,分别加入正常浓度葡萄糖、甘露醇、高糖及不同浓度的铁皮枫斗,观察p-38MAPK的活性及下游TGF-β1、CTGF的表达。结果:动物实验发现,与模型组比较,铁皮枫斗各组大鼠的肾脏指数、Scr、BUN、24 h UP、肾皮质MDA等指标均显著降低(P<0.05或P<0.01),肾脏组织病理学改善明显,大鼠肾皮质中TGF-β1、CTGF的表达显著降低,SOD活性显著升高(P<0.05或P<0.01)。体外实验发现,与高糖组比较,铁皮枫斗各组p-38MAPK、TGF-β1、CTGF表达显著降低(P<0.05或P<0.01)。结论:铁皮枫斗可能通过p-38MAPK-TGF-β-CTGF通路抑制糖尿病肾病中肾纤维化,发挥保护肾脏的作用。
文摘Objective: To study the molecular mechanisms of TNF--a expression induced by lipopolysaccharide (LPS) for exploring novel methods to prevent or treat clinical patients with endotoxic shock. Methods:Protein kinase assay was used to detect the kinase activity stimulated by LPS; Con focal laser scan technique was used to show the translocation of p38 on the activation; RT PCR and reporter gene system were used to study the molecular mechanism of TNF -a gene transcription. Results: In RAW cells it was found that p38 was activated on the stimulation of LPS. and activated p38 moved into nucleus from cytosol; TNF--a mRNA increased on the stimulation of LPS and the increased promoter transactivity induced by LPS could be inhibited significantly by specific inhibitor for p38. Conclusion: p38 mitogen activated protein kinase (MAPK ) was activated by the stimulation of LPS,which brought about its entry to the nucleus to act on transcription factors to regulate cellular processes. p38 MAPK Is an important regulator of TNF--a gene expression induced by LPS.
文摘目的探讨人参二醇组皂苷(PDS)20(s)对大脑中动脉梗塞(MCAO)老年小鼠p-erk1/2、p-JNK2、P-38蛋白表达的影响及其机制。方法 C57BL/6老年小鼠40只,制备老年小鼠MCAO模型,随机分为4组:90 min MCAO组、PDS小剂量组、PDS中剂量组、PDS大剂量组,应用激光多普勒血流仪进行术中脑血流监测,应用Western印迹方法观察各组p-erk1/2、p-JNK2、P-38蛋白表达的变化。结果与90 min MCAO组比较,中、大剂量PDS组p-erk1/2、p-JNK2蛋白表达明显增高,P-38蛋白表达无变化。结论 PDS促进MCAO老年小鼠脑p-erk1/2、p-JNK2蛋白表达早期明显升高。
