脓毒败血症（sepsis）是一种高发病率和死亡率的急性综合征，以广泛的炎症反应及感染的器官细胞死亡为特征，最终导致多器官功能衰竭（multiple organ failure，MOF），其中肝损伤是多器官功能衰竭的一个重要标志。氧化应激、线粒体功...脓毒败血症（sepsis）是一种高发病率和死亡率的急性综合征，以广泛的炎症反应及感染的器官细胞死亡为特征，最终导致多器官功能衰竭（multiple organ failure，MOF），其中肝损伤是多器官功能衰竭的一个重要标志。氧化应激、线粒体功能障碍、展开更多
Objective To study the signaling transduction mechanism of leptin, including phosphatidylinositol 3-kinase/AKT (PI3-K/AKT) and cPLA2 signal pathway. Methods MTT colorimetric assay and Annexin V-FITC/PI double staining...Objective To study the signaling transduction mechanism of leptin, including phosphatidylinositol 3-kinase/AKT (PI3-K/AKT) and cPLA2 signal pathway. Methods MTT colorimetric assay and Annexin V-FITC/PI double staining for flow cytometry were used to demonstrate the inhibitory effect of leptin on lipopolysaccharide(LPS)-induced toxicity and apoptosis of thymocytes with a cPLA2 activity kit. RT-PCR was performed to show the suppressive effect of leptin on cPLA2 activity and cPLA2 mRNA level in proteins and genes. Effect of a specific inhibitor (LY294002) of PI3-K on apoptosis of thymocytes was detected by flow cytometry. Caspase3 mRNA was determined by RT-PCR. Results Leptin inhibited lipopolysaccharid(eLPS)-induced toxicity and apoptosis of thymocytes, decreased the cPLA2 activity and cPLA2 mRNA level in proteins and genes. Conclusion Leptin inhibits toxicity and apoptosis of thymocytes through the PI3-K/AKT and cPLA2 signal pathway.展开更多
基金supported by the National Natural Science Foundation of China(30670821)The National Key Technology R&D Program(2006BAF07B01)
文摘Objective To study the signaling transduction mechanism of leptin, including phosphatidylinositol 3-kinase/AKT (PI3-K/AKT) and cPLA2 signal pathway. Methods MTT colorimetric assay and Annexin V-FITC/PI double staining for flow cytometry were used to demonstrate the inhibitory effect of leptin on lipopolysaccharide(LPS)-induced toxicity and apoptosis of thymocytes with a cPLA2 activity kit. RT-PCR was performed to show the suppressive effect of leptin on cPLA2 activity and cPLA2 mRNA level in proteins and genes. Effect of a specific inhibitor (LY294002) of PI3-K on apoptosis of thymocytes was detected by flow cytometry. Caspase3 mRNA was determined by RT-PCR. Results Leptin inhibited lipopolysaccharid(eLPS)-induced toxicity and apoptosis of thymocytes, decreased the cPLA2 activity and cPLA2 mRNA level in proteins and genes. Conclusion Leptin inhibits toxicity and apoptosis of thymocytes through the PI3-K/AKT and cPLA2 signal pathway.
