AIM: To investigate the effects of prednisolone on cell membrane bleb formation, calpain μ activation and talin degradation during hepatic ischemia-reperfusion injury in rats. METHODS: The hilar area of the left late...AIM: To investigate the effects of prednisolone on cell membrane bleb formation, calpain μ activation and talin degradation during hepatic ischemia-reperfusion injury in rats. METHODS: The hilar area of the left lateral and median lobes of rat liver (68%) was clamped for 60 min and followed by 120 min reperfusion. Prednisolone was administered at 1.0, 3.0, or 10 mg/kg at 30 min before ischemia. In addition to biochemical and microscopic analyses, activation of calpain μ was determined using specific antibodies against the intermediate (activated) form of calpain μ. Degradation of talin was also studied by Western blotting. RESULTS: In the control and prednisolone (1.0 mg/kg) groups, serum aspartate transaminase (AST) and alanine transaminase (ALT) level were elevated, and cell membrane bleb formation was observed after 120 min of reperfusion. Moreover, calpain μ activation and talin degradation were detected. Infusion of prednisolone at 3.0 or 10 mg/kg significantly suppressed serum AST and ALT, and prevented cell membrane bleb formation. At 10 mg/kg, prednisolone markedly suppressed calpain μ activation and talin degradation. CONCLUSION: Prednisolone can suppress ischemia- reperfusion injury of the rat liver. Its cytoprotective effect is closely associated with the suppression of calpain μ activation and talin degradation.展开更多
研究了改性小麦秸秆对赤潮异弯藻的去除作用和机制.结果表明,在与未改性秸秆相同用量(0.10 g/L)的情况下,在120 m in时,改性秸秆对赤潮异弯藻的去除率可以从10%左右提高到80%以上.为了探讨改性秸秆对赤潮异弯藻的去除机制,测定了核苷酸...研究了改性小麦秸秆对赤潮异弯藻的去除作用和机制.结果表明,在与未改性秸秆相同用量(0.10 g/L)的情况下,在120 m in时,改性秸秆对赤潮异弯藻的去除率可以从10%左右提高到80%以上.为了探讨改性秸秆对赤潮异弯藻的去除机制,测定了核苷酸在260 nm时的吸光度,结果发现水体内核苷酸物质浓度增大,说明在此作用过程中,藻细胞膜结构遭到破坏,核苷酸物质由胞内释放.当改性秸秆用量为0.15 g/L时,释放核苷酸在260nm时吸光度与正常细胞的吸光度比值为1.17,此时改性秸秆对赤潮异弯藻造成的损害是不可逆的.实验发现,改性秸秆对赤潮异弯藻同时具有吸附作用和灭杀作用.当浓度较低时,改性秸秆通过吸附细胞体,或者与细胞膜结合,从而导致部分藻细胞的絮凝;而当浓度进一步增加时,改性秸秆可以破坏细胞膜的结构,导致大量膜内物质的释放,进而导致藻细胞的死亡.展开更多
文摘AIM: To investigate the effects of prednisolone on cell membrane bleb formation, calpain μ activation and talin degradation during hepatic ischemia-reperfusion injury in rats. METHODS: The hilar area of the left lateral and median lobes of rat liver (68%) was clamped for 60 min and followed by 120 min reperfusion. Prednisolone was administered at 1.0, 3.0, or 10 mg/kg at 30 min before ischemia. In addition to biochemical and microscopic analyses, activation of calpain μ was determined using specific antibodies against the intermediate (activated) form of calpain μ. Degradation of talin was also studied by Western blotting. RESULTS: In the control and prednisolone (1.0 mg/kg) groups, serum aspartate transaminase (AST) and alanine transaminase (ALT) level were elevated, and cell membrane bleb formation was observed after 120 min of reperfusion. Moreover, calpain μ activation and talin degradation were detected. Infusion of prednisolone at 3.0 or 10 mg/kg significantly suppressed serum AST and ALT, and prevented cell membrane bleb formation. At 10 mg/kg, prednisolone markedly suppressed calpain μ activation and talin degradation. CONCLUSION: Prednisolone can suppress ischemia- reperfusion injury of the rat liver. Its cytoprotective effect is closely associated with the suppression of calpain μ activation and talin degradation.
