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目的 :观察亚砷酸钠 (SA )预处理对大鼠常温下肝脏缺血再灌注损伤的保护作用。方法 :Westernblot分析 SA预处理诱导大鼠肝脏合成热休克蛋白 (HSP)。复制大鼠肝脏缺血再灌注模型 ,SA组缺血前 18小时以 6 m g/ kg静注 SA,动态观察血清丙氨酸转氨酶 (AL T)、乳酸脱氢酶 (L DH)、肝组织 ATP及能荷 (EC)、血浆内皮素 (ET)和肝组织学变化及生存率。结果 :SA预处理可诱导大鼠肝脏合成 HSP。肝脏缺血再灌注后 ,血清 AL T、L DH、血浆 ET水平逐渐升高 ,ATP、EC急剧下降 ,恢复缓慢 ;SA预处理组与同期缺血再灌注组 (对照组 )相比 ,血清 AL T、L DH、血浆 ET水平降低 (P均 <0 .0 5 ) ,肝组织 ATP、EC水平增高 (P均 <0 .0 1) ,肝组织破坏程度 SA预处理组明显轻于对照组 ,生存率高于对照组 (P<0 .0 1)。结论 :SA预处理对大鼠肝脏缺血再灌注损伤具有明显的保护作用 ,HSP可能是细胞保护的物质基础。
AIM: To observe the protective effects of sodium arsenite (SA) preconditioning on liver ischemia-reperfusion injury at room temperature in rats. Methods: SA pretreatment induced the synthesis of heat shock protein (HSP) in rat liver by Western blot. Rat liver ischemia-reperfusion model was duplicated. In SA group, SA was injected intravenously 6 mg / kg 18 hours before ischemia, serum ALT, L DH, And energy charge (EC), plasma endothelin (ET) and liver histology and survival rate. Results: SA preconditioning induced HSP synthesis in rat liver. Serum ALT, L DH and plasma ET levels gradually increased after ischemia-reperfusion in liver, while ATP and EC decreased sharply and recovered slowly. Compared with the ischemia-reperfusion group (control group), serum AL (P <0.05). The level of ATP and EC in liver tissue were increased (P <0.01), the degree of liver damage was significantly lower in SA pretreatment group than in control group The survival rate was higher than that of the control group (P <0.01). CONCLUSION: SA preconditioning has a protective effect on hepatic ischemia-reperfusion injury in rats. HSP may be the material basis of cell protection.