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目的:探讨黄芩苷对大鼠重症急性胰腺炎相关性肾损伤的保护作用及其机制。方法:将60只SD大鼠随机分为假手术组(S组)、重症急性胰腺炎相关性肾损伤组(M组)和黄芩苷治疗组(T组),各20只。用4%牛磺胆酸钠逆行胰胆管注射方法建立大鼠重症急性胰腺炎模型。造模成功后,T组经尾静脉持续(2 m L/h)注入5%黄芩苷0.2 m L/100 g,而SO组和M组予等量生理盐水。采用自动生化仪检测血清淀粉酶(AMY)、血尿素氮(BUN)、血肌酐(Cr)水平,Western blotting法检测肾组织核因子相关因子2(NF-E2-related factor 2,Nrf2)、超氧化物歧化酶(superoxide dismutase,SOD)、血红素加氧酶l(hemeoxygenase 1,HO-1)蛋白表达。结果:与SO组比较,M组的血清AMY、BUN、Cr的表达均明显升高,肾组织Nrf2、SOD、HO-1蛋白表达均的显著升高。与M组比较,T组的血清AMY、BUN、Cr的表达均明显下降,肾组织Nrf2、SOD、HO-1蛋白表达均明显降低。结论:黄芩苷对重症急性胰腺相关性肾损伤有良好保护作用,其作用机制可能与激活Nrf2,上调SOD、HO-1蛋白的表达有关。
Objective: To investigate the protective effect of baicalin on renal injury induced by severe acute pancreatitis in rats and its mechanism. Methods: Sixty Sprague-Dawley rats were randomly divided into sham operation group (S group), severe acute pancreatitis-related renal injury group (M group) and baicalin treatment group (T group). Rat model of severe acute pancreatitis was established by injecting 4% sodium taurocholate into pancreaticobiliary duct. After successful modeling, 5% baicalin 0.2 m L / 100 g was injected into tail vein (2 m L / h) in T group, and normal saline in SO group and M group. Serum amylase (AMY), blood urea nitrogen (BUN) and serum creatinine (Cr) were detected by automatic biochemical analyzer. The expression of NF-E2-related factor 2 (Nrf2) Superoxide dismutase (SOD), hemeoxygenase 1 (HO-1) protein expression. Results: Compared with SO group, the expressions of AMY, BUN and Cr in serum of M group were significantly increased, and the expression of Nrf2, SOD and HO-1 in renal tissue were significantly increased. Compared with M group, the expression of serum AMY, BUN and Cr in T group were significantly decreased, while the expression of Nrf2, SOD and HO-1 in renal tissue were significantly decreased. CONCLUSION: Baicalin has a good protective effect on severe acute pancreatitis-associated renal injury. Its mechanism may be related to activating Nrf2 and up-regulating the expression of SOD and HO-1.