摘要
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 associated renal injury in rats with severe acute pancreatitis and its mechanism. Methods :60 SD rats were randomly divided into sham operation group (group SO), severe acute pancreatitis associated renal injury group (group M) and baicalin treatment group (group T) ,20 rats for each. The severe acute pancreatitis rat model was set up with 4% sodium taurocholate retrograde pancreatic duct injection method. After the success of modeling,group T via the tail vein continuous (2 mL/h) was injected 5% baicalin 0.2 mL/100 g, while group SO and group M were treated with normal saline. Serum amylase (AMY) ,blood urea nitrogen (BUN) and serum creatinine (Cr) were detected by automatic biochemical analyzer. Related factors such as renal tissues was 2 ( Nrf2), superoxide dismutase (SOD) and heme oxygenase L ( HO - 1 ) were detected with Western blotting method. Results : Compared with group SO, the group M' s expressions on AMY, BUN and Cr were significantly increased and Nrf2, SOD and HO - 1 protein in renal tissue were significantly higher and the difference was statistically significant (P 〈 O. 05 ). Compared with group M, the group T' s expressions on AMY, BUN and Cr were significantly decreased, and Nrf2, SOD and HO - 1 protein in renal tissue were obviously decreased and the difference was statistically significant (P 〈 0. 05 ). Conclusion : Baicalin has a good protective effect on severe acute pancreatitis associated renal injury and its mechanism may be related to activation of Nrf2 and up - regulation of the expressions of SOD and HO - 1.
出处
《中华中医药学刊》
CAS
北大核心
2015年第10期2476-2478,共3页
Chinese Archives of Traditional Chinese Medicine