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作 者:沈轶瑶[1] 汤伟[1] 朱爱红[1] 周跃[1] 朱建华[1]
出 处:《中国临床医学》2008年第6期828-829,共2页Chinese Journal of Clinical Medicine
摘 要:目的:探讨清肝灵煎剂(清肝灵)对α-萘异硫氰酸酯(Alpha-naphthylisothi,ANIT)所致急性肝损伤大鼠脂质过氧化反应的影响。方法:SD大鼠48只,随机分为正常对照组、模型组、茵栀黄注射液治疗组、清肝灵预保护组、清肝灵低剂量组以及清肝灵高剂量组。除正常对照组外,其它5组均用ANIT(100mg.kg-1体重)灌胃以制备大鼠急性肝损伤模型。清肝灵预保护组于ANIT攻毒前3d起给药,所有实验组均于ANIT攻毒后分别给予相应药物治疗。ANIT攻毒后72h,检测各组大鼠的血清谷丙转氨酶(ALT)、谷草转氨酶(AST)和胆红素(TBil)平、肝组织和血清的丙二醛(MDA)含量以及血清超氧化物歧化酶(SOD)活性和谷胱甘肽(GSH)浓度。结果:与模型组比较,各清肝灵治疗组的ALT、AST、TBil、MDA含量均明显降低,而SOD活性、GSH的含量均明显升高。结论:清肝灵可提高急性肝损伤大鼠体内清除氧自由基和抗脂质过氧化反应的能力,减轻脂质过氧化损伤。Objective:To investigate the protective effects of Qingganling(QGL) apozem on lipid peroxidation of rats with acute hepatic injury induced by Alpha-naphthylisothi (ANIT). Methods: Forty-eight Sprague Dawley rats were randomly divided into six groups: the normal control group, the model group, Yinzhihuang injection group, the pretreatment group of QGL, the low dose group of QGL and the high dose group of QGL. All experimental rats except those of the normal control group were given a single dose of ANIT (100mg · kg^-1 , ig ) to make the acute hepatic injury model. The rats of the pretreatment group of QGL had been treated with QGI. in low dose for three days before ANIT ig, and the rats of all experimental groups were respectively treated with corresponsive drugs after given ANIT. The serum biochemical indexes including ALT, AST and TBil of rats were monitored at 72 h after the rats were given ANIT, meanwhile, the content of malondialdehyde(MDA) in liver tissue and the concentration of MDA, Glutathione-SH(GSH) as well as the activity of Superoxide dismutase(SOD) in serum were detected. Results: In comparison with the modal group, the levels of ALT, AST, TBil, the levels of MDA in hepatic tissue as well as in serum of the rats of three QGL groups were markedly lower, but the activity of SOD and the content of GSH of the rats of three QGL groups were higher. Conclusion: QGL apozem can enhance the abilities of the rat with acute hepatic injury to pellate oxygen free radical and abate the injury caused by lipid peroxidation.
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