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刘秀英, 王翔朴, 贺全仁, 高泽宣, 王夷平, 曾庆善. 甘草甜素和齐墩果酸对大鼠镉中毒性肝损伤的防护作用与机理[J]. 中国公共卫生, 2000, 16(1): 21-24. DOI: 10.11847/zgggws2000-16-01-14
引用本文: 刘秀英, 王翔朴, 贺全仁, 高泽宣, 王夷平, 曾庆善. 甘草甜素和齐墩果酸对大鼠镉中毒性肝损伤的防护作用与机理[J]. 中国公共卫生, 2000, 16(1): 21-24. DOI: 10.11847/zgggws2000-16-01-14
Liu Xiuying, . Protective Effects and Mechanisms of Glycyrrhizin and Oleanolic Acid Against Cadmium induced Hepatic Injury in Rats[J]. Chinese Journal of Public Health, 2000, 16(1): 21-24. DOI: 10.11847/zgggws2000-16-01-14
Citation: Liu Xiuying, . Protective Effects and Mechanisms of Glycyrrhizin and Oleanolic Acid Against Cadmium induced Hepatic Injury in Rats[J]. Chinese Journal of Public Health, 2000, 16(1): 21-24. DOI: 10.11847/zgggws2000-16-01-14

甘草甜素和齐墩果酸对大鼠镉中毒性肝损伤的防护作用与机理

Protective Effects and Mechanisms of Glycyrrhizin and Oleanolic Acid Against Cadmium induced Hepatic Injury in Rats

  • 摘要: 为探讨甘草甜素(GL)和齐墩果酸(OA)对大鼠镉中毒性肝损伤的防护作用及其作用机理,给大鼠腹腔注射CdCl2溶液(0.8mgCd2+/kg体重),两组染镉大鼠分别同时皮下注射GL的生理盐水溶液(20mg/kg,每周3次)和OA的吐温-生理盐水混悬液(60mg/kg,每周5次),测定血清转氨酶、肝镉(Cd)、金属硫蛋白(MT)含量,检查肝组织病理形态学.结果显示:GL和OA延缓、降低了镉引起的血清转氨酶的升高,显着减轻了肝细胞肿胀、坏死及肝线粒体、滑面内质网病变的程度,明显减少了染镉初期镉在肝脏的蓄积,显着提高了肝内诱导的MT量.提示GL和OA对大鼠镉中毒性肝损伤有防护作用,此作用可能与其减少染镉初期镉在肝脏的蓄积及诱导MT或促进镉对MT的诱导有关.

     

    Abstract: To examine the hepatoprotecive effects of Gly cyr rhizin(GL) and Oleanolic acid(OA)against Cadmium(Cd)-induced liver injury in rats and the mechanisms of protection,SD rats were injected ip with CdCl2(0.8mg/kg Cd2+/kg body weight,five times a week).Two cadmium-challenged groups were concomitantly injected sc with GL(20mg/kg,three times a week)and OA(60mg/kg,five times a week)respectively.Serum activities of alanine aminotransferase(ALT)and aspartate aminotr ansferase(AST)indicative of hepatic injury were measured,and livers were examined mor phologically and analyzed for cadmium and metallothio nein (MT).Bo th GLand OA delayed and attenuated the elevation of serum ALT and AST activities,ameliorated hepatic parenchymal swelling and necrosis produced by cadmium.Electron microscopy showed the pathological changes of hepatocellular mitochondr ia and smooth endo plasmic reticulum were less severe in Cd-GL,CdOA-cotreated rats compared with Cd-treated ones.In the early stage of cadmium exposure,GLnd OA also decreased hepatic cadmium accumulation and increased hepatic MT induction,which in turn elevated MT amount available to every cadmium unit.It show s that both GLand OA can protect rats against Cd-induced hepatotoxicity in subchronic Cd exposure.The protection may be in partrelated to decrease of cadmium accumulation and additional increase of MT induction in the target or gan.

     

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