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目的探讨四氯化碳(CCl4)致大鼠慢性肾损伤的毒性机制。方法将健康的Wistar大鼠随机分为对照组和染毒组,对照组腹部皮下注射生理盐水;染毒组腹部皮下注射CCl4大豆油溶液。于第8周末分别检测血清中尿素氮(BUN)和肌酐(CRE)含量;血清和肾组织中丙二醛(MDA)、NO含量及超氧化物歧化酶(SOD)的活力,并作肾组织病理检查。结果与对照组比较,染毒组血清中BUN、CRE明显增高(P<0.01),血清和肾组织中SOD活力明显降低、MDA和NO含量增加(P<0.01)。染毒组肾组织病理学变化明显。结论CCl4能诱发肾脏损伤,其机制可能与体内自由基增加和细胞脂质过氧化有关。
Objective To investigate the toxic mechanism of carbon tetrachloride (CCl4) -induced chronic kidney injury in rats. Methods Healthy Wistar rats were randomly divided into control group and exposure group. The control group was injected subcutaneously with normal saline. CCl4 soybean oil solution was injected subcutaneously into the abdomen. Serum urea nitrogen (BUN) and creatinine (CRE) were measured at the end of the 8th week. Malondialdehyde (MDA), NO content and superoxide dismutase (SOD) activity in serum and kidney tissue were measured. Pathological examination. Results Compared with the control group, the serum levels of BUN and CRE in the treated group were significantly increased (P <0.01). The activities of SOD and GSH in serum and kidney tissue were significantly decreased (P <0.01). The pathological changes of renal tissue in exposed group were obvious. Conclusion CCl4 can induce renal injury, the mechanism may be related to the increase of free radicals and lipid peroxidation in the body.