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目的 :探讨金属硫蛋白(MT)对硫酸镍致小鼠肾脏损伤的治疗效果及作用机制。方法 :60只清洁级昆明(KM)种小鼠,雌雄各半,随机分为5组,对照组,硫酸镍(Ni+2)染毒组,低、中、高剂量MT治疗组。对照组灌胃生理盐水,镍染毒组灌胃2.5 mg/kg“bw硫酸镍溶液;M”I’治疗组在给予Ni+2染毒后再分别按5.0,10.0,20.0 mg/kg“bw剂量灌胃MT。各组灌胃时间均为15d,每日一次;灌胃体积均为0.1 ml/IO g”bw。实验结束麻醉处死动物采血,取双肾脏作病理学检测;全自动生化分析仪检测血清BUN和CRE含量;试剂盒检测肾组织SOD活性和MDA含量。结果 :与对照组比较,镍染毒小鼠血清BUN和CRE增高、肾组织SOD活力下降、MDA含量增高(P<0.05)o M’I,治疗后与镍染毒组比较小鼠血清BUN和CRE降低,SOD活力升高、MDA含量下降(P<0.05);MT治疗后肾病理损伤明显减轻,细胞管形消失,核坏死、出血等病变明显改善,其中以高剂量MZ,治疗肾损伤效果更佳。结论 :金属硫蛋白对镍致小鼠肾损伤有治疗作用,其机制与抗氧化损伤有关。
Objective: To investigate the therapeutic effect and mechanism of metallothionein (MT) on kidney injury induced by nickel sulfate in mice. Methods: Sixty clean Kunming (KM) mice were randomly divided into 5 groups: control group, nickel sulfate (Ni + 2) group and low, medium and high dose MT groups. The rats in the control group were fed with normal saline, and the rats in the nickel-exposed group were fed with 2.5 mg / kg bw nickel sulfate solution. The mice in the M group were treated with Ni + 2 at 5.0, 10.0 and 20.0 mg / kg “bw dose gavage MT. Each group gavage time were 15d, once daily; gavage volume was 0.1 ml / IOg ” bw. At the end of the experiment, blood samples were collected from anesthetized animals and pathological examination was performed on both kidneys. Serum levels of BUN and CRE were detected by automatic biochemical analyzer. SOD activity and MDA content in renal tissues were detected by kit. Results: Compared with the control group, the serum levels of BUN and CRE were increased in the nickel-exposed mice, the activities of SOD in the renal tissue were decreased, and the levels of MDA were increased (P <0.05) o M’I. Compared with the nickel- CRE decreased, SOD activity increased and MDA content decreased (P <0.05). After MT treatment, the pathological changes of kidney were alleviated obviously, the tubular disappearance, nuclear necrosis and hemorrhage were significantly improved. High dose MZ treatment of renal injury Better. CONCLUSIONS: Metallothionein has a therapeutic effect on renal injury induced by nickel in mice and the mechanism is related to anti-oxidative damage.