姜黄素对染镉6周大鼠肾损伤的影响
Effects of Curcumin on Renal Damage in Rats Exposed to Cadmium
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摘要:
目的 探讨姜黄素(curcumin)对氯化镉染毒大鼠亚慢性肾损伤的影响,为镉中毒的发病机制和防治提供实验依据。 方法 将48只Wistar大鼠按体重随机分成4组,每组12只,第1组为对照组,第2组为低剂量染镉组,第3组为高剂量染镉组,第4组为姜黄素干预组。周一至周五每天进行染毒,第1组腹腔注射生理盐水,第2~4组分别腹腔注射3、6、6μmol/kg氯化镉溶液;每周一、三、五染毒前2 h进行干预,第1~3组皮下注射生理盐水,第4组皮下注射50 mg/kg姜黄素,注射容积均为5 mL/kg;连续处理6周,最后一次染毒结束后24 h,检测尿乳酸脱氢酶(LDH)、尿碱性磷酸酶(ALP)及尿N-乙酰-β-氨基葡萄糖苷酶(NAG)活性,尿蛋白含量,血清尿素氮(BUN)含量,肾皮质还原型谷胱甘肽(GSH)、丙二醛(MDA)含量和超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性,肾细胞内ROS水平及细胞凋亡率。 结果 与对照组比较,各染镉组大鼠的体重增长幅度均降低;高剂量染镉组大鼠尿蛋白、血清BUN含量,尿LDH、ALP、NAG活性,肾皮质MDA含量均增加分别为(2.51& #177;0.57)g/g肌酐、(32.82& #177;4.99)mmol/L,(1180.54& #177;293.55)、(211.53& #177;46.39)、(104.94& #177;18.58)U/g肌酐,(4.59& #177;0.67)μmol/g蛋白,肾皮质GSH含量,SOD、GSH-Px活性均下降分别为(26.75& #177;6.92)μmol/g蛋白,(35.65& #177;6.27)、(62.91& #177;20.50)U/mg蛋白,肾细胞内ROS的含量升高(527.50& #177;60.12)平均荧光强度,细胞凋亡率增大(41.88& #177;4.10)%;姜黄素干预组与高剂量染镉组比较,各项指标均得到不同程度的改善。 结论 给大鼠亚慢性染镉可对肾脏产生明显的氧化损伤作用;姜黄素处理对镉引起的肾损伤具有一定的拮抗作用。 Abstract:Objective To observe the effects of curcumin on nephrotoxicity of rats induced by sub-chronic cadmium exposure, and provide experimental evidence for the mechanism of cadmium poisoning and its prevention and treatment. Methods Forty-eight Wistar rats were randomly divided into four groups by body weight:control group (saline), low-dose cadmium chloride group (3 μmol/kg cadmium chloride), high-dose cadmium chloride group (6 μmol/kg), and curcumin intervention group (6 μmol/kg). Exposure started from Monday to Friday by daily intraperitoneal injection and lasted for six weeks. Two hours before the exposure on every Monday, Wednesday, and Friday, the rats in the control, low-dose, and high-dose groups were injected subcutaneously with normal saline, while the rats in the intervention group was injected subcutaneously with 50 mg/kg curcumin, all lasted for six weeks. After the last injection of cadmium chloride, the following indicators were determined:24-hour urine lactate dehydrogenase (LDH), alkaline phosphatase (ALP), N-acetyl-beta-D-glucosaminidase (NAG), urine protein, serum urea nitrogen (BUN), glutathione (GSH), malonydialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and renal cells reactive oxygen species (ROS) and apoptosis. Results Compared with the control group, the increased body weights in the cadmium administered rats were reduced. In the high-dose cadmium chloride group, the contents of urine protein(2.51±0.57) g/g creatinine and BUN(32.82± 4.99) mmol/L, the activities of LDH(1180.54±293.55) U/g creatinine, ALP(211.53±46.39) U/g creatinine, and NAG(104.94± 18.58) U/g creatinine, the content of MDA(4.59±0.67) μmol/g protein, ROS(527.50±60.12) median fluorescence intensity and the apoptosis rate of renal samples(41.88±4.10)% were increased, while the content of GSH(26.75±6.92) μmol/g protein and the activities of SOD(35.65±6.27) U/mg protein and GSH-Px(62.91±20.50) U/mg protein were decreased. Compared with the highdose cadmium chloride group, the curcumin intervention group showed varying degrees of antagonistic activity against nephrotoxicity of cadmium. Conclusion Sub-chronic administration of cadmium could result in renal damage, and curcumin might present a potential antagonistic effect on the renal damage induced by cadmium.
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