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目的观察对氨基水杨酸钠(PAS-Na)对锰致大鼠肾线粒体、微粒体抗氧化酶、病理学改变的影响。方法 50只雄性SD大鼠按体重随机分为对照组、染锰组。染锰组腹腔注射(ip)MnCl2.4H2O 15mg/kg,对照组ip等容量生理盐水,1次/d,每周5 d,连续6周。然后,将染锰组按体重随机分为染锰组、低、中、高(L、M、H)-PAS干预组。L、M、H-PAS干预组大鼠分别背部皮下注射(sc)PAS-Na 100、200和300 mg/kg,对照组、染锰组背部sc等容量生理盐水,1次/d,每周4 d,连续4周。末次干预后72 h,处死大鼠取肾。试剂盒检测肾线粒体、微粒体超氧化物歧化酶(SOD,WST-1法)、谷胱甘肽过氧化物酶(GSH-Px,DTNB比色法)活性,显微镜观察肾组织病理学改变。结果染锰组肾线粒体SOD活性比对照组低,差异有统计学意义(P<0.05)。经4周干预,PAS-Na干预组肾线粒体、微粒体SOD、GSH-Px活性与染锰组比较,差异无统计学意义。肾病理学检查显示,染锰组出现肾小管蛋白管型、肾小管上皮细胞水肿,部分肾小球出现毛细血管扩张,M-PAS干预组蛋白管型等病理改变恢复明显,L-PAS、H-PAS干预组与染锰组比较也有所恢复。结论染锰可抑制大鼠肾线粒体SOD活性,使大鼠出现肾小管蛋白管型、肾小管上皮细胞水肿、肾小球毛细血管扩张,PAS-Na干预可使其病理形态学改变明显好转。
Objective To observe the effect of sodium para-aminosalicylate (PAS-Na) on the activities of antioxidant enzymes and pathological changes of renal mitochondria and microsomes induced by manganese in rats. Methods Fifty male SD rats were randomly divided into control group and manganese group. The rats in the Mn-treated group were intraperitoneally injected with MnCl2.4H2O 15 mg / kg and the control group ip with the same volume of normal saline once a day for 5 days for 6 weeks. Then, the manganese-exposed groups were randomly divided into Mn-dosed group, L, M, H-PAS-treated groups according to body weight. Rats in the L, M, H-PAS intervention groups were subcutaneously injected with 100, 200 and 300 mg / kg of PAS-Na, sc, 4 d, for 4 weeks. 72 h after the last intervention, rats were sacrificed and kidneys were sacrificed. The activity of renal mitochondria, microsomal SOD, GSH-Px and DTNB colorimetric assay was detected by kit, and pathological changes of renal tissue were observed by microscope. Results Compared with control group, SOD activity in renal mitochondria of manganese-exposed group was significantly lower than that of control group (P <0.05). After 4 weeks’ intervention, the activities of SOD, GSH-Px in renal mitochondria and microsome of PAS-Na intervention group were not significantly different from those of the control group. Nephropathy examination showed that tubulointerstitial tubular epithelial cell edema, part of glomerular capillary dilatation occurred in Mn-Mn group, histopathological changes recovered obviously after M-PAS intervention. L-PAS, H- PAS intervention group and manganese group also recovered. Conclusion Mn can inhibit the activity of SOD in rat renal mitochondria, and lead to tubular protein tubular type, tubular epithelial cell edema, glomerular capillary dilatation in rats. PAS-Na intervention can significantly improve the pathological changes.