PAS-Na对锰致大鼠肝肾抗氧化酶和病理学改变的影响
发布时间：2018-07-26 06:39
【摘要】：目的观察对氨基水杨酸钠(PAS-Na)对锰致大鼠肝肾线粒体、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) MnCl2·4H2015mg/kg,对照组ip等容量生理盐水,每日1次,每周5天,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-Na100、200或300mg/kg,对照组、染锰组背部sc等容量生理盐水,每日1次,每周4天,连续4周。末次治疗后72小时,处死大鼠取肝、肾。试剂盒检测肝、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,显微镜观察肝、肾组织病理学改变。 结果染锰组肾线粒体SOD比对照组低,差异有统计学意义(P0.05)。经4周治疗,各治疗组肝、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。光镜下染锰组大鼠可见肝脏汇管区炎性淋巴细胞及中性粒细胞浸润,肝小叶内出现点状坏死,甚至部分灶性坏死,部分肝细胞出现脂肪变性,M-PAS治疗组点状坏死灶减少明显(几乎很难看到),L、H-PAS治疗组治疗组点状坏死灶也有所减少。肾病理学检查显示,染锰组可见肾小管蛋白管型,肾小管上皮细胞水肿,部分肾小球出现毛细血管扩张,M-PAS治疗组蛋白管型等病理改变恢复明显,L-PAS、H-PAS治疗组与染锰组比较也有所恢复。 结论染锰大鼠肝脏汇管区炎性淋巴细胞及中性粒细胞浸润,肝小叶点状坏死,甚至部分灶性坏死,肝细胞脂肪变性,肾脏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治疗可使其病理形态学改变明显好转。
[Abstract]:Objective to observe the effect of sodium p-aminosalicylate (PAS-Na) on the changes of liver and kidney mitochondria, microsomal antioxidant enzymes and pathological changes in rats induced by manganese. Methods 50 male Sprague-Dawley rats were randomly divided into two groups according to their body weight. (ip) MnCl2 4H2015 mg / kg was injected intraperitoneally in the manganese exposed group, and the control group was given IP of the same volume of normal saline once a day, 5 days a week for 6 weeks. Then, the manganese exposed group was randomly divided into two groups according to their body weight: low, medium and high (Lomm, H) -pas intervention group. The rats in the LHP-PAS group were subcutaneously injected with (sc) PAS-Na100200 or 300mg / kg, respectively. The control group and the manganese exposed group received normal saline of the same volume in the back of the back, once a day, 4 days a week, respectively. 4 weeks in a row. 72 hours after the last treatment, the rats were killed to take liver and kidney. The activities of liver and kidney mitochondria, microsomes (SODX WST-1 method) and glutathione peroxidase (GSH-PXX DTNB colorimetric method) were detected by the kit. The pathological changes of liver and kidney were observed by microscope. Results the SOD of kidney mitochondria in manganese group was lower than that in control group (P 0.05). After 4 weeks treatment, the activity of GSH-PX in liver, kidney mitochondria and microsome was not significantly different from that in manganese group. Under light microscope, inflammatory lymphocytes and neutrophils were infiltrated in the portal area of the liver, and dotted necrosis or even partial focal necrosis occurred in the hepatic lobules in the rats exposed to manganese under light microscope. In the M-PAS treatment group, the point necrotic foci were decreased significantly (hardly seen) in some of the liver cells, and the dotted necrotic foci were also decreased in the LH-PAS treatment group. Renal pathological examination showed that tubuloprotein tubule type and edema of renal tubular epithelial cells were observed in manganese exposed group. The pathological changes such as capillary dilatation and histone tubules in some glomeruli recovered significantly in the L-PAS-H-PAS group as compared with those in the manganese exposed group. Conclusion inflammatory lymphocytes and neutrophils infiltrate the hepatic catchment area of the rats exposed to manganese, dotted necrosis of hepatic lobules, even partial focal necrosis, steatosis of hepatocytes, renal tubuloprotein tubule type and edema of renal tubular epithelial cells. PAS-Na therapy of glomerular capillary dilatation can obviously improve the pathomorphology of glomerular capillary dilatation.
【学位授予单位】：广西医科大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R114
[Abstract]:Objective to observe the effect of sodium p-aminosalicylate (PAS-Na) on the changes of liver and kidney mitochondria, microsomal antioxidant enzymes and pathological changes in rats induced by manganese. Methods 50 male Sprague-Dawley rats were randomly divided into two groups according to their body weight. (ip) MnCl2 4H2015 mg / kg was injected intraperitoneally in the manganese exposed group, and the control group was given IP of the same volume of normal saline once a day, 5 days a week for 6 weeks. Then, the manganese exposed group was randomly divided into two groups according to their body weight: low, medium and high (Lomm, H) -pas intervention group. The rats in the LHP-PAS group were subcutaneously injected with (sc) PAS-Na100200 or 300mg / kg, respectively. The control group and the manganese exposed group received normal saline of the same volume in the back of the back, once a day, 4 days a week, respectively. 4 weeks in a row. 72 hours after the last treatment, the rats were killed to take liver and kidney. The activities of liver and kidney mitochondria, microsomes (SODX WST-1 method) and glutathione peroxidase (GSH-PXX DTNB colorimetric method) were detected by the kit. The pathological changes of liver and kidney were observed by microscope. Results the SOD of kidney mitochondria in manganese group was lower than that in control group (P 0.05). After 4 weeks treatment, the activity of GSH-PX in liver, kidney mitochondria and microsome was not significantly different from that in manganese group. Under light microscope, inflammatory lymphocytes and neutrophils were infiltrated in the portal area of the liver, and dotted necrosis or even partial focal necrosis occurred in the hepatic lobules in the rats exposed to manganese under light microscope. In the M-PAS treatment group, the point necrotic foci were decreased significantly (hardly seen) in some of the liver cells, and the dotted necrotic foci were also decreased in the LH-PAS treatment group. Renal pathological examination showed that tubuloprotein tubule type and edema of renal tubular epithelial cells were observed in manganese exposed group. The pathological changes such as capillary dilatation and histone tubules in some glomeruli recovered significantly in the L-PAS-H-PAS group as compared with those in the manganese exposed group. Conclusion inflammatory lymphocytes and neutrophils infiltrate the hepatic catchment area of the rats exposed to manganese, dotted necrosis of hepatic lobules, even partial focal necrosis, steatosis of hepatocytes, renal tubuloprotein tubule type and edema of renal tubular epithelial cells. PAS-Na therapy of glomerular capillary dilatation can obviously improve the pathomorphology of glomerular capillary dilatation.
【学位授予单位】：广西医科大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R114
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