PAS-Na對錳致大鼠肝腎抗氧化酶和病理學(xué)改變的影響
發(fā)布時間：2018-07-26 06:39
【摘要】：目的觀察對氨基水楊酸鈉(PAS-Na)對錳致大鼠肝腎線粒體、微粒體抗氧化酶、病理學(xué)改變的影響。 方法50只雄性SD大鼠按體重隨機分為對照組、染錳組。染錳組腹腔注射(ip) MnCl2·4H2015mg/kg,對照組ip等容量生理鹽水,每日1次,每周5天,連續(xù)6周。然后,將染錳組按體重隨機分為染錳組、低、中、高(L、M、 H)-PAS干預(yù)組。L、M、H-PAS干預(yù)組大鼠分別背部皮下注射(sc)PAS-Na100、200或300mg/kg,對照組、染錳組背部sc等容量生理鹽水,每日1次,每周4天,連續(xù)4周。末次治療后72小時,處死大鼠取肝、腎。試劑盒檢測肝、腎線粒體、微粒體(超氧化物歧化酶(SOD,WST-1法)、谷胱甘肽過氧化物酶(GSH-PX,DTNB比色法)活性,顯微鏡觀察肝、腎組織病理學(xué)改變。 結(jié)果染錳組腎線粒體SOD比對照組低,差異有統(tǒng)計學(xué)意義(P0.05)。經(jīng)4周治療,各治療組肝、腎線粒體、微粒體SOD、GSH-PX活性與染錳組比較,差異無統(tǒng)計學(xué)意義。光鏡下染錳組大鼠可見肝臟匯管區(qū)炎性淋巴細胞及中性粒細胞浸潤,肝小葉內(nèi)出現(xiàn)點狀壞死,甚至部分灶性壞死,部分肝細胞出現(xiàn)脂肪變性,M-PAS治療組點狀壞死灶減少明顯(幾乎很難看到),L、H-PAS治療組治療組點狀壞死灶也有所減少。腎病理學(xué)檢查顯示,染錳組可見腎小管蛋白管型,腎小管上皮細胞水腫,部分腎小球出現(xiàn)毛細血管擴張,M-PAS治療組蛋白管型等病理改變恢復(fù)明顯,L-PAS、H-PAS治療組與染錳組比較也有所恢復(fù)。 結(jié)論染錳大鼠肝臟匯管區(qū)炎性淋巴細胞及中性粒細胞浸潤,肝小葉點狀壞死,甚至部分灶性壞死,肝細胞脂肪變性,腎臟出現(xiàn)腎小管蛋白管型、腎小管上皮細胞水腫,腎小球毛細血管擴張,PAS-Na治療可使其病理形態(tài)學(xué)改變明顯好轉(zhuǎn)。
[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.
【學(xué)位授予單位】：廣西醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2013
【分類號】：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.
【學(xué)位授予單位】：廣西醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2013
【分類號】：R114
【參考文獻】
相關(guān)期刊論文 前10條
1 張留保;真炳攸;;硫酸錳對肝細胞酶活性的影響[J];電子顯微學(xué)報;1990年03期
2 劉軍;陳愛敬;胡先勤;汪明;黃峰;榮克明;;多糖復(fù)合物對鯽魚軀體生化組成、臟器指數(shù)及白細胞數(shù)目的影響[J];飼料工業(yè);2009年24期
3 高利民;馮義朝;王恬;王建馗;;肝性腦病發(fā)病機制的研究進展[J];國際消化病雜志;2010年02期
4 江泉觀;李玉瑞;;中毒機理的一種學(xué)說:脂質(zhì)過氧化[J];國外醫(yī)學(xué)(衛(wèi)生學(xué)分冊);1980年06期
5 劉起展,趙躍,董國賓,趙曼平,翟中波,彭建英;錳作業(yè)者血中微量元素和脂質(zhì)過氧化的改變[J];工業(yè)衛(wèi)生與職業(yè)病;1999年04期
6 姜岳明,陸繼培,謝佩意,廖小勤,楊洪,關(guān)文堅;錳對接觸工人肝功能的影響[J];工業(yè)衛(wèi)生與職業(yè)病;2000年03期
7 朱圣陶,傅春玲,江偉威,王小平,麥峰,陸曉靜,劉葉花;某些營養(yǎng)素對短期染毒鉛鎘汞在小鼠體內(nèi)分布的影響[J];工業(yè)衛(wèi)生與職業(yè)病;2005年05期
8 劉，
本文編號：2145179
本文鏈接：http://sikaile.net/yixuelunwen/yufangyixuelunwen/2145179.html
最近更新
教材專著
