中华内分泌代谢杂志
中華內分泌代謝雜誌
중화내분비대사잡지
CHINESE JOURNAL OF ENDOCRINOLOGY AND METABOLISM
2010年
10期
875-880
,共6页
亚硒酸钠%糖尿病肾病%脂联素%Nephrin
亞硒痠鈉%糖尿病腎病%脂聯素%Nephrin
아서산납%당뇨병신병%지련소%Nephrin
Sodium selenite%Diabetic nephropathy%Adiponectin%Nephrin
目的 探讨亚硒酸钠对糖尿病肾病大鼠肾脏脂联素和nephrin表达的影响及其相互间的关系,从而研究亚硒酸钠与脂联素、nephrin在糖尿病肾病中的作用机制.方法 通过链脲佐菌素法加高脂饮食诱导模拟大鼠糖尿病肾病模型,实验设完全空白对照组、糖尿病组、糖尿病药物干预组,药物干预组每日给予亚硒酸钠溶液灌胃,其它组给予等量盐水溶液灌胃.10周后处死大鼠,取血、尿标本测相关生化指标,取肾脏组织分别提取DNA和蛋白质标本,石蜡切片光镜观察病理改变及免疫组化分析蛋白表达定位,实时定量PCR法检测脂联素mRNA表达、RT-PCR法检测nephrin mRNA表达,Western印迹法检测脂联素和nephrin蛋白表达.结果 亚硒酸钠干预组大鼠生化指标较糖尿病组明显改善,光镜下观察亚硒酸钠干预组病理改变较糖尿病组明显减轻.免疫组化分析,亚硒酸钠干预组脂联素蛋白着色较糖尿病组明显增强,且肾小管、肾小球内均有着色;糖尿病组nephrin蛋白表达着色较空白对照组减少,亚硒酸钠干预组较糖尿病组着色明显增多.亚硒酸钠干预组脂联素mRNA和蛋白表达明显高于糖尿病组和正常对照组,差异有统计学意义(均P<0.05).亚硒酸钠干预组nephrin mRNA和蛋白表达均较糖尿病组明显增加,但仍较空白对照组降低,差异均有统计学意义(P<0.05).结论 亚硒酸钠能促进大鼠肾脏脂联素和nephrin表达,表明亚硒酸钠、脂联素和nephrin在延缓和防治糖尿病肾病的发生发展中可能起重要作用.
目的 探討亞硒痠鈉對糖尿病腎病大鼠腎髒脂聯素和nephrin錶達的影響及其相互間的關繫,從而研究亞硒痠鈉與脂聯素、nephrin在糖尿病腎病中的作用機製.方法 通過鏈脲佐菌素法加高脂飲食誘導模擬大鼠糖尿病腎病模型,實驗設完全空白對照組、糖尿病組、糖尿病藥物榦預組,藥物榦預組每日給予亞硒痠鈉溶液灌胃,其它組給予等量鹽水溶液灌胃.10週後處死大鼠,取血、尿標本測相關生化指標,取腎髒組織分彆提取DNA和蛋白質標本,石蠟切片光鏡觀察病理改變及免疫組化分析蛋白錶達定位,實時定量PCR法檢測脂聯素mRNA錶達、RT-PCR法檢測nephrin mRNA錶達,Western印跡法檢測脂聯素和nephrin蛋白錶達.結果 亞硒痠鈉榦預組大鼠生化指標較糖尿病組明顯改善,光鏡下觀察亞硒痠鈉榦預組病理改變較糖尿病組明顯減輕.免疫組化分析,亞硒痠鈉榦預組脂聯素蛋白著色較糖尿病組明顯增彊,且腎小管、腎小毬內均有著色;糖尿病組nephrin蛋白錶達著色較空白對照組減少,亞硒痠鈉榦預組較糖尿病組著色明顯增多.亞硒痠鈉榦預組脂聯素mRNA和蛋白錶達明顯高于糖尿病組和正常對照組,差異有統計學意義(均P<0.05).亞硒痠鈉榦預組nephrin mRNA和蛋白錶達均較糖尿病組明顯增加,但仍較空白對照組降低,差異均有統計學意義(P<0.05).結論 亞硒痠鈉能促進大鼠腎髒脂聯素和nephrin錶達,錶明亞硒痠鈉、脂聯素和nephrin在延緩和防治糖尿病腎病的髮生髮展中可能起重要作用.
목적 탐토아서산납대당뇨병신병대서신장지련소화nephrin표체적영향급기상호간적관계,종이연구아서산납여지련소、nephrin재당뇨병신병중적작용궤제.방법 통과련뇨좌균소법가고지음식유도모의대서당뇨병신병모형,실험설완전공백대조조、당뇨병조、당뇨병약물간예조,약물간예조매일급여아서산납용액관위,기타조급여등량염수용액관위.10주후처사대서,취혈、뇨표본측상관생화지표,취신장조직분별제취DNA화단백질표본,석사절편광경관찰병리개변급면역조화분석단백표체정위,실시정량PCR법검측지련소mRNA표체、RT-PCR법검측nephrin mRNA표체,Western인적법검측지련소화nephrin단백표체.결과 아서산납간예조대서생화지표교당뇨병조명현개선,광경하관찰아서산납간예조병리개변교당뇨병조명현감경.면역조화분석,아서산납간예조지련소단백착색교당뇨병조명현증강,차신소관、신소구내균유착색;당뇨병조nephrin단백표체착색교공백대조조감소,아서산납간예조교당뇨병조착색명현증다.아서산납간예조지련소mRNA화단백표체명현고우당뇨병조화정상대조조,차이유통계학의의(균P<0.05).아서산납간예조nephrin mRNA화단백표체균교당뇨병조명현증가,단잉교공백대조조강저,차이균유통계학의의(P<0.05).결론 아서산납능촉진대서신장지련소화nephrin표체,표명아서산납、지련소화nephrin재연완화방치당뇨병신병적발생발전중가능기중요작용.
Objective To investigate the influence of sodium selenite on the expression of adiponectin and nephrin in the kidney of rats with diabetic nephropathy, the relation of sodium selenite with adiponectin and nephrin, and to study the roles played by these factors in diabetic nephropathy. Methods Rat models of diabetic nephropathy were established by injecting intraperitoneally streptozocin combined with high fat diet. Three groups of rats were employed: control group, diabetic nephropathy group, and selenite-treated group. The selenite-treated rats were given selenite solution by intragastric administration every day, and other groups were given same volume of saline. After 10 weeks, all rats were sacrificed, blood and urine samples were collected. The kidneys were used to observe pathological changes with light microscope, and to locate protein expression with immunohistochemistry analysis. The mRNA and protein expressions of adiponectin and nephrin were analyzed via real-time PCR, RT PCR, and Western blot. Results The basic condition, biochemical parameters, and pathological images in selenite-treated group were better than those in diabetic nephropathy group. Immunohistochemistry analysis showed that the expression of adiponectin was in both glomeruli and renal tubules in selenite-treated group, and the coloration was enhanced as compared with diabetic nephropathy group. The mRNA and protein expressions of adiponectin in selenite-treated group were significantly higher than those in diabetic nephropathy group and the control group (all P<0. 05 ). Nephrin expression in selenite-treated group was also higher than that in diabetic nephropathy group, but lower than that in control group. Conclusion Sodium selenite can enhance the mRNA and protein expressions of adiponectin and nephrin in kindey of rats with diabetic nephropathy. Sodium selenite,adiponectin, and nephrin may play important roles in delaying and preventing the development of diabetic nephropathy.