中国医药
中國醫藥
중국의약
CHINA MEDICINE
2011年
9期
1075-1078
,共4页
金芪降糖片%糖尿病肾病%晚期糖化终末产物%晚期糖化终末产物受体%核转录因子-κBp65%单核细胞趋化蛋白1
金芪降糖片%糖尿病腎病%晚期糖化終末產物%晚期糖化終末產物受體%覈轉錄因子-κBp65%單覈細胞趨化蛋白1
금기강당편%당뇨병신병%만기당화종말산물%만기당화종말산물수체%핵전록인자-κBp65%단핵세포추화단백1
Jinqi tablet%Diabetic nephropathy%Advanced glycation end products%Receptor of advanced glycation end products%Nuclear transcription factor-κBp65%Monocyte chemoattractant protein-1
目的 观察金芪降糖片对糖尿病大鼠肾组织晚期糖化终末产物(AGEs)及其受体(RAGE)、核转录因子-κBp65(NF-κBp65)和单核细胞趋化蛋白1(MCP-1)表达的影响.方法 测定造模后20周糖尿病模型组(DM组)、糖尿病给药组(DD组)和正常对照组(N组)大鼠24 h尿微量白蛋白定量(UMA)、平均血糖、TG、TC、内生肌酐清除率(Ccr)水平及肾皮质AGEs、RAGE、NF-κBp65、MCP-1水平,同时观察各组大鼠肾脏形态学改变,评价金芪降糖片的肾脏保护作用.结果 DM组和DD组平均血糖、TC差异无统计学意义,DD组Ccr[(2.72±0.36)ml/min]高于DM组[(2.31±0.23)ml/min],而UMA、TG、AGEs、RAGE、NF-κBP65、MCP-1水平降低[(6.95±2.65)mg/d比(14.52±5.90)mg/d、(2.87±0.56)mmol/L比(4.35±0.92)mmol/L、(38.24±8.36)AFU/mg比(70.49±15.21)AFU/mg、(8.26±4.47)比(17.44±7.91)、(3.40±2.62)比(5.95±3.22)、(1.52±0.34)比(2.17±0.56)],差异有统计学意义(P＜0.05);光镜和电镜下,DD组肾组织损伤程度均轻于DM组.结论 金芪降糖片可以减轻糖尿病慢性肾损伤的程度,其肾脏保护作用可能与其降脂及降低AGEs、RAGE、NF-κBp65、MCP-1水平有关.
目的 觀察金芪降糖片對糖尿病大鼠腎組織晚期糖化終末產物(AGEs)及其受體(RAGE)、覈轉錄因子-κBp65(NF-κBp65)和單覈細胞趨化蛋白1(MCP-1)錶達的影響.方法 測定造模後20週糖尿病模型組(DM組)、糖尿病給藥組(DD組)和正常對照組(N組)大鼠24 h尿微量白蛋白定量(UMA)、平均血糖、TG、TC、內生肌酐清除率(Ccr)水平及腎皮質AGEs、RAGE、NF-κBp65、MCP-1水平,同時觀察各組大鼠腎髒形態學改變,評價金芪降糖片的腎髒保護作用.結果 DM組和DD組平均血糖、TC差異無統計學意義,DD組Ccr[(2.72±0.36)ml/min]高于DM組[(2.31±0.23)ml/min],而UMA、TG、AGEs、RAGE、NF-κBP65、MCP-1水平降低[(6.95±2.65)mg/d比(14.52±5.90)mg/d、(2.87±0.56)mmol/L比(4.35±0.92)mmol/L、(38.24±8.36)AFU/mg比(70.49±15.21)AFU/mg、(8.26±4.47)比(17.44±7.91)、(3.40±2.62)比(5.95±3.22)、(1.52±0.34)比(2.17±0.56)],差異有統計學意義(P＜0.05);光鏡和電鏡下,DD組腎組織損傷程度均輕于DM組.結論 金芪降糖片可以減輕糖尿病慢性腎損傷的程度,其腎髒保護作用可能與其降脂及降低AGEs、RAGE、NF-κBp65、MCP-1水平有關.
목적 관찰금기강당편대당뇨병대서신조직만기당화종말산물(AGEs)급기수체(RAGE)、핵전록인자-κBp65(NF-κBp65)화단핵세포추화단백1(MCP-1)표체적영향.방법 측정조모후20주당뇨병모형조(DM조)、당뇨병급약조(DD조)화정상대조조(N조)대서24 h뇨미량백단백정량(UMA)、평균혈당、TG、TC、내생기항청제솔(Ccr)수평급신피질AGEs、RAGE、NF-κBp65、MCP-1수평,동시관찰각조대서신장형태학개변,평개금기강당편적신장보호작용.결과 DM조화DD조평균혈당、TC차이무통계학의의,DD조Ccr[(2.72±0.36)ml/min]고우DM조[(2.31±0.23)ml/min],이UMA、TG、AGEs、RAGE、NF-κBP65、MCP-1수평강저[(6.95±2.65)mg/d비(14.52±5.90)mg/d、(2.87±0.56)mmol/L비(4.35±0.92)mmol/L、(38.24±8.36)AFU/mg비(70.49±15.21)AFU/mg、(8.26±4.47)비(17.44±7.91)、(3.40±2.62)비(5.95±3.22)、(1.52±0.34)비(2.17±0.56)],차이유통계학의의(P＜0.05);광경화전경하,DD조신조직손상정도균경우DM조.결론 금기강당편가이감경당뇨병만성신손상적정도,기신장보호작용가능여기강지급강저AGEs、RAGE、NF-κBp65、MCP-1수평유관.
Objective To observe the effect of jinqi tablet on the expression of advanced glycation end products(AGEs), advanced glycation end products receptor(RAGE), nuclear transcription factor(NF)-κBp65 and monocyte chemoattractant protein(MCP)-1 in the kidney of diabetic rats. Methods The level of AGEs, RAGE,NF-κBp65 NF-κBp65 and MCP-1 were determined in the kidney of diabetes group (group DM), diabetes with jinqi tablet(group DD)and control group(group N)at the 20th week. The average plasma glucose(APG) ,triglyceride (TG) ,total cholesterol (TC), endogenous creatinine clearance (Ccr)and urine microal bumin were collected.Results Compared with the group DM, the level of UMA, TG, AGEs, RAGE, NF-κBp65, MCP-1 in group DD was lower, but the Ccr was higher. The pathological changes in group DD were not as significant as that in DM group.Conclusions Jinqi tablet may decrease the renal damage of diabetes. The renal protection of jinqi tablet is not related to the control of blood sugar and it maybe related to the inhibition of AGEs, RAGE, NF-κBp65 and MCP-1.
