浙江医学
浙江醫學
절강의학
ZHEJIANG MEDICAL JOURNAL
2013年
16期
1490-1493
,共4页
雷公藤内酯醇%糖尿病肾病%肾小球足细胞裂孔隔膜%核心蛋白
雷公籐內酯醇%糖尿病腎病%腎小毬足細胞裂孔隔膜%覈心蛋白
뢰공등내지순%당뇨병신병%신소구족세포렬공격막%핵심단백
Triptolide%DN%GPSD%Core protein
目的观察雷公藤内酯醇（TP）干预高糖环境培养的小鼠肾小球足细胞裂孔隔膜nephrin、podocin和CD2AP的表达，探讨雷公藤治疗糖尿病肾病（DN）蛋白尿的分子生物学机制。方法培养成熟的小鼠足细胞随机分为对照组1、对照组2、高糖组和TP干预组，TP干预组进一步分为低剂量、中剂量和高剂量组。用不同浓度的TP（8、16和32ng/ml）干预高糖（25mmol/L的Glu）培养24h后的小鼠足细胞，用 RT- PCR法检测干预前后nephrin、podocin和CD2AP mRNA的表达；用间接免疫荧光法检测16ng/ml TP干预后nephrin和podocin蛋白的表达。结果（1）与对照组相比，高糖诱导的足细胞nephrin、podocin和CD2AP mRNA表达均明显减弱（均P＜0.01）。（2）TP显著上调高糖诱导的足细胞nephrin、podocin和CD2AP mRNA的表达（均P＜0.05）。（3）16ng/ml TP能明显上调高糖对足细胞nephrin和podocin（均P＜0.05）蛋白表达的抑制。结论 TP显著上调高糖诱导的足细胞nephrin、podocin和CD2AP的表达，可能是其降低DN蛋白尿的机制之一。
目的觀察雷公籐內酯醇（TP）榦預高糖環境培養的小鼠腎小毬足細胞裂孔隔膜nephrin、podocin和CD2AP的錶達，探討雷公籐治療糖尿病腎病（DN）蛋白尿的分子生物學機製。方法培養成熟的小鼠足細胞隨機分為對照組1、對照組2、高糖組和TP榦預組，TP榦預組進一步分為低劑量、中劑量和高劑量組。用不同濃度的TP（8、16和32ng/ml）榦預高糖（25mmol/L的Glu）培養24h後的小鼠足細胞，用 RT- PCR法檢測榦預前後nephrin、podocin和CD2AP mRNA的錶達；用間接免疫熒光法檢測16ng/ml TP榦預後nephrin和podocin蛋白的錶達。結果（1）與對照組相比，高糖誘導的足細胞nephrin、podocin和CD2AP mRNA錶達均明顯減弱（均P＜0.01）。（2）TP顯著上調高糖誘導的足細胞nephrin、podocin和CD2AP mRNA的錶達（均P＜0.05）。（3）16ng/ml TP能明顯上調高糖對足細胞nephrin和podocin（均P＜0.05）蛋白錶達的抑製。結論 TP顯著上調高糖誘導的足細胞nephrin、podocin和CD2AP的錶達，可能是其降低DN蛋白尿的機製之一。
목적관찰뢰공등내지순（TP）간예고당배경배양적소서신소구족세포렬공격막nephrin、podocin화CD2AP적표체，탐토뢰공등치료당뇨병신병（DN）단백뇨적분자생물학궤제。방법배양성숙적소서족세포수궤분위대조조1、대조조2、고당조화TP간예조，TP간예조진일보분위저제량、중제량화고제량조。용불동농도적TP（8、16화32ng/ml）간예고당（25mmol/L적Glu）배양24h후적소서족세포，용 RT- PCR법검측간예전후nephrin、podocin화CD2AP mRNA적표체；용간접면역형광법검측16ng/ml TP간예후nephrin화podocin단백적표체。결과（1）여대조조상비，고당유도적족세포nephrin、podocin화CD2AP mRNA표체균명현감약（균P＜0.01）。（2）TP현저상조고당유도적족세포nephrin、podocin화CD2AP mRNA적표체（균P＜0.05）。（3）16ng/ml TP능명현상조고당대족세포nephrin화podocin（균P＜0.05）단백표체적억제。결론 TP현저상조고당유도적족세포nephrin、podocin화CD2AP적표체，가능시기강저DN단백뇨적궤제지일。
Objective To investigate the effect of triptolide (TP) on the expression of GPSD core proteins in mouse podocytes induced by high glucose. Methods The cultured mouse podocyte were randomly divided into control group1, control group2, high glucose group and TP treatment groups, which were further divided into low, middle and high dose subgroups. Podocyte exposed to 25 mmol/L glucose were treated with different doses of triptolide (8,16 and 32ng/ml). The expressions of nephrin, podocin and CD2AP mRNA were examined by RT- PCR. The expressions of nephrin and podocin protein were detected by indirect immunoflorescence technique (IIFT). Results Compared to control group, the expression of nephrin, podocin and CD2AP mRNA in high glucose group were significantly decreased (P<0.05 or P<0.01). Compared to high glucose group, the expression of nephrin, podocin and CD2AP mRNA were significantly up- regulated (P<0.05) in 3 TP- treatment groups, and the expression was highest in middle dose group (P<0.05). IIFT demonstrated that the inhibited expression of nephrin and podocin by high- glucose was significantly up- regulated in the middle dose group. Conclusion The expressions of nephrin, podocin and CD2AP in the mouse podocyte are inhibited in high glucose condition. These core proteins inhibited in high glucose can be sig-nificantly up- regulated by triptolide, indicating that it may attenuate the proteinuria in diabetic hephropathy.
