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
2008年
3期
308-311
,共4页
p38丝裂原活化蛋白激酶%NF-κB%单核细胞趋化蛋白1%糖尿病肾病%大鼠肾小球系膜细胞株HBZY-1
p38絲裂原活化蛋白激酶%NF-κB%單覈細胞趨化蛋白1%糖尿病腎病%大鼠腎小毬繫膜細胞株HBZY-1
p38사렬원활화단백격매%NF-κB%단핵세포추화단백1%당뇨병신병%대서신소구계막세포주HBZY-1
p38 mitogen-activated protein kinase%NF-κB%Monocyte chemoattractant protein-1%Diabetic nephropathies%Rat mesangial cell line HBZY-1
目的 探讨p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase, p38MAPK)与NF-κB、单核细胞趋化蛋白1(monocyte chemoattractant protein-1, MCP-1)之间的关系,从而研究p38MAPK和NF-κB、MCP-1在糖尿病肾病中的作用机制.方法 分别以高葡萄糖、高胰岛素、H2O2和糖基化终产物孵育大鼠肾小球系膜细胞株HBZY-1;先以p38MAPK特异抑制剂SB203580预处理细胞株HBZY-1,再给予上述4种因素孵育细胞株HBZY-1,观察其p38MAPK和NF-κB、MCP-1的表达.结果 高葡萄糖、高胰岛素、H2O2和糖基化终产物均可独立激活p38MAPK,使其磷酸化表达量增加,NF-κB、MCP-1表达也明显增加;SB203580预处理后,NF-κB、MCP-1表达被显著抑制.结论 p38MAPK可能通过激活NF-κB、MCP-1而诱导糖尿病时肾脏的损害,p38MAPK和NF-κB、MCP-1在糖尿病肾病的发生发展过程中可能起重要作用.
目的 探討p38絲裂原活化蛋白激酶(p38 mitogen-activated protein kinase, p38MAPK)與NF-κB、單覈細胞趨化蛋白1(monocyte chemoattractant protein-1, MCP-1)之間的關繫,從而研究p38MAPK和NF-κB、MCP-1在糖尿病腎病中的作用機製.方法 分彆以高葡萄糖、高胰島素、H2O2和糖基化終產物孵育大鼠腎小毬繫膜細胞株HBZY-1;先以p38MAPK特異抑製劑SB203580預處理細胞株HBZY-1,再給予上述4種因素孵育細胞株HBZY-1,觀察其p38MAPK和NF-κB、MCP-1的錶達.結果 高葡萄糖、高胰島素、H2O2和糖基化終產物均可獨立激活p38MAPK,使其燐痠化錶達量增加,NF-κB、MCP-1錶達也明顯增加;SB203580預處理後,NF-κB、MCP-1錶達被顯著抑製.結論 p38MAPK可能通過激活NF-κB、MCP-1而誘導糖尿病時腎髒的損害,p38MAPK和NF-κB、MCP-1在糖尿病腎病的髮生髮展過程中可能起重要作用.
목적 탐토p38사렬원활화단백격매(p38 mitogen-activated protein kinase, p38MAPK)여NF-κB、단핵세포추화단백1(monocyte chemoattractant protein-1, MCP-1)지간적관계,종이연구p38MAPK화NF-κB、MCP-1재당뇨병신병중적작용궤제.방법 분별이고포도당、고이도소、H2O2화당기화종산물부육대서신소구계막세포주HBZY-1;선이p38MAPK특이억제제SB203580예처리세포주HBZY-1,재급여상술4충인소부육세포주HBZY-1,관찰기p38MAPK화NF-κB、MCP-1적표체.결과 고포도당、고이도소、H2O2화당기화종산물균가독립격활p38MAPK,사기린산화표체량증가,NF-κB、MCP-1표체야명현증가;SB203580예처리후,NF-κB、MCP-1표체피현저억제.결론 p38MAPK가능통과격활NF-κB、MCP-1이유도당뇨병시신장적손해,p38MAPK화NF-κB、MCP-1재당뇨병신병적발생발전과정중가능기중요작용.
Objective To investigate the relationship among p38 mitogen-activated protein kinase (p38MAPK), NF-KB and monocyte chemoattractant protein-1 (MCP-1), and to study the role of p38MAPK, NF-κB and MCP-1 in diabetic nephropathy. Methods Protein expressions of p38MAPK and NF-κB, and mRNA expression of MCP-1 were initially investigated in rat mesangial cell line HBZY-1, which were incubated separately with 25mmol/L glucose, 100nmol/L insulin, 100 μmol/L H2 O2 and 100mg/L advanced glycosylation end products (AGEs). The relationship among p38MAPK, NF-κB and MCP-1 expression Was observed by usingSB203580, a specific inhibitor of p38MAPK. Results The expressions of p38MAPK, NF-κB and MCP-1 were increased in HBZY-1 cells incubated separately with 25mmol/L glucose, 100nmol/L insulin, 100μmol/L H2 O2and 100 mg/L AGEs. Expressions of NF-κB and MCP-1 were significantly reduced when p38MAPK was inhibited by SB203580. Conclusion p38MAPK, NF-κB and MCP-1 are involved in development of diabetic nephropathy, and p38MAPK stimulation is essential for the expressions of NF-κB and MCP-1.
