中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2015年
8期
1066-1070,1071
,共6页
覃媛%何艳华%张根水%张贵平%罗健东
覃媛%何豔華%張根水%張貴平%囉健東
담원%하염화%장근수%장귀평%라건동
内皮祖细胞%1 型糖尿病%Sonic hedgehog信号通路%增殖%迁移%小管形成%衰老
內皮祖細胞%1 型糖尿病%Sonic hedgehog信號通路%增殖%遷移%小管形成%衰老
내피조세포%1 형당뇨병%Sonic hedgehog신호통로%증식%천이%소관형성%쇠로
endothelial progenitor cells%type 1 diabe-tes mellitus%Sonic hedgehog pathway%proliferation%migration%tube formation%senescence
目的:研究激活Sonic hedgehog通路对1型糖尿病小鼠内皮祖细胞( EPCs)生物学功能的影响。方法用链脲佐菌素( STZ)诱导建立1型糖尿病小鼠模型;采用密度梯度离心法分离并培养糖尿病小鼠骨髓 EPCs;体外给予 Sonic hedgehog( Shh)信号通路配体蛋白Shh和受体激动剂SAG,通过MTT法、改良Boyden小室、Matrigel和β-半乳糖苷酶分别检测各组EPCs的增殖、迁移、小管形成和衰老的功能性指标。结果1型糖尿病小鼠EPCs与正常对照组相比功能明显下降,体外给予Shh蛋白和受体激动剂SAG,可促进糖尿病EPCs增殖,减少衰老,改善迁移和小管形成能力。结论体外激活Sonic hedgehog通路可以改善1型糖尿病小鼠内皮祖细胞受损的功能。
目的:研究激活Sonic hedgehog通路對1型糖尿病小鼠內皮祖細胞( EPCs)生物學功能的影響。方法用鏈脲佐菌素( STZ)誘導建立1型糖尿病小鼠模型;採用密度梯度離心法分離併培養糖尿病小鼠骨髓 EPCs;體外給予 Sonic hedgehog( Shh)信號通路配體蛋白Shh和受體激動劑SAG,通過MTT法、改良Boyden小室、Matrigel和β-半乳糖苷酶分彆檢測各組EPCs的增殖、遷移、小管形成和衰老的功能性指標。結果1型糖尿病小鼠EPCs與正常對照組相比功能明顯下降,體外給予Shh蛋白和受體激動劑SAG,可促進糖尿病EPCs增殖,減少衰老,改善遷移和小管形成能力。結論體外激活Sonic hedgehog通路可以改善1型糖尿病小鼠內皮祖細胞受損的功能。
목적:연구격활Sonic hedgehog통로대1형당뇨병소서내피조세포( EPCs)생물학공능적영향。방법용련뇨좌균소( STZ)유도건립1형당뇨병소서모형;채용밀도제도리심법분리병배양당뇨병소서골수 EPCs;체외급여 Sonic hedgehog( Shh)신호통로배체단백Shh화수체격동제SAG,통과MTT법、개량Boyden소실、Matrigel화β-반유당감매분별검측각조EPCs적증식、천이、소관형성화쇠로적공능성지표。결과1형당뇨병소서EPCs여정상대조조상비공능명현하강,체외급여Shh단백화수체격동제SAG,가촉진당뇨병EPCs증식,감소쇠로,개선천이화소관형성능력。결론체외격활Sonic hedgehog통로가이개선1형당뇨병소서내피조세포수손적공능。
Aim To study the effect of activating Sonic hedgehog( Shh) pathway on the function of endothelial progenitor cells ( EPCs ) in type 1 diabetic mice. Methods EPCs were isolated and cultured by density gradient method from diabetic mice. The effects of Shh N-terminal peptide and agonist SAG on EPCs prolifera-tion were evaluated by using the MTT colorimetric as-say. EPCs migration was measured by Transwell meth-od. EPCs tube formation ability was estimated by Matrigel . EPCs senescence activity was determined by β-galactosidase staining. Results Compared with control mice, the function of EPCs in type 1 diabetic mice was impaired. The proliferation, migration and tube formation of diabetic EPCs could be promoted by Shh peptide and agonist SAG. The senescence of dia-betic EPCs could be decreased by Shh peptide and ag-onist SAG. Conclusion Activating Shh signaling pathway can improve the impared function of diabetic EPCs in type 1 diabetic mice.