重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2013年
21期
2496-2499
,共4页
肾小球系膜细胞%细胞增殖%细胞周期%商陆皂苷甲
腎小毬繫膜細胞%細胞增殖%細胞週期%商陸皂苷甲
신소구계막세포%세포증식%세포주기%상륙조감갑
mesangial cells%cell proliferation%cell cycle%esculentoside A
目的观察商陆皂苷甲（EsA ）对白细胞介素（IL ）-1β诱导的大鼠肾小球系膜细胞（rGM C ）增殖和细胞周期依赖性蛋白激酶（CDK2）及其抑制蛋白（P27）表达的影响。方法噻唑蓝（MTT）法检测EsA对 rGMC增殖与毒性的影响；碘化丙啶（PI）染色法，流式细胞仪检测细胞周期；蛋白免疫印迹法（Western blotting ）检测CDK2、P27的表达。结果观察剂量中EsA对rG-MC没有细胞毒作用，EsA（2．5～5．0 mg/L）作用rGMC 48 h后明显抑制其增殖；IL-1β减少了rGMC的G1期细胞数并增加了S期的细胞数，促进了rGMC的CDK2的表达，抑制了P27的表达；EsA增加了IL-1β诱导的rGMC的G1期的细胞数并减少了S期的细胞数，抑制了IL-1β诱导的rGMC的CDK2的表达，并促进了P27的表达。结论 rGMC可能是EsA的作用靶细胞，EsA通过抑制CDK2及激活P27的表达抑制了IL-1β诱导的rGMC的增殖，阻滞了细胞周期的进程。
目的觀察商陸皂苷甲（EsA ）對白細胞介素（IL ）-1β誘導的大鼠腎小毬繫膜細胞（rGM C ）增殖和細胞週期依賴性蛋白激酶（CDK2）及其抑製蛋白（P27）錶達的影響。方法噻唑藍（MTT）法檢測EsA對 rGMC增殖與毒性的影響；碘化丙啶（PI）染色法，流式細胞儀檢測細胞週期；蛋白免疫印跡法（Western blotting ）檢測CDK2、P27的錶達。結果觀察劑量中EsA對rG-MC沒有細胞毒作用，EsA（2．5～5．0 mg/L）作用rGMC 48 h後明顯抑製其增殖；IL-1β減少瞭rGMC的G1期細胞數併增加瞭S期的細胞數，促進瞭rGMC的CDK2的錶達，抑製瞭P27的錶達；EsA增加瞭IL-1β誘導的rGMC的G1期的細胞數併減少瞭S期的細胞數，抑製瞭IL-1β誘導的rGMC的CDK2的錶達，併促進瞭P27的錶達。結論 rGMC可能是EsA的作用靶細胞，EsA通過抑製CDK2及激活P27的錶達抑製瞭IL-1β誘導的rGMC的增殖，阻滯瞭細胞週期的進程。
목적관찰상륙조감갑（EsA ）대백세포개소（IL ）-1β유도적대서신소구계막세포（rGM C ）증식화세포주기의뢰성단백격매（CDK2）급기억제단백（P27）표체적영향。방법새서람（MTT）법검측EsA대 rGMC증식여독성적영향；전화병정（PI）염색법，류식세포의검측세포주기；단백면역인적법（Western blotting ）검측CDK2、P27적표체。결과관찰제량중EsA대rG-MC몰유세포독작용，EsA（2．5～5．0 mg/L）작용rGMC 48 h후명현억제기증식；IL-1β감소료rGMC적G1기세포수병증가료S기적세포수，촉진료rGMC적CDK2적표체，억제료P27적표체；EsA증가료IL-1β유도적rGMC적G1기적세포수병감소료S기적세포수，억제료IL-1β유도적rGMC적CDK2적표체，병촉진료P27적표체。결론 rGMC가능시EsA적작용파세포，EsA통과억제CDK2급격활P27적표체억제료IL-1β유도적rGMC적증식，조체료세포주기적진정。
Objective To observe the effect of esculemoside A (EsA)on the proliferation and expression of CDK2 and P27 of rats glomerular mesangial cell .Methods rGMC was cultured in vitro ,The cell growth and cell toxicity were detected by MTT assay ;rGMC proliferation was observed by Rnase/PI-Flous ;The expression of CDK2 and P27 were measured by Western blotting .Results EsA at observed dose has not apparent cytotoxicity effect on rGMC .EsA(2 .5-5 .0 mg/L) inhibited the proliferation of rGMC after 48h .EsA increased the number of the G1 phase and reduced the number of the S phase of IL-1βinduced rGMC .At the same time ,EsA inhibited the expression of CDK2 and promoted the expression of P27 of IL-1βinduced rGMC .Conclusion The GMC is one of the mainly target cell which EsA bing therapeu tical action .EsA inhibited proliferation of IL-1βinduced the GMC ,inhibited the expression of CDK2 and activated the expression of P27 may be its mechanism .
