中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2008年
12期
923-926
,共4页
CD40配体%胰岛素抗药性%血小板膜糖蛋白Ⅱb
CD40配體%胰島素抗藥性%血小闆膜糖蛋白Ⅱb
CD40배체%이도소항약성%혈소판막당단백Ⅱb
CD40 ligand%Insulin resistance%Platelet,membrane glyeoprotein Ⅱb
目的 观察罗格列酮对胰岛素抵抗大鼠血小板CD40配体(CD40L)变化的影响,进一步明确胰岛素抵抗、CD40L之间的关系. 方法 健康SD大鼠60只,随机分为普食组、高脂组、小剂量干预组和大剂量干预组.普食组给予基础饲料,高脂组、小剂量干预组、大剂量干预组均给予高脂饲料.喂养12周后小剂量干预组每天给予5 mg/kg罗格列酮灌胃,大剂量干预组每天给予10mg/kg罗格列酮灌胃,高脂组、普食组则给予相应剂量的生理盐水灌胃.干预治疗4周后(第16周)用稳态模型评估法计算胰岛素抵抗指数(HOMA-IR),以ELISA法测定循环sCD40L浓度,以免疫沉淀、免疫印迹测定血小板膜蛋白CD40L表达. 结果 高脂组与普食组比较,HOMA-IR(9.8±3.2比5.9±1.7)、循环sCD40L(367.3±35.3比232.3±120.6)、血小板CD40L(2.1±0.4比1.4±0.2)均明显升高(均为P<0.05).罗格列酮干预后,大剂景组HOMA(5.4±1.1)、循环sCD40L(276.9±54.0)、血小板CD40L(1.4±0.3)均明显降低(均为P<0.05). 结论 胰岛素抵抗大鼠血小板CD40L表达升高;大剂最罗格列酮干预后,CD40L随着胰岛素抵抗的改善而下降.
目的 觀察囉格列酮對胰島素牴抗大鼠血小闆CD40配體(CD40L)變化的影響,進一步明確胰島素牴抗、CD40L之間的關繫. 方法 健康SD大鼠60隻,隨機分為普食組、高脂組、小劑量榦預組和大劑量榦預組.普食組給予基礎飼料,高脂組、小劑量榦預組、大劑量榦預組均給予高脂飼料.餵養12週後小劑量榦預組每天給予5 mg/kg囉格列酮灌胃,大劑量榦預組每天給予10mg/kg囉格列酮灌胃,高脂組、普食組則給予相應劑量的生理鹽水灌胃.榦預治療4週後(第16週)用穩態模型評估法計算胰島素牴抗指數(HOMA-IR),以ELISA法測定循環sCD40L濃度,以免疫沉澱、免疫印跡測定血小闆膜蛋白CD40L錶達. 結果 高脂組與普食組比較,HOMA-IR(9.8±3.2比5.9±1.7)、循環sCD40L(367.3±35.3比232.3±120.6)、血小闆CD40L(2.1±0.4比1.4±0.2)均明顯升高(均為P<0.05).囉格列酮榦預後,大劑景組HOMA(5.4±1.1)、循環sCD40L(276.9±54.0)、血小闆CD40L(1.4±0.3)均明顯降低(均為P<0.05). 結論 胰島素牴抗大鼠血小闆CD40L錶達升高;大劑最囉格列酮榦預後,CD40L隨著胰島素牴抗的改善而下降.
목적 관찰라격렬동대이도소저항대서혈소판CD40배체(CD40L)변화적영향,진일보명학이도소저항、CD40L지간적관계. 방법 건강SD대서60지,수궤분위보식조、고지조、소제량간예조화대제량간예조.보식조급여기출사료,고지조、소제량간예조、대제량간예조균급여고지사료.위양12주후소제량간예조매천급여5 mg/kg라격렬동관위,대제량간예조매천급여10mg/kg라격렬동관위,고지조、보식조칙급여상응제량적생리염수관위.간예치료4주후(제16주)용은태모형평고법계산이도소저항지수(HOMA-IR),이ELISA법측정순배sCD40L농도,이면역침정、면역인적측정혈소판막단백CD40L표체. 결과 고지조여보식조비교,HOMA-IR(9.8±3.2비5.9±1.7)、순배sCD40L(367.3±35.3비232.3±120.6)、혈소판CD40L(2.1±0.4비1.4±0.2)균명현승고(균위P<0.05).라격렬동간예후,대제경조HOMA(5.4±1.1)、순배sCD40L(276.9±54.0)、혈소판CD40L(1.4±0.3)균명현강저(균위P<0.05). 결론 이도소저항대서혈소판CD40L표체승고;대제최라격렬동간예후,CD40L수착이도소저항적개선이하강.
Objective To investigate the effect of rosiglitazone on the expression of platelet CD40 ligand (CD40L) in insulin-resistant rats, and to further determine the relationship between CD40L and insulin resistance. Methods 60 healthy male SD rats [(200±20)g] were randomly divided into 4 groups: control group (C), high fat group (HF), low dose rosiglitazone group (LR) and high dose rosiglitazone group (HR). Rats in group C were fed normal chow diet, and the others were given high fat chow diet. After 12 weeks, high dose of rosiglitazone (10mg/kg) was given to rats in group HR and low dose of rosiglitazone (5 mg/kg) was given to rats in group LR for 4 weeks. Rats in group HF and group C were given 0.9% sodium chloride solution. The level of sCD40L was measured by ELISA and the expression of platelet membrane CD40L was detected by immunoprecipitation and Western blot. The insulin resistance (IR) index was calculated by homeostasis model assessment (HOMA). Results HOMA-IR, sCD40L level and platelet membrane CD40L expression were higer in group HF than in group C (9.8±3.2 vs. 5.9±1.7, 367.3 ±35.3 vs. 232.3±120.6, 2.1±0.4 vs. 1.4±0.2, respectively, all P<0.05). Compared with the group HF, HOMA-IR, sCD40L level and platelet membrane CD40L expression were obviously decreased in group HR(5.4±1.1, 276.9±54.0, 1.4±0.3, respectively, all P<0.05), and there were no significant differences in HOMA-IR, sCD40L level and platelet membrane CD40L expression between group HF and group LR (P>0.05). Conclusions In insulin-resistant rats, the level of sCD40L and the expression of platelet membrane CD40L were higher. After treatment with high dose of rosiglitazone, sCD40L level and platelet membrane CD40L expression were decreased with the improvement of insulin resistance.
