摘要
目的:探讨FK506对血糖调节的副作用,并研究其机制。方法:健康SD大鼠12只,随机分为2组:对照组(生理盐水,1 mL·kg-1·d-1)、给药组(FK506,1 mg·kg-1·d-1)。每天监测体重,每2 d测空腹血糖。在第15天取脂肪组织,实时荧光定量PCR检测脂联素(adiponectin)、瘦素(leptin)、内酯素(visfatin)、抵抗素(resistin)、视黄醇结合蛋白4(RBP4)及氧化物酶体增殖物激活受体γ(PPAR-γ)mRNA的表达;Western blotting检测PPAR-γ及脂联素蛋白的表达。结果:第10天开始,给药组大鼠空腹血糖逐渐升高,显著高于对照组(P<0.05);第14天,给药组空腹血糖由(5.10±0.62)mmol/L升到(7.73±0.73)mmol/L,对照组空腹血糖无明显变化;与对照组相比,给药组大鼠脂肪组织adiponectin和leptin mRNA的表达量显著降低(P<0.01),而visfatin、resistin和RBP4 mRNA表达明显升高(P<0.05);与对照组相比,给药组脂肪组织PPAR-γmRNA表达量降低(P<0.01);与对照组相比,给药组脂肪组织PPAR-γ及脂联素蛋白表达量明显降低(P<0.01)。结论:FK506可能通过抑制PPAR-γ的表达,影响脂肪因子的表达,影响血糖。
AIM：ToinvestigatetheeffectofimmunosuppressantFK506onserumglucoseinratsandtoex-plore its mechanism .METHODS： Sprague-Dawley rats （ n =12 ） were randomly divided into drug group and normal group.The rats in drug group were intraperitoneally injected with FK 506 at dose of 1 mg＆#183; kg-1 ＆#183; d-1 and the rats in nor-mal group received saline （1 mL＆#183; kg-1 ＆#183; d-1 , ip） for 14 d.The fasting weight and fasting glucose were regularly meas-ured every 2 d.Visceral fat was isolated from the rats at the end of experiment .The mRNA expression of adiponectin , lep-tin, visfatin, resistin, retinol-binding protein 4 （ RBP4） and peroxisome proliferator-activated receptors γ（ PPAR-γ） was determined by real-time fluorescence quantitative PCR .The protein expression of PPAR-γand adiponectin was measured by Western blotting .RESULTS：Compared with normal group , the concentration of fasting blood glucose in model group was significantly increased from the 10th day （P＆lt;0.05）.At day 14, the fasting blood glucose of the model group increased from （5.10 ＆#177;0.62） mmol/L to （7.73 ＆#177;0.73） mmol/L.No significant change of blood glucose in normal group between the 10th day and the 14th day [from （4.66 ＆#177;0.32） mmol/L to （5.80 ＆#177;0.10） mmol/L] was observed.Compared with normal group , the mRNA expression of PPAR-γ, adiponectin and leptin in the adipose tissue of model group was signifi-cantly decreased （ P ＆lt;0.01 ） , whereas the expression of visfatin , resistin and RBP4 was significantly increased （ P ＆lt;0.05）.Compared with normal group, the expression of PPAR-γand adiponectin in model group was decreased （P ＆lt;0.01）.CONCLUSION：FK506 may decrease the expression of PPAR-γto change the expression of adipocytokines and induce hyperglycemia in rats .
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2014年第8期1363-1367,共5页
Chinese Journal of Pathophysiology
基金
浙江省教育厅外科学重中之重学科资助项目
浙江省自然科学基金资助项目(No.Y2110944
No.LY12H1004)
浙江省卫生厅营养学支撑学科(No.11-ZC24)
