论文部分内容阅读
目的探讨代谢综合征(MS)大鼠肠系膜脂肪组织中肾素-血管紧张素系统(RAS)变化及拮抗血管紧张素Ⅱ(AngⅡ)对脂肪细胞成脂作用的影响。方法30只8周龄健康雄性Wistar大鼠随机分为MS组和正常对照组,分别给予高脂饲料和普通饲料喂养24周,造成MS模型后,取出肠系膜脂肪组织,应用RT-PCR和Westernblot法检测脂肪组织中mRNA和蛋白质表达。同时,将前脂肪细胞(3T3-L1)进行诱导分化,油红O染色观察脂滴形成情况,比率荧光倒置显微镜检测脂肪细胞内钙水平([Ca2+]i)。给予AngⅡ刺激,并观察血管紧张素Ⅱ受体阻断剂(ARB)坎地沙坦或血管紧张素转换酶抑制剂(ACEI)巯甲丙脯酸对脂滴形成及细胞内钙水平([Ca2+]i)的作用。结果MS大鼠肠系膜脂肪组织的血管紧张素原(AGT)、血管紧张素转换酶(ACE)和血管紧张素Ⅱ受体亚型1(AT1R)表达均显著高于正常对照组(P<0·05,P<0·01);未诱导前脂肪细胞和经AngⅡ处理的成熟脂肪细胞未见明显脂滴形成,给予ACEI和ARB的成熟脂肪细胞有明显的脂滴形成;AngⅡ可致前脂肪细胞内钙水平([Ca2+]i)显著增加(P<0·01),巯甲丙脯酸和坎地沙坦可阻断其效应,而对成熟脂肪细胞,AngⅡ介导的细胞内钙水平([Ca2+]i)升高受到抑制,但坎地沙坦能恢复AngⅡ的效应,巯甲丙脯酸与AngⅡ组比较细胞内钙水平([Ca2+]i)差异无显著性。结论代谢综合征大鼠肠系膜脂肪组织中RAS系统处于激活状态,拮抗RAS能恢复脂肪细胞的基本功能。
Objective To investigate the changes of renin - angiotensin system (RAS) in mesenteric adipose tissue of rats with metabolic syndrome (MS) and the effect of antagonizing angiotensin Ⅱ (Ang Ⅱ) on the adipogenic effect of adipocytes. Methods Thirty healthy male Wistar rats, aged 8 weeks, were randomly divided into MS group and normal control group. The rats were fed with high-fat diet and normal diet for 24 weeks respectively. After MS model was induced, mesenteric adipose tissue was removed. RT-PCR and Western blot Detection of adipose tissue mRNA and protein expression. At the same time, adipocytes (3T3-L1) were induced to differentiate, the formation of lipid droplets was observed with oil red O staining, and the ratio of intracellular calcium ([Ca2 +] i) was measured by fluorescence inverted microscopy. Ang Ⅱ was given to the rats and the effects of angiotensin II receptor blocker (ARB) and angiotensin-converting enzyme inhibitor (ACEi) captopril on lipid drop formation and intracellular calcium level ([Ca 2+] ] i) role. Results The expressions of angiotensinogen (AGT), angiotensin converting enzyme (ACE) and angiotensin Ⅱ receptor type 1 (AT1R) in mesenteric adipose tissue of MS rats were significantly higher than those of normal control rats (P <0 · 05, P <0.01). No lipid droplet formation was observed in uninduced preadipocytes and mature adipocytes treated with AngⅡ. Adipocytes were found to form lipid droplets in mature adipocytes treated with ACEI and ARB. Ang Ⅱ preadipocytes (P <0.01). Captopril and candesartan could block the effect of Ca (superscript 2 +) on intracellular calcium (Ca2 + [Ca2 +] i) was inhibited, but candesartan restored the effect of AngⅡ. There was no significant difference in intracellular calcium level ([Ca2 +] i) between captopril and AngⅡgroup. Conclusion The RAS system in mesenteric adipose tissue of rats with metabolic syndrome is activated and antagonism of RAS can restore the basic functions of adipocytes.