摘要
目的探讨黄芪甲苷对棕榈酸诱导脂肪细胞炎症因子分泌的作用及其机制。方法 3T3-L1脂肪细胞分为空白对照组、模型组、黄芪甲苷组。黄芪甲苷(100μmol·L^(-1))预孵育3T3-L1脂肪细胞4 h后,再用500μmol·L^(-1)的棕榈酸处理24 h。Real-time PCR测定炎症因子IL-6和TNF-αmRNA的相对表达量;ELISA法测定细胞培养上清液中IL-6和TNF-α的分泌量,Western blot测定IκBα和p-IκBα蛋白的相对表达量;免疫荧光检测NF-κB的核转位。结果与空白组相比,棕榈酸可使脂肪细胞炎症因子IL-6、TNF-α的mRNA和蛋白表达增加。黄芪甲苷可缓解棕榈酸诱导的炎症因子表达升高。免疫印迹检测发现黄芪甲苷降低IκBα表达,增加IκBα的磷酸化;免疫荧光发现黄芪甲苷可降低棕榈酸诱导的NF-κB核转位。结论黄芪甲苷可降低棕榈酸诱导脂肪细胞炎症因子的表达,其机制与降低细胞内NF-κB的激活有关。
Objective To determine the effect and mechanism of astragaloside Ⅳ （AS-Ⅳ） on the expression of inflammatory factors in palmitic acid （PA）-induced 3T3-L1 adipocytes. Methods The 3T3-L1 adipocytes were divided into 3 groups： a control group, a PA group and a PA ＋ AS-IV group. After pre-incubation with AS-IV, the 3T3-L1 adipocytes were treated with PA （500 μmol · L - 1） for 24 h. The level of mRNA and protein expression of IL-6 and TNF-a were detected with Real-time PCR and ELISA, respectively. The NF- IκBa and IκBa expressions were measured by Western blot; the NF-κB nuclear translocation was determined by immunofluorescence. Results Compared with the control group, PA-treated 3T3-L1 adipocytes strongly increased the mRNA and protein expression of IL-6 and TNF-a. The increased inflammatory cytokines were inhibited by AS-IV pre-incubation. Meanwhile, pretreatment with AS-IV decreased the IκBa expression and nuclear translocation. Conclusion AS-IV decreases the expression of 3T3-L1 adipocytes inflammatory cytokines induced by PA via inhibiting NF-κB activity.
出处
《中南药学》
CAS
2017年第12期1721-1724,共4页
Central South Pharmacy
