首页|灯盏花乙素通过PPARγ-PGC1α-UCP1通路改善小鼠肥胖作用及机制

灯盏花乙素通过PPARγ-PGC1α-UCP1通路改善小鼠肥胖作用及机制

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目的 探究灯盏花乙素对肥胖小鼠的干预作用及可能的分子机制,为肥胖的治疗提供借鉴.方法 采用高脂膳食构建小鼠肥胖模型,并采用灯盏花乙素(400mg·kg-1)干预8周,测定各组小鼠肥胖相关指标,包括体质量变化、脂肪组织质量、血脂指标[总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)及高密度脂蛋白胆固醇(HDL-C)]等;采用苏木精-伊红(HE)染色法分析脂肪组织形态的改变;分别采用免疫荧光方法、实时荧光定量PCR(qRT-PCR)及Western blotting法检测脂肪组织中脂质代谢相关基因[过氧化酶体增殖物激活受体γ(PPARγ)、PPARγ共激活因子1α(PGC1α)与解偶联蛋白1(UCP1)]、蛋白(PPARγ、PGC1α及UCP-1)表达水平的变化.结果 结果显示,灯盏花乙素干预可显著降低高脂喂养小鼠的体质量及脂肪组织质量(P＜0.05、0.01);另外,灯盏花乙素可改善血脂指标——TC、TG、LDL-C及HDL-C;组织病理学结果显示,灯盏花乙素可以减轻脂肪组织中的脂质沉积.进一步qRT-PCR结果显示,灯盏花乙素极显著提高肥胖小鼠脂肪组织中PPARγ的mRNA表达水平(P＜0.05),同时还能升高PGC1α与UCP1的mRNA表达水平,差异具有极显著性(P＜0.01).Western blotting结果则进一步验证了灯盏花乙素能显著提高高脂喂养小鼠脂肪组织PPARγ、PGC1α以及UCP1的蛋白表达水平(P＜0.05).结论 灯盏花乙素可以改善高脂喂养小鼠肥胖,该作用可能与激活PPARγ-PGC1α-UCP1信号通路,调节脂肪组织的能量代谢有关.
Scutellarin ameliorates obesity in high-fat fed mice by regulating PPARγ-PGC1α-UCP1 signaling pathway
To explore the intervention effect of scutellarin(SCU)on obese mice fed with high-fat diet and its possible molecular mechanism,and provide reference for the treatment of obesity.Firstly,a mouse obesity model was constructed with a high-fat diet,and SCU was used to intervene for 8 weeks.Obesity-related indexes,such as weight change,adipose tissue weight and lipid indexes,were measured in each group.The changes of adipose tissue morphology were analyzed by HE staining.Immunofluorescence,quantitative real-time fluorescence polymerase chain reaction(qRT-PCR)and Western blotting were used to detect the expression levels of lipid metabolism-related genes and proteins in adipose tissue.The results showed that the body weight and adipose tissue weight of high-fat fed mice could be significantly reduced after SCU intervention.In addition,SCU could improve total cholesterol(TC),triglyceride(TG),low density lipoprotein cholesterol(LDL-C)and high density lipoprotein cholesterol(HDL-C)(P＜0.05,0.01).Histopathological results showed that SCU could reduce lipid deposition in adipose tissue.Further,qRT-PCR results showed that SCU significantly increased the mRNA expression level of peroxidase proliferator-activated receptor γ(PPARγ)in adipose tissue of high-fat fed mice(P＜0.01),and significantly increased the mRNA expression level of PGC1α and uncoupling protein-1(UCP1)in high-fat fed mice(P＜0.01).Western blotting results further demonstrated that SCU significantly increased the protein expression levels of PPARγ,PGC1α and UCP1 in adipose tissue of high-fat fed mice(P＜0.01).Conclusion SCU can effectively improve obesity in high-fat fed mice,and the improvement may be related to the PPARγ-PGC1α-UCP1 signaling pathway.

scutellarinobesityPPARγ-PGC1α-UCP1 signaling pathwayblood lipidlipid metablishment

张琦、田冲冲、张洋、方晨曦、卜薇、李凤

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江苏医药职业学院药学院,江苏盐城 224005

灯盏花乙素 肥胖 PPARγ-PGC1α-UCP1信号通路 血脂 脂质代谢

江苏省盐城市卫生健康委员会2023年度医学科研立项项目江苏省盐城市卫生健康委员会2023年度医学科研立项项目江苏高校哲学社会科学研究一般项目江苏省高职院校青年教师企业实践计划江苏医药职业学院自然科学基金研究重点项目江苏医药职业学院自然科学基金研究重点项目江苏医药职业学院校本教育教学研究课题江苏医药职业学院校本教育教学研究课题

YK2023032YK20230972022SJYB20752023QYSJ0472021410720214103Q202303Y202322

2024

10.7501/j.issn.1674-6376.2024.08.012

药物评价研究
天津药物研究院 中国药学会

药物评价研究

CSTPCD北大核心
影响因子：1.199
ISSN：1674-6376
年,卷(期)：2024.47(8)