目的 探究燈盞花乙素對肥胖小鼠的干預(yù)作用及可能的分子機制，為肥胖的治療提供借鑒。方法 采用高脂膳食構(gòu)建小鼠肥胖模型，并采用燈盞花乙素（400 mg·kg^-1）干預(yù)8周，測定各組小鼠肥胖相關(guān)指標(biāo)，包括體質(zhì)量變化、脂肪組織質(zhì)量、血脂指標(biāo)［總膽固醇（TC）、三酰甘油（TG）、低密度脂蛋白膽固醇（LDL-C）及高密度脂蛋白膽固醇（HDL-C）］等；采用蘇木精-伊紅（HE）染色法分析脂肪組織形態(tài)的改變；分別采用免疫熒光方法、實時熒光定量PCR（qRT-PCR）及Western blotting法檢測脂肪組織中脂質(zhì)代謝相關(guān)基因［過氧化酶體增殖物激活受體γ （PPARγ）、PPARγ共激活因子1α（PGC1α）與解偶聯(lián)蛋白1（UCP1）］、蛋白（PPARγ、PGC1α及UCP-1）表達水平的變化。結(jié)果 結(jié)果顯示，燈盞花乙素干預(yù)可顯著降低高脂喂養(yǎng)小鼠的體質(zhì)量及脂肪組織質(zhì)量（P＜0.05、0.01）；另外，燈盞花乙素可改善血脂指標(biāo)——TC、TG、LDL-C及HDL-C；組織病理學(xué)結(jié)果顯示，燈盞花乙素可以減輕脂肪組織中的脂質(zhì)沉積。進一步qRT-PCR結(jié)果顯示，燈盞花乙素極顯著提高肥胖小鼠脂肪組織中PPARγ的mRNA表達水平（P＜0.05），同時還能升高PGC1α與UCP1的mRNA表達水平，差異具有極顯著性（P＜0.01）。Western blotting結(jié)果則進一步驗證了燈盞花乙素能顯著提高高脂喂養(yǎng)小鼠脂肪組織PPARγ、PGC1α以及UCP1的蛋白表達水平（P＜0.05）。結(jié)論 燈盞花乙素可以改善高脂喂養(yǎng)小鼠肥胖，該作用可能與激活PPARγ-PGC1α-UCP1信號通路，調(diào)節(jié)脂肪組織的能量代謝有關(guān)。

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.

R739.5

江蘇省鹽城市衛(wèi)生健康委員會2023年度醫(yī)學(xué)科研立項項目（YK2023032，YK2023097）;江蘇高校哲學(xué)社會科學(xué)研究一般項目資助（2022SJYB2075）;江蘇省高職院校青年教師企業(yè)實踐計劃（2023QYSJ047）;江蘇醫(yī)藥職業(yè)學(xué)院自然科學(xué)基金研究重點項目（20214107，20214103）;江蘇醫(yī)藥職業(yè)學(xué)院校本教育教學(xué)研究課題（Q202303，Y202322）