甘草素通过激活 PI3K/AKT 通路调节胰岛素敏感性并改善非酒精性脂肪肝中的炎症反应,Chemical Biology & Drug Design

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甘草素通过激活 PI3K/AKT 通路调节胰岛素敏感性并改善非酒精性脂肪肝中的炎症反应
Chemical Biology & Drug Design ( IF 3.2 ) Pub Date : 2023-07-16 , DOI: 10.1111/cbdd.14292
Lei Bao ₁ , Pei Hao ₂ , Meiju Jiang ₁ , Weijiang Chu ₃

Affiliation

非酒精性脂肪肝（NAFLD）是世界上一种流行的长期疾病。甘草素 (LQ) 对多种肝毒素具有保护作用。在此，我们报告了 LQ 对高脂饮食 (HFD) 诱导的 NAFLD 的潜在机制。采用HFD 12周、LQ治疗1周建立NAFLD小鼠模型。市售检测试剂盒可测量肝脏甘油三酯 (TG) 和总胆固醇 (TC) 水平。还通过生化监测血浆 TC、TG、高密度脂蛋白 (HDL-C) 和低密度脂蛋白胆固醇 (LDL-C) 水平。采用酶联免疫吸附测定（ELISA）试剂盒分析促炎因子，并测定腹腔葡萄糖耐量试验（IPGTT）、胰岛素耐量试验（IPITT）和血清胰岛素。采用GO和KEGG通路富集分析来分析LQ靶点和NAFLD发展相关靶点的重叠基因。对富集信号通路的关键蛋白进行蛋白质印迹。HFD 小鼠血脂中肝脏 TG 和 TC 以及血浆 TC、TG 和 LDL-C 显着升高，而 HDL-C 显着降低，LQ 治疗逆转了它们的水平（p < 0.05 ）。LQ 还减轻了 HFD 引起的 IPGTT、IPITT 和胰岛素抵抗稳态模型评估 (HOMA-IR) 水平的升高。LQ 也抑制了促炎因子的血清水平。KEGG 通路富集后 PI3K/AKT 通路得到富集，LQ 处理后其关键蛋白 p-PI3K 和 p-AKT 升高（p < 0.05）。我们首次发现LQ可以改善NAFLD小鼠的脂质积累、减轻胰岛素抵抗并抑制炎症反应，这可能与PI3K/AKT通路的激活有关。

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Liquiritigenin regulates insulin sensitivity and ameliorates inflammatory responses in the nonalcoholic fatty liver by activation PI3K/AKT pathway

Nonalcoholic fatty liver disease (NAFLD) is a prevalent long-term disease in the world. Liquiritigenin (LQ) is protective against a variety of hepatotoxins. Herein, we report the potential mechanism of LQ on a high-fat diet (HFD) induced NAFLD. NAFLD mice model was established by HFD for 12 weeks, and LQ treatment for 1 week. Commercially available assay kits measure liver triglycerides (TG) and total cholesterol (TC) levels. Plasm TC, TG, high-density-lipoprotein (HDL-C), and low-density-lipoprotein cholesterol (LDL-C) levels were also monitored by biochemistry. Enzyme linked immunosorbent assay (ELISA) kits were performed to analyze the pro-inflammatory factors, and intraperitoneal glucose tolerance test (IPGTT), insulin tolerance test (IPITT), and serum insulin were also determined. GO and KEGG pathway enrichment analysis was employed to analyze the overlapping genes of LQ targets and NAFLD development-related targets. Western blot was performed on key proteins of the enriched signaling pathway. HFD mice showed significant increases in hepatic TG and TC, and plasm TC, TG, and LDL-C in blood lipids, while HDL-C significantly decreased, and LQ treatment reversed their levels (p < 0.05). LQ also alleviated HFD-induced elevated levels of IPGTT, IPITT, and homeostasis model assessment of insulin resistance (HOMA-IR). And serum levels of the pro-inflammatory factor were also suppressed by LQ. PI3K/AKT pathway was enriched by KEGG pathway enrichment, and its key proteins p-PI3K and p-AKT were elevated after LQ treatment (p < 0.05). We found for the first time that LQ improves lipid accumulation, alleviates insulin resistance, and suppresses inflammatory responses in NAFLD mice, which might be associated with the activation of the PI3K/AKT pathway.

更新日期：2023-07-16

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