Cui Zhen-Yu, Han Xin, Jiang Yu-Chen, Dou Jia-Yi, Yao Kun-Chen, Hu Zhong-He, Yuan Ming-Hui, Bao Xiao-Xue, Zhou Mei-Jie, Liu Yue, Lian Li-Hua, Zhang Xian, Nan Ji-Xing, Wu Yan-Ling
Key Laboratory for Traditional Chinese Korean Medicine of Jilin Province, College of Pharmacy, Yanbian University, Yanji, China.
Chinese Medicine Processing Centre, College of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, China.
Front Pharmacol. 2021 Oct 8;12:738689. doi: 10.3389/fphar.2021.738689. eCollection 2021.
(AVL) is a traditional medicinal plant recorded in the Compendium of Materia Medica (the Ming Dynasty). In general, it is used for hemostasis, analgesia, anti-inflammation, antioxidation, and to especially facilitate hepatoprotective effect. In recent years, it has received more and more attention due to its special nutritional and medicinal value. The present study investigates the effect and potential mechanism of AVL against alcoholic liver disease (ALD). C57BL/6 mice were fed Lieber-DeCarli liquid diet containing 5% ethanol plus a single ethanol gavage (5 g/kg), and followed up with the administration of AVL or silymarin. AML12 cells were stimulated with ethanol and incubated with AVL. AVL significantly reduced serum transaminase and triglycerides in the liver and attenuated histopathological changes caused by ethanol. AVL significantly inhibited SREBP1 and its target genes, regulated lipin 1/2, increased PPARα and its target genes, and decreased PPARγ expression caused by ethanol. In addition, AVL significantly enhanced FXR, LXRs, Sirt1, and AMPK expressions compared with the EtOH group. AVL also inhibited inflammatory factors, NLRP3, and F4/80 and MPO, macrophage and neutrophil markers. , AVL significantly reduced lipid droplets, lipid metabolism enzymes, and inflammatory factors depending on FXR activation. AVL could ameliorate alcoholic steatohepatitis, lipid deposition and inflammation in ALD by targeting FXR activation.
（AVL）是《本草纲目》（明代）记载的一种传统药用植物。一般来说，它用于止血、镇痛、抗炎、抗氧化，尤其有助于发挥肝脏保护作用。近年来，由于其特殊的营养和药用价值，受到越来越多的关注。本研究探讨了AVL对酒精性肝病（ALD）的作用及潜在机制。给C57BL/6小鼠喂食含5%乙醇的Lieber-DeCarli液体饮食并单次灌胃乙醇（5 g/kg），随后给予AVL或水飞蓟宾。用乙醇刺激AML12细胞并与AVL共同孵育。AVL显著降低了肝脏中的血清转氨酶和甘油三酯，并减轻了乙醇引起的组织病理学变化。AVL显著抑制SREBP1及其靶基因，调节lipin 1/2，增加PPARα及其靶基因，并降低乙醇引起的PPARγ表达。此外，与乙醇组相比，AVL显著增强了FXR、LXRs、Sirt1和AMPK的表达。AVL还抑制炎症因子、NLRP3以及巨噬细胞和中性粒细胞标志物F4/80和MPO。AVL通过激活FXR显著减少脂滴、脂质代谢酶和炎症因子。AVL可通过靶向激活FXR改善ALD中的酒精性脂肪性肝炎、脂质沉积和炎症。
