AIST-INDIA DAILAB, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba 305-8565, Japan.
Graduate School of Science and Technology, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8577, Japan.
Int J Mol Sci. 2024 Nov 14;25(22):12256. doi: 10.3390/ijms252212256.
We investigated the effect of purified withanolides and extracts derived from Ashwagandha on steatosis, the abnormal accumulation of fat that can lead to non-alcoholic fatty liver disease (NAFLD). Collaborator of ARF (CARF, also known as CDKN2AIP, a protein that regulates hepatic lipid metabolism, fat buildup, and liver damage) was used as an indicator. Six withanolides (Withaferin A, Withanone, Withanolide B, Withanoside IV, Withanoside V, and Withanostraminolide-12 deoxy) reversed the decrease in CARF caused by exposure to free fatty acids (FFAs) in liver-derived cells (HepG2 hepatocytes). After analyzing the effects of these withanolides on CARF mRNA and protein levels, FFA accumulation, protein aggregation, and oxidative and DNA damage stresses, we selected Withaferin A and Withanone for molecular analyses. Using the palmitic-acid-induced fatty acid accumulation stress model in Huh7 cells, we found a significant reduction in the activity of the key regulators of lipogenesis pathways, including sterol regulatory element-binding protein-1c (SREBP-1c), fatty acid synthase (FASN), and peroxisome proliferator-activated receptors (PPARγ and PPARα). This in vitro study suggests that low, non-toxic doses of Withaferin A, Withanone, or Ashwagandha extracts containing these withanolides possess anti-steatosis and antioxidative-stress properties. Further in vivo and clinical studies are required to investigate the therapeutic potential of these Ashwagandha-derived bioactive ingredients for NAFLD.
我们研究了纯化的醉茄内脂和醉茄提取物对脂肪变性的影响,脂肪变性是一种异常的脂肪堆积,可导致非酒精性脂肪性肝病(NAFLD)。ARF(也称为 CDKN2AIP 的合作因子,一种调节肝脏脂质代谢、脂肪堆积和肝损伤的蛋白质)被用作指标。六种醉茄内脂(醉茄酮 A、醉茄素酮、醉茄内脂 B、醉茄皂苷 IV、醉茄皂苷 V 和 12-脱氧醉茄内脂)逆转了游离脂肪酸(FFAs)暴露于肝源性细胞(HepG2 肝细胞)导致的 CARF 减少。在分析这些醉茄内脂对 CARF mRNA 和蛋白水平、FFA 积累、蛋白聚集以及氧化和 DNA 损伤应激的影响后,我们选择了醉茄酮 A 和醉茄素酮进行分子分析。在 Huh7 细胞的棕榈酸诱导的脂肪酸积累应激模型中,我们发现参与脂生成途径的关键调节因子的活性显著降低,包括固醇调节元件结合蛋白-1c(SREBP-1c)、脂肪酸合酶(FASN)和过氧化物酶体增殖物激活受体(PPARγ 和 PPARα)。这项体外研究表明,低剂量、非毒性的醉茄酮 A、醉茄素酮或含有这些醉茄内脂的醉茄提取物具有抗脂肪变性和抗氧化应激特性。需要进一步的体内和临床研究来研究这些源自 Ashwagandha 的生物活性成分对 NAFLD 的治疗潜力。