杂志名称：Food Science & Nutrition
影响因子：3.9
文章题目：Penthorum chinense Pursh extract ameliorates hepatic steatosis by suppressing pyroptosis via the NLRP3/Caspase-1/GSDMD pathway
DOI：https://doi.org/10.1002/fsn3.4165
第一作者：Ruixi Luo，Yudie Hu， La Wang，Zunli Ke，Wenjia Wang，Ping Wang， Weiyi Tian
作者单位：贵州中医药大学
引用YOBIBIO产品：
U96-1964E  Human IL-18 ELISA Kit

文章摘要：
The primary catalyst for nonalcoholic fatty liver disease (NAFLD) is widely recognized as the induction of lipotoxicity in hepatocytes by an excess of fatty acids. In China, Penthorum chinense Pursh (PcP) is commonly employed as a functional food due to its known hepatoprotective properties. The present study aimed to investigate the influence of PcP extract on in vivo and in vitro models of NAFLD. We found that PcP extract can attenuate palmitic acid (PA)‐induced lipotoxicity in HepG2 cells. PA was observed to trigger pyroptosis, as indicated by the increased expression of NLRP3 and GSDMD/N, activation of Caspase‐1, and subsequent release of IL‐1β and IL‐18. However, these changes were reversed after PcP was administered. Furthermore, the application of an NLRP3 agonist inhibited the protective effects of PcP on lipotoxicity, indicating that PcP decreased lipotoxicity by inhibiting the NLRP3/Caspase‐1/GSDMD pathway. Ultimately, we established a rat model of NAFLD through the administration of a high‐fat diet (HFD), followed by the oral delivery of PcP extracts. The results demonstrated that the administration of PcP extract effectively decreased dyslipidemia and hepatic steatosis, which coincided with a decrease in hepatic pyroptosis through modulation of the NLRP3/Caspase‐1/GSDMD pathway in liver tissues. Overall, our findings provide insight into the mechanism by which PcP extracts alleviate hepatic steatosis, highlighting the potential significance of modulating the NLRP3/Caspase‐1/GSDMD pathway in the context of pyroptosis.

非酒精性脂肪肝（NAFLD）的主要催化剂被广泛认为是通过过量的脂肪酸诱导肝细胞的脂肪毒性。在中国，中国粉（PcP）因其已知的肝保护特性而被用作功能性食品。本研究旨在探讨PcP提取物对NAFLD体内外模型的影响。我们发现PcP提取物可以减弱棕榈酸（PA）诱导的HepG2细胞的脂肪毒性。通过NLRP3和GSDMD/N的表达增加，Caspase-1的激活，以及随后的IL-1β和IL-18的释放来表明，PA可以触发焦亡。然而，这些变化在PcP后被逆转。此外，NLRP3激动剂的应用抑制了PcP对脂肪毒性的保护作用，表明PcP通过抑制NLRP3/Caspase-1/ GSDMD通路来降低脂肪毒性。最终，我们通过给予高脂饮食（HFD），然后口服PcP提取物，建立了一个大鼠NAFLD模型。结果表明，PcP提取物可有效降低脱脂作用。