雜志名稱：Food Science & Nutrition
影響因子：3.9
文章題目：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
作者單位：貴州中醫(yī)藥大學
引用YOBIBIO產品：
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）的主要催化劑被廣泛認為是通過過量的脂肪酸誘導肝細胞的脂肪毒性。在中國，中國粉（PcP）因其已知的肝保護特性而被用作功能性食品。本研究旨在探討PcP提取物對NAFLD體內外模型的影響。我們發(fā)現(xiàn)PcP提取物可以減弱棕櫚酸（PA）誘導的HepG2細胞的脂肪毒性。通過NLRP3和GSDMD/N的表達增加，Caspase-1的激活，以及隨后的IL-1β和IL-18的釋放來表明，PA可以觸發(fā)焦亡。然而，這些變化在PcP后被逆轉。此外，NLRP3激動劑的應用抑制了PcP對脂肪毒性的保護作用，表明PcP通過抑制NLRP3/Caspase-1/ GSDMD通路來降低脂肪毒性。最終，我們通過給予高脂飲食（HFD），然后口服PcP提取物，建立了一個大鼠NAFLD模型。結果表明，PcP提取物可有效降低脫脂作用。
