NLRP3 炎性小体缺失可调节衰老过程中 KO NLRP3 小鼠的肝纤维化进展、脂质代谢和炎症。
The Absence of NLRP3-inflammasome Modulates Hepatic Fibrosis Progression, Lipid Metabolism, and Inflammation in KO NLRP3 Mice during Aging.
机构信息
Unit for Clinical Management of Digestive Diseases and CIBERehd, Valme University Hospital, 41014 Seville, Spain.
Research Laboratory, Oral Medicine Department, University of Sevilla, 41009 Sevilla, Spain.
出版信息
Cells. 2020 Sep 23;9(10):2148. doi: 10.3390/cells9102148.
Aging is associated with metabolic changes and low-grade inflammation in several organs, which may be due to NLRP3 inflammasome activation. Methods: Here, we asked whether age-related liver changes such as lipid metabolism and fibrosis are reduced in aged mice lacking the NLRP3 inflammasome. We report reduced protein levels of lipid markers (MTP, FASN, DGAT1), SOD activity, oxidative stress marker PTPRG, and the fibrotic markers TPM2β, COL1-α1 associated with increased GATA4, in NLRP3 deficient mice. Fibrotic, lipid, and oxidative reduction in liver tissues of mice was more pronounced in those old KO NLRP3 mice than in the younger ones, despite their greater liver damage. These results suggest that absence of the NLRP3 inflammasome attenuates age-related liver fibrotic pathology in mice, suggesting that pharmacological targeting may be beneficial.
衰老是与几个器官的代谢变化和低度炎症相关的，这可能是由于 NLRP3 炎性小体的激活。方法：在这里，我们询问 NLRP3 炎性小体缺失的老年小鼠的肝脏是否会减少与年龄相关的肝脏变化，如脂质代谢和纤维化。我们报告了脂质标志物（MTP、FASN、DGAT1）、SOD 活性、氧化应激标志物 PTPRG 的蛋白水平降低，与纤维化相关的标志物 TPM2β、COL1-α1 与 GATA4 的增加有关，在 NLRP3 缺陷型小鼠中。尽管 NLRP3 缺失的老年 KO 小鼠的肝损伤更大，但它们的肝脏组织中的纤维化、脂质和氧化减少更为明显。这些结果表明，NLRP3 炎性小体的缺失可减轻小鼠与年龄相关的肝纤维化病理，表明药物靶向可能是有益的。
Zotero 插件