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Carbon tetrachloride does not promote hepatic fibrosis in ob/ob mice via downregulation of lipocalin-2 protein
Redox Biology ( IF 10.7 ) Pub Date : 2025-01-16 , DOI: 10.1016/j.redox.2025.103506
Hyun Joo Shin, Kyung Eun Kim, Hyeong Seok An, Eun Ae Jeong, Jiwon Oh, Yundong Sun, Dong-Ju Park, Jaewoong Lee, Jinsung Yang, Gu Seob Roh

Although leptin-deficient ob/ob mice have been investigated to determine whether hepatic steatosis promotes susceptibility to hepatotoxic insults, carbon tetrachloride (CCl4)-induced hepatic fibrosis in ob/ob mice remains largely unknown. In this study, we evaluate the pathogenic mechanisms of hepatic fibrosis in CCl4-treated wild-type (WT) and ob/ob mice and analyze some parameters related to lipogenesis, inflammation, fibrosis, oxidative stress, apoptosis, and autophagy. CCl4 treatment attenuated liver weight and lipogenesis in ob/ob mice. Increased hepatic fibrosis-related proteins were reduced in CCl4-treated ob/ob mice compared with CCl4-treated WT mice. Specifically, the expression of lipocalin-2 (LCN2) was markedly reduced in CCl4-treated ob/ob mice versus CCl4-treated WT mice. Compared with CCl4-treated WT mice, CCl4-treated ob/ob mice had reduced expression of neutrophil-related inflammatory genes and proteins. Hepatic heme oxygenase-1 protein was reduced in CCl4-treated ob/ob mice compared with CCl4-treated WT mice. However, CCl4 did not promote hepatic apoptosis in ob/ob mice. Therefore, these findings highlight LCN2 as a key signaling factor in CCl4-induced hepatic fibrosis.

中文翻译:


四氯化碳不会通过下调脂质运载蛋白-2 蛋白促进 ob/ob 小鼠的肝纤维化



尽管已经研究了瘦素缺陷的 ob/ob 小鼠以确定肝脂肪变性是否会促进对肝毒性损伤的易感性,但四氯化碳 (CCl4) 诱导的 ob/ob 小鼠肝纤维化在很大程度上仍然未知。在这项研究中,我们评估了 CCl4 处理的野生型 (WT) 和 ob/ob 小鼠肝纤维化的致病机制,并分析了与脂肪生成、炎症、纤维化、氧化应激、细胞凋亡和自噬相关的一些参数。CCl4 处理减轻了 ob/ob 小鼠的肝脏重量和脂肪生成。与 CCl4 处理的 WT 小鼠相比,CCl4 处理的 ob/ob 小鼠肝纤维化相关蛋白的增加减少。具体来说,与 CCl4 处理的 WT 小鼠相比,CCl4 处理的 ob/ob 小鼠中脂质运载蛋白-2 (LCN2) 的表达显著降低。与 CCl4 处理的 WT 小鼠相比,CCl4 处理的 ob/ob 小鼠中性粒细胞相关炎症基因和蛋白的表达降低。与 CCl4 处理的 WT 小鼠相比,CCl4 处理的 ob/ob 小鼠的肝血红素加氧酶-1 蛋白降低。然而,CCl4 不会促进 ob/ob 小鼠的肝细胞凋亡。因此,这些发现突出了 LCN2 是 CCl4 诱导的肝纤维化的关键信号因子。
更新日期:2025-01-16
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