Wang Jianwei, Cheng Quancheng, Fang Jinyu, Ding Huiru, Liu Huaicun, Fang Xuan, Chen Chunhua, Zhang Weiguang
Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Peking University, Beijing 100191, China.
Antioxidants (Basel). 2021 Dec 1;10(12):1933. doi: 10.3390/antiox10121933.
As a small-molecule reductant substance, hydrogen gas has an obvious antioxidant function. It can selectively neutralize hydroxyl radicals (OH) and peroxynitrite (ONOO) in cells, reducing oxidative stress damage. The purpose of this study was to investigate the effect of hydrogen gas (3%) on early chronic liver injury (CLI) induced by CCl and to preliminarily explore the protective mechanism of hydrogen gas on hepatocytes by observing the expression of uncoupling protein 2 (UCP2) in liver tissue. Here, 32 rats were divided into four groups: the control group, CCl group, H (hydrogen gas) group, and CCl + H group. The effect of hydrogen gas on early CLI was observed by serological tests, ELISA, hematoxylin and eosin staining, and oil red O staining. Immunohistochemical staining and Western blotting were used to observe the expression of UCP2 in liver tissues. We found that CCl can induce significant steatosis in hepatocytes. When the hydrogen gas was inhaled, hepatocyte steatosis was reduced, and the UCP2 expression level in liver tissue was increased. These results suggest that hydrogen gas might upregulate UCP2 expression levels, reduce the generation of intracellular oxygen free radicals, affect lipid metabolism in liver cells, and play a protective role in liver cells.
作为一种小分子还原物质,氢气具有明显的抗氧化功能。它可以选择性地中和细胞中的羟自由基(OH)和过氧亚硝酸根(ONOO),减轻氧化应激损伤。本研究旨在探讨氢气(3%)对四氯化碳诱导的早期慢性肝损伤(CLI)的影响,并通过观察肝组织中解偶联蛋白2(UCP2)的表达,初步探讨氢气对肝细胞的保护机制。在此,将32只大鼠分为四组:对照组、四氯化碳组、氢气组和四氯化碳+氢气组。通过血清学检测、酶联免疫吸附测定、苏木精-伊红染色和油红O染色观察氢气对早期CLI的影响。采用免疫组织化学染色和蛋白质免疫印迹法观察肝组织中UCP2的表达。我们发现四氯化碳可诱导肝细胞发生明显的脂肪变性。吸入氢气后,肝细胞脂肪变性减轻,肝组织中UCP2表达水平升高。这些结果表明,氢气可能上调UCP2表达水平,减少细胞内氧自由基的产生,影响肝细胞脂质代谢,从而对肝细胞起到保护作用。