Dihydromyricetin Suppresses Lipopolysaccharide-Induced Intestinal Injury Through Reducing Reactive Oxygen Species Generation and NOD-Like Receptor Pyrin Domain Containing 3 Inflammasome Activation
文献类型： 外文期刊
作者： Chang, Yicong 1 ; Jiang, Xinru 1 ; Ji, Zhenghua 1 ; Gong, Yingchao 1 ; Fan, Xianan 1 ; Hao, Beili 1 ; Yuan, Liang 1 ; Muhammad, Ishfaq 1 ; Li, Rui 1 ; Li, Changwen 3 ; Liu, Fangping 1 ;
作者机构： 1.Northeast Agr Univ, Coll Vet Med, Dept Basic Vet Sci, Harbin, Peoples R China
2.Heilongjiang Key Lab Anim Dis Control & Pharmaceut, Harbin, Peoples R China
3.Chinese Acad Agr Sci, Harbin Vet Res Inst, Harbin, Peoples R China
关键词： dihydromyricetin; intestinal injury; lipopolysaccharide; NLRP3 inflammasome; ROS
期刊名称：JOURNAL OF ANIMAL PHYSIOLOGY AND ANIMAL NUTRITION （ 影响因子：2.4； 五年影响因子：2.7 ）
ISSN： 0931-2439
年卷期： 2025 年 109 卷 2 期
页码：
收录情况： SCI
摘要： As an integral component of the gram-negative bacterial cellular envelope, excess production of lipopolysaccharide (LPS) regularly precipitates causing intestinal damage and barrier dysfunction in avian species. Dihydromyricetin (DHM), a naturally occurring constituent in rattan tea, exhibits protective characteristics against various tissue injuries. However, the intervention mechanism of DHM on intestinal injury induced by LPS in chickens has not been determined. Consequently, this study aimed to elucidate the mechanisms through which DHM mitigates LPS-induced intestinal damage in chickens through the reactive oxygen species (ROS)-NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome. Primary intestinal epithelial cells (IECs) were isolated and cultured from 14-day-old specific pathogen free (SPF) chicken embryos, and DHM ranging from 20 to 320 mu mol/L increased cell survival rates. Additionally, DHM at 20 and 40 mu mol/L demonstrated reduction in oxidative stress and ROS accumulation, mirroring the impact of ROS inhibitor (2.5 mmol/L NAC). DHM efficiently regulated ROS production, thereby augmenting ZO-1, occludin and claudin-1 expression to enhance barrier function; upregulating bcl-2 expression and downregulating bax and caspase-3 expression to regulate apoptosis and suppressing inflammation in IECs. Suppression of ROS subsequently attenuates NLRP3 inflammasome activation, leading to a remarkable downregulation of IL-1 beta, IL-18 and lactate dehydrogenase (LDH) secretion, consistent with direct inactivation of NLRP3 inflammasome (10 mu mol/L MCC950). Notably, DHM diminished IL-1 beta and IL-18 levels and LDH activity via suppression of ROS-regulated NLRP3 and caspase-1 expression and activation. In summary, DHM prevents LPS-induced intestinal impairment by modulating ROS generation and NLRP3 inflammasome activation.
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