Calycosin, a Bioactive Isoflavone, Ameliorates Oxidative Stress and Inflammation in Lipopolysaccharide-Induced Intestinal Cell Damage Model via the Nrf2 and NF-κB Signaling Pathways

文献类型： 外文期刊

第一作者： Li, Lu

作者： Li, Lu;Che, Yuyan;Zhu, Longlong;Liu, Zeqing;Song, Yanchen;Chen, Meixia;Wang, Jing;Li, Lu;Che, Yuyan;Song, Yanchen;Zhu, Longlong;Liu, Zeqing;Wu, Qiong;Chen, Meixia;Wang, Jing

作者机构：

关键词： calycosin; cell damage; inflammation; LPS; NF-kappa B pathway; Nrf2 pathway; oxidative stress

期刊名称：FASEB JOURNAL （ 影响因子：4.2； 五年影响因子：4.5 ）

ISSN： 0892-6638

年卷期： 2025 年 39 卷 8 期

页码：

收录情况： SCI

摘要： Calycosin (CA), a bioactive isoflavone derived from Astragali Radix, has garnered interest in food sciences and pharmacology due to its potential antioxidant and anti-inflammatory properties. Our previous studies found that CA induced host defense peptide production in porcine IPEC-J2 cells and alleviated hydrogen peroxide-induced cellular oxidative damage. However, it is still unknown whether CA can protect against pathogenic microorganisms or toxins that cause intestinal cell damage. In this study, we aimed to investigate the protective effects of CA against LPS-induced intestinal cell damage. Using IPEC-J2 intestinal cells to develop a damage model, we found that LPS exposure caused significant morphological damage and apoptosis. However, pretreatment with CA effectively attenuated these adverse effects. Mechanistically, CA alleviated LPS-induced oxidative stress by reducing reactive oxygen species, malondialdehyde, 8-hydroxy-2'-deoxyguanine and carbonyl production, while enhancing antioxidant enzyme activities and gene expression. Furthermore, CA restored the LPS-induced decrease in nuclear erythroid 2-related factor 2 (Nrf2) expression, and Nrf2 silencing abolished the protective effects of CA, indicating that its action is mediated through the Nrf2 pathway. Additionally, CA suppressed LPS-induced inflammation by downregulating inflammation-related gene expression and inhibiting the nuclear factor (NF)-kappa B pathway. Collectively, our findings demonstrate that CA protects intestinal cells from LPS-induced damage by mitigating oxidative stress and inflammation via the Nrf2 and NF-kappa B pathways. These results suggest that CA has potential to be developed as a feed additive to prevent intestinal injury in animals, warranting further investigation in vivo.

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