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
作者： Li, Lu 1 ; Che, Yuyan 1 ; Zhu, Longlong 1 ; Liu, Zeqing 1 ; Song, Yanchen 1 ; Wu, Qiong 5 ; Chen, Meixia 1 ; Wang, Jing 1 ;
作者机构： 1.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing, Peoples R China
2.Hebei Univ Engn, Coll Life Sci & Food Engn, Handan, Peoples R China
3.Gansu Agr Univ, Coll Anim Sci & Technol, Lanzhou, Gansu, Peoples R China
4.Henan Univ Sci & Technol, Coll Anim Sci & Technol, Luoyang, Peoples R China
5.Beijing Univ Agr, Anim Sci & Technol Coll, Beijing, Peoples R China
6.Beijing Acad Agr & Forestry Sci, Sino US Joint Lab Anim Sci, Beijing, Peoples R China
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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