Yuan Lin, Li Wanli, Li Guoxi, Jin Wei, Wang Bingxun, Li Shengli, Wang Haoyu
Key Laboratory of Livestock and Poultry Breeding and Nutrition Regulation in Henan Province, Institute of Animal Husbandry, Henan Academy of Agricultural Sciences, Zhengzhou 450002, China.
Key Laboratory of Livestock and Poultry Breeding and Nutrition Regulation in Henan Province, Institute of Animal Husbandry, Henan Academy of Agricultural Sciences, Zhengzhou 450002, China; The Shennong Laboratory, Zhengzhou Henan 450002, China.
Poult Sci. 2025 Aug 12;104(11):105677. doi: 10.1016/j.psj.2025.105677.
This study sought to explore the effects of and potential mechanisms underlying berberine (BBR) in lipopolysaccharide (LPS)-induced intestinal epithelium injury in broilers. Ninety 19-day-old male AA broilers were randomly divided into five groups: the negative control group (NC), positive control group (PC), and three treatment groups (T1, T2, and T3). On the 21st day of age, the control group was orally administered saline, the LPS-challenged group was orally administered LPS (3 mg/kg body weight), and the treatment groups were orally administered BBR (6, 12, 18 mg/kg body weight) along with LPS (3 mg/kg body weight). Afterwards, in vitro cell experiments were used for validation. The results revealed that the oral administration of LPS caused intestinal inflammation and cell apoptosis and disrupted the intestinal barrier and function. However, simultaneous administration of high-dose BBR alleviated LPS-induced adverse changes in intestinal morphology and mucosal barrier integrity by decreasing the expression of inflammatory cytokines and apoptotic proteins, increasing the expression of tight junction proteins, and inhibiting LPS-induced increases in mA methylation and METTL3 expression. Our findings indicated that BBR addition attenuated LPS-induced intestinal epithelium injury by increasing the expression of tight junction proteins and increasing the anti-inflammatory and antiapoptotic capacity of broiler chickens, possibly via coregulating METTL3 protein expression and mA methylation levels. The research will provide theoretical support for the application of natural alkaloid anti-inflammatory additives in poultry farming.
本研究旨在探讨小檗碱（BBR）对脂多糖（LPS）诱导的肉鸡肠道上皮损伤的影响及潜在机制。将90只19日龄的雄性AA肉鸡随机分为五组：阴性对照组（NC）、阳性对照组（PC）和三个处理组（T1、T2和T3）。在21日龄时，对照组口服生理盐水，LPS攻击组口服LPS（3 mg/kg体重），处理组口服BBR（6、12、18 mg/kg体重）并同时口服LPS（3 mg/kg体重）。之后，采用体外细胞实验进行验证。结果显示，口服LPS会导致肠道炎症和细胞凋亡，并破坏肠道屏障和功能。然而，同时给予高剂量BBR可通过降低炎性细胞因子和凋亡蛋白的表达、增加紧密连接蛋白的表达以及抑制LPS诱导的mA甲基化和METTL3表达增加，减轻LPS诱导的肠道形态和黏膜屏障完整性的不良变化。我们的研究结果表明，添加BBR可通过增加紧密连接蛋白的表达以及提高肉鸡的抗炎和抗凋亡能力来减轻LPS诱导的肠道上皮损伤，可能是通过共同调节METTL3蛋白表达和mA甲基化水平实现的。该研究将为天然生物碱抗炎添加剂在家禽养殖中的应用提供理论支持。
