Effect of berberine on LPS-induced intestinal epithelial injury and mA methylation in broilers.

Abstract

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.