Overexpression of SIRT1 alleviates oxidative damage and barrier dysfunction in CPB2 toxin-infected IPEC-J2 cells.

Clostridium perfringens (C. perfringens) beta2 (CPB2) toxin may induce necrotizing enteritis (NE) in pigs. Sirtuin1 (SIRT1) is involved in inflammatory intestinal diseases and affects intestinal barrier function. However, the effects of SIRT1 on piglet intestinal disease caused by CPB2 toxin are unclear. This study revealed the role of pig SIRT1 in CPB2 toxin-exposed intestinal porcine epithelial cells (IPEC-J2). Herein, we manifested that SIRT1 was dramatically decreased in IPEC-J2 cells infected with CPB2 toxin. Subsequently, we silenced and overexpressed SIRT1 using siRNA and a overexpression vector in CPB2 toxin-treated IPEC-J2 cells. The results indicated that overexpression of SIRT1 suppressed reactive oxygen species (ROS) generates, the expression tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and Bax, nuclear factor-kappa B (NF-κB p65), phospho (p)-NF-kB p65 and lactate dehydrogenase (LDH) activity and apoptosis in CPB2 toxin-treated IPEC-J2 cells, and increased IL-10, mitochondrial membrane potential (ΔΨm), Bcl-2, Claudin1 and Occludin levels and cell viability. These results indicated that SIRT1 protects IPEC-J2 cells against CPB2 toxin-induced oxidative damage and tight junction (TJ) disruption, which provides a theoretical basis for further study of the molecular regulatory mechanism of SIRT1 in C. perfringens-infected NE in piglets.