Protective effects of Curcumin-Zinc complex on inflammatory damage of IPEC-J2 cells induced by bacterial lipopolysaccharide.

Abstract

The present study aimed to investigate the potential mitigative effects of the Curcumin-Zinc Complex (Cur-Zn) on bacterial lipopolysaccharide (LPS)-induced inflammatory damage in porcine small intestinal epithelial cells (IPEC-J2). IPEC-J2 cells were initially assigned to one of six treatment groups for 24 h (N = 6): the control group (0 µM Cur-Zn and 0 µg.mL− 1 LPS), the LPS group (0 µM Cur-Zn and 1 µg.mL− 1 LPS), and four cotreatment groups receiving varying concentrations of Cur-Zn (5, 10, 20, and 40 µM, respectively) combined with a constant LPS concentration (1 µg.mL− 1). Cell viability, apoptosis rate, and lactate dehydrogenase (LDH) level were detected. The results showed that 20 µM or 40 µM Cur-Zn significantly increased cell viability and significantly decreased apoptosis rate and LDH release in IPEC-J2 cells challenged with LPS, so 20 µM Cur-Zn was adopted for the mechanistic assays. Then, IPEC-J2 cells were randomly assigned to one of three treatment groups for 24 h (N = 6): the control group (CON; 0 µM Cur-Zn and 0 µg.mL− 1 LPS), the LPS group (LPS; 0 µM Cur-Zn and 1 µg.mL− 1 LPS), and Cur-Zn and LPS co-treated groups (Cur-Zn + LPS; 20 µM Cur-Zn and 1 µg.mL− 1 LPS). The results indicated that Cur-Zn treatment significantly increased the genes and proteins expression of zonula occluden-1 (ZO-1), Claudin-1, Occludin, and mucin 2 (MUC2), and significantly decreased the gene and protein expression of Caspase 3 in LPS-induced IPEC-J2 cells. Treatment of LPS-stimulated IPEC-J2 cells with Cur-Zn significantly reduced nitric oxide (NO), interleukin (IL)-1β, IL-6 and tumor necrosis factor α (TNF-α) production, and decreased the genes and proteins expression of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factor-κB (NF-κB). Furthermore, Cur-Zn increased the production of anti-inflammatory cytokine IL-13 in LPS-challenged IPEC-J2 cells. It provides preliminary evidence that Cur-Zn may alleviate inflammatory responses by inhibiting the TLR4/ NF-κB signaling pathway. In conclusion, Cur-Zn can mitigate the inflammatory damage induced by LPS stimulation in IPEC-J2 cells by enhancing barrier and immune functions while reducing the inflammatory response.