Baicalin Alleviates LPS-Induced Oxidative Stress via NF-κB and Nrf2-HO1 Signaling Pathways in IPEC-J2 Cells

Baicalin is a natural plant extract with anti-inflammatory and anti-oxidant activities. However, the molecular mechanism of baicalin on oxidative stress in IPEC-J2 cells exposed to LPS remains to be unclear. In this study, LPS stimulation significantly increased Toll-like receptor 4, tumor necrosis factor-alpha, and interleukins (IL-6 and IL-1 beta) expression in IPEC-J2 cells, and it activated the nuclear factor (NF-kappa B) expression. While, baicalin exerted anti-inflammatory effects by inhibiting NF-kappa B signaling pathway. LPS stimulation significantly increased the levels of the oxidative stress marker MDA, inhibited the anti-oxidant enzymes catalase and superoxide dismutase, which were all reversed by baicalin pre-treatment. It was found that baicalin treatment activated the nuclear import of nuclear factor-erythroid 2 related factor 2 (Nrf2) protein, and significantly increased the mRNA and protein expression of its downstream anti-oxidant factors such as heme oxygenase-1 and quinone oxidoreductase-1, which suggested that baicalin exerted anti-oxidant effects by activating the Nrf2-HO1 signaling pathway. Thus, pretreatment with baicalin inhibited LPS - induced oxidative stress and protected the normal physiological function of IPEC-J2 cells via NF-kappa B and Nrf2-HO1 signaling pathways.

Automated summary

Baicalin exerts anti-inflammatory effects by inhibiting the NF-κB signaling pathway and exerts antioxidant effects by activating the Nrf2-HO1 signaling pathway, thereby inhibiting LPS-induced oxidative stress and protecting the normal physiological function of IPEC-J2 cells.