Betulinic acid attenuates T-2 toxin-induced lung injury by activating Nrf2 signaling pathway and inhibiting MAPK/NF- κB signaling pathway

Toxicon. 2024 Feb 21:107652. doi: 10.1016/j.toxicon.2024.107652. Online ahead of print.ABSTRACTT-2 toxin, a type-A trichothecene mycotoxin, exists ubiquitously in mildewed foods and feeds. Betulinic acid (BA), a pentacyclic triterpenoid derived from plants, has the effect of relieving inflammation and oxidative stress. The purpose of this study was to investigate whether BA mitigates lung impairment caused by T-2 toxin and elucidate the underlying mechanism. The results indicated that T-2 toxin triggered the inflammatory cell infiltration, morphological alterations and cell apoptosis in the lungs. It is gratifying that BA ameliorated T-2 toxin-caused lung injury. The protein expression of nuclear factor erythrocyte 2-related factor 2 (Nrf2) pathway and the markers of antioxidative capability were improved in T-2 toxin induced lung injury by BA mediated protection. Simultaneously, BA supplementation could suppress T-2 toxin-induced mitogen-activated protein kinase (MAPK)/nuclear factor-kappa B (NF-κB)-dependent inflammatory response and mitochondrial apoptotic pathway. Therefore, T-2 toxin gave rise to pulmonary toxicity, but these changes were moderated by BA administration through regulation of the Nrf2/MAPK/NF-κB pathway, which may be offer a viable alternative for mitigating the lung impairments caused by the mycotoxin.PMID:38395262 | DOI:10.1016/j.toxicon.2024.107652

Source: Toxicon - February 23, 2024 Category: Toxicology Authors: Chunlin Huang Zhaoping Ou Li Kong You Huang Wenjiang Yang Jiayu He Mingqi Yang Jing Wu Siting Xiang Yu Zhou Jine Yi Source Type: research