Tanshinone IIA protects intestinal epithelial cells from deoxynivalenol-induced pyroptosis

Maintaining the Mitochondrial Quality Control System Was a Key Event of Tanshinone IIA against Deoxynivalenol-Induced Intestinal Toxicity

“…Tan IIA's protective effect against LPS-induced small intestine injury may be attributed to its ability to inhibit inflammatory factors and enhance autophagy [26]. In our previous studies, Tan IIA was found to improve intestinal epithelial cell damage induced by DON by modulating the cell pyroptosis signaling pathway [27]. During the research process, we observed a significant impact of Tan IIA on the mitochondrial-related genes of IPEC-J2 cells.…”

“…Recent studies have found that the concentration of Tanshinone in the digestive tract is higher than that in the cardiovascular system after oral administration, suggesting that Tan IIA may play a role in intestinal health [34]. Our previous research has indicated that Tan IIA mitigates cell pyroptosis in DON-induced IPEC-J2 cells by inhibiting the accumulation of ROS and the activation of NLRP3 inflammasomes [27]. Since damaged mitochondria are the primary sites for ROS generation, excessive ROS accumulation can trigger oxidative stress and activate NLRP3 inflammasomes [35][36][37].…”

Overview of T-2 Toxin Enterotoxicity: From Toxic Mechanisms and Detoxification to Future Perspectives

“…Two weeks after intraperitoneal injection of T-2 toxin at a dose of 4 mg/kg, the intestinal MDA concentration in mice increased significantly, and the antioxidant enzyme activity decreased markedly, resulting in oxidative stress and activation of the NF-κB pathway. The levels of the inflammatory molecules IL-1β, IL-6, and TNF-α were increased, and the level of the anti-inflammatory factor IL-10 was decreased, thus inducing an inflammatory response in the intestines. − Treatment of IPEC-J2 cells with T-2 toxin (0, 1, 2, or 4 ng/mL) for a 24 h period demonstrated that the toxin triggered the release of TNF-α, IL-6, and IL-1β, which resulted in an inflammatory response. In addition, T-2 toxin increased the phosphorylation of key factors in the MAPK signaling pathway (p38, JNK, and ERK), thereby demonstrating that in IPEC-J2 cells, T-2 toxin initiates the MAPK signaling pathway.…”

“…In recent years, natural plant extracts have been shown to have prominent effects on relieving mycotoxin-induced toxicity. , Plant extracts can protect the intestine from oxidative damage by strengthening the intestinal physical barrier and immune barrier. The pentacyclic triterpenoid betulinic acid (BA), which is generated from plants, may have biological effects that include immunomodulatory, antioxidant, and anti-inflammatory effects.…”