Wogonin Alleviates Aconitine-induced Gastric Tissue Damage in Gastric Cancer through PI3K/Akt Signaling Pathway

Background and Objectives Aconitine is a toxic substance capable of causing damage to the nervous system, digestive system, and gastric tissue. Wogonin exhibits significant antibacterial, antioxidant, and potential anticancer effects. The PI3K/Akt pathway is known to engage in the development of cancer cells. Consequently, it is of great significance to investigate the potential of wogonin on aconitine-induced gastric tissue damage in gastric cancer (GC) and its correlation with the signaling pathway. Materials and Methods Forty modelled mice were divided into a normal group, normal saline group, aconitine (low, high) dose group, wogonin (high, medium, low) dose group, celecoxib group, and Weifuchun group. After treatment, we detected the mouse’s tumor volume and survival day, as well as determined the expression of PI3K/Akt, LC3B, and p62. Results During modeling, HE staining revealed that the low-dose aconitine group exhibited improved pathological conditions, reduced tumor volume and mass compared to the saline group, and elevated survival days. After modeling, tumor volume and mass decreased concentration-dependent in each wogonin dose group. Wogonin treatment greatly prolongs survival days and effectively inhibits tumor growth. The expressions of LC3B, P62, PI3K, Akt, and mTOR mRNA were all decreased compared to the model group. Meanwhile, the treatment promoted the expression of LC3 and Beclin1 proteins related to the autophagy pathway. Conclusion Wogonin effectively ameliorates gastric tissue damage induced by aconitine in GC, prolongs the survival days of mice, and inhibits tumor growth through activation of the PI3K/Akt signaling pathway and reduction of P62 protein.