摘要
Objectives:Petasites japonicus(PJ)is a traditional medicinal herb widely used in East Asia for treating diverse ailments.However,its anticancer properties and underlying mechanisms have not been elucidated.This study investigated the anticancer potential and molecular mechanisms of the methanol extract of Petasites japonicus(PJE)in human adenocarcinoma gastric stomach(AGS)cells.Methods:AGS cells were treated with various concentrations of PJE,and cell viability was measured using MTT and CCK-8 assays.Apoptotic cell death was evaluated by the cell cycle,caspase-3 and-9 activity assays,and western blotting.To elucidate the underlying signaling mechanisms,we also examined the generation of reactive oxygen species(ROS)and the activation of mitogen-activated protein kinase(MAPK).Results:PJE significantly decreased AGS cell viability and increased the sub-G1 population,indicating apoptosis.PJE upregulated Bcl-2-associated X protein(Bax)expression while downregulating B-cell lymphoma 2(Bcl-2)and surviving.Increased cleavage of caspase-3,caspase-9,and poly(ADP-ribose)polymerase(PARP)-1 confirmed the activation of the intrinsic apoptotic pathway.Moreover,PJE induced phosphorylation of MAPKs and induced a dose-dependent increase in ROS generation.Conclusions:PJE triggers apoptosis in gastric cancer cells through ROS-dependent mitochondrial and MAPK signaling,leading to potent anticancer effects.These findings highlight PJ as a promising natural source for developing new therapeutic agents for gastric cancer.
出处
《BIOCELL》
2025年第12期2365-2375,共11页
生物细胞(英文)
基金
supported by a 2-Year Research Grant of Pusan National University。
