To explore the mechanism of isoquercitrin in the induction of apoptosis in cervical cancer cells through endoplasmic reticulum stress and autophagy pathways.Methods:The SiHa cells were randomly divided into a control group,and low-(20 μmol/L),medium-(40 μmol/L),and high-dose(80 μmol/L) isoquercitrin groups.The cells in the isoquercitrin groups were cultured with corresponding drugs,and those in the control group with normal medium.The cell proliferation was detected at 24 h,48 h,and 72 h using CCK-8 kits.EDU was used to detect the proliferation of cells in each group at 72 h.The expression of endoplasmic reticulum stress-related genes was detected by qRT-PCR.The protein expression in each group was detected by Western blot.Cell apoptosis was detected by flow cytometry.Results:Compared with the control group,the isoquercitrin groups showed reduced OD values in cells,increased expression levels of glucose-regulated protein 78(GRP78) mRNA,CHOP mRNA,GRP78 protein,CHOP protein,Caspase-12 protein,Beclin 1 protein,Bax protein,Cl-caspase-3 protein,and the LC3 Ⅱ/LC3 Ⅰ ratio,decreased expression levels of p62 protein,Bcl-2 protein,p-JAK2 protein,and p-STAT3 protein,and elevated apoptosis rate(P<0.05).The effect of isoquercitrin was in a dose-dependent manner.Conclusion:Isoquercitrin can induce apoptosis of cervical cancer cells through endoplasmic reticulum stress and autophagy pathways.