山柰酚-3-O-芸香糖苷对H2O2诱导的HepG2细胞氧化损伤的保护作用OA

To investigate the protective effects of kaempferol-3-O-rutinoside(K3R)against H2O2-induced oxidative damage in HepG2 cells,the regulatory mechanisms of such effects were systematically analyzed using an in vitro model.After pre-treatment with 10,20,and 30 μmol·L-1 K3R for 24 hours,the cells were exposed to 400 μmol·L-1 H2O2 for four hours.Cellular viability,reactive oxygen species(ROS)levels,oxidative damage status,and antioxidant capacity were assessed across experimental groups.Apoptosis was evaluated using Annexin V-FITC/PI staining and TUNEL assays.Western blotting was performed to analyze the expression of antioxidant proteins(HO-1 and NQO1),apoptosis-related proteins(Bax,Caspase3,and Bcl-2),and key components of the MAPK/NF-κB signaling pathway.The results demonstrated that cell viability was significantly increased to 99.93％in the K3R-protected groups,accompanied by reduced ROS levels approaching normal ranges,enhanced antioxidant enzyme activity,and effective suppression of apoptosis.HO-1,NQO1,and Bcl-2 expressions were upregulated,whereas Bax and Caspase3 expressions were downregulated.Furthermore,phosphorylation of P38,JNK,ERK1/2,and NF-κB p65 in the MAPK/NF-κB pathway was effectively inhibited.In summary,K3R alleviates H2O2-induced oxidative damage in HepG2 cells by suppressing MAPK/NF-κB pathway activation,enhancing antioxidant capacity,and regulating apoptosis-related proteins.This study provides a theoretical basis for the application of K3R in the development of antioxidant functional foods and drugs.