Abstract: Objective To investigate the effect of Qihong capsules on mitochondrial oxidative stress in mice with coronary microvascular disease(CMVD)via the TLR4/NF-κB/GPX4 pathway.Methods Twenty CMVD model mice were randomly assigned to 2 groups:model group and Qihong capsules treatment group[0.648 g/(kg·d),intragastric administration for 4 weeks],and additional 10 mice were served as the control group.Hematoxylin-eosin(HE)staining,oil red O staining,and immunohistochemistry were employed to assess coronary pathology and macrophage infiltration.Western blotting and enzyme-linked immunosorbent assay(ELISA)were utilized to detect the expression of relevant proteins and levels of reactive oxygen species(ROS).Results Compared with the control group,the model group exhibited severe coronary artery injury,elevated expression of inflammatory cytokines(TNF-α,IL-1β,IL-6),enhanced activation of the TLR4/NF-κB pathway,downregulated expression of GPX4,Sirt1,and HO-1,and increased ROS levels(all P<0.001).Following intervention with Qihong capsules,the aforementioned pathological changes were significantly ameliorated,inflammation and oxidative stress were suppressed,and the expression of protective proteins was upregulated(all P<0.001).Conclusion Qihong capsules can alleviate oxidative stress by inhibiting the TLR4/NF-κB inflammatory pathway and upregulating the expression of GPX4/Sirt1/HO-1,thereby improving microvascular dysfunction in CMVD mice.Its mechanism may be associated with the inhibition of ferroptosis,reflecting its potential for multi-target intervention.

Key words: coronary microvascular disease, Qihong capsule, oxidative stress, TLR4/NF-κB/GPX4 pathway, ferroptosis