Ischemic stroke is a disease resulting from the cerebral ischemia and hypoxia caused by the blockage of brain vessels in the brain,and is characterized by the focal neurological signs.Pathologically,neuronal necrosis in the infarcted area and the neuronal degeneration or delayed death of neurons in the ischemic penumbra,contribute to the morphological basis of the disease.Ischemic stroke is regulated by multiple processes,including ferroptosis,apoptosis,and autophagy.Ferroptosis,a type of iron-dependent cell death,is closely associated with ischemic stroke.Nuclear factor erythroid 2-related factor 2(Nrf2),a key transcription factor,plays a critical role in maintaining cellular redox balance and regulating inflammatory responses.Nrf2 promotes the expression of solute carrier family 7 member 11(SLC7A11)and glutathione peroxidase 4(GPX4),thereby activating the Nrf2 signaling pathway to counteract ferroptosis and protect cells from damage.This article reviews and analyzes recent experimental studies on traditional Chinese medicine(TCM)therapy targeting the Nrf2/SLC7A11/GPX4 pathway to suppress ferroptosis.The studies have found that TCM therapy with herbal compounds,Chinese patent medicines,single herbal components and their active ingredients,and acupuncture and moxibustion can inhibit ferroptosis by activating the Nrf2/SLC7A11/GPX4 signaling pathway,which will provide novel strategies for the TCM intervention of ischemic stroke.

Aim To observe the analgesic effect of oxymatrine(OMT)and its mechanism.Methods A peripheral mononeuropathy was produced in adult mice by placing loosely constrictive ligatures around the common sciatic nerve.The antinociceptive effects of the OMT were assessed in mechanical allodynia and cold allodynia tests.The CAMKII inhibitor KN-93 and AIP were adopted to investigate the influence of OMT on the analgesic effect and analyze its analgesic mecha-nisms.Western blot was used to evaluate the expres-sions of tCaMKII and pCaMKII protein.Results The intraperitoneal administration of OMT (1 60,80 mg· kg -1 )increased the paw withdrawal threshold in the
mechanical allodynia test (P <0.05 ),OMT (1 60, 80,40 mg·kg -1 ,ip)remarkably decreased the paw lifts in the cold allodynia test (P <0.05).Ith KN-93 (1 .25 μg/site),AIP (0.02 μg/site)significantly en-hanced the analgesic effect of OMT (35 mg·kg -1 ) (P <0.01 ).Protein expression of pCaMKII was de-creased by OMT(1 60 mg·kg -1 ).Conclusion OMT has significant protective effects on chronic constriction injury(CCI)in mice,and the effective mechanism of OMT inhibits the expression of CaMKII receptor.