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OBJECTIVE:To evaluate the anti-apoptotic efficacy of Qingnao Yizhi formula(清脑益智方,QNYZ)in cultured cerebral cortical neuronal cells(CNCs)and the regulation of the NogoA-Nogo receptor(NgR)/Rho-Rho kinase(ROCK)signaling pathway.METHODS:Primary cultured CNCs were randomly divided into the following groups:normal control group(N-C),hypoxia-reoxygenation group(H/R),high-dose QNYZ group(Q-H),low-dose QNYZ group(Q-L)butylphthalide(NBP)group,and Y-27632(a selective ROCK transduction pathway in-hibiter)group.Except those in the N-C group,CNCs were placed in hypoxic conditions for 24 h and then in reoxygenation conditions for 24 h.Cell me-dia was changed every 48 h,and various assays were performed on the 7th day.Cell viability was evaluated by measuring mitochondrial dehydroge-nase activity,using a CCK-8 assay,in triplicate.Syn-apsin(SYN)protein concentrations were evaluated by enzyme-linked immunosorbent assay.NogoA and RhoA protein expression were evaluated through Western blotting.The gene expression of NogoA,NgR,RhoA,and ROCK was evaluated by re-verse transcription-polymerase chain reaction.Cell apoptosis was measured using a terminal deoxynu-cleotidyl transferase biotin-dUTP nick end labeling assay.RESULTS:Compared with the N-C group,the cell vi-ability of the H/R group decreased significantly(P＜0.05).The cell viability values for the Q-H and Q-L groups increased compared with that for the H/R group,and the difference was significant for the Q-H group(P＜0.05).The NogoA and RhoA protein levels and the NogoA,NgR,RhoA,and ROCK mRNA expression levels increased in the H/R group,com-pared with the N-C group,and decreased signifi-cantly in the Q-H and Q-L groups(P＜0.05)and in the Y-27632 group(P＜0.05)compared with the H/R group.The SYN levels in the Q-H,Q-L,and NBP groups significantly increased compared with that in the H/R group(P＜0.05).Compared with the H/R group,the numbers of apoptotic cells in the Q-H,Q-L,and NBP groups significantly decreased(P＜0.05).CONCLUSION:The presented study demonstrated that QNYZ exerted anti-apoptotic effects on H/R-in-duced CNCs,possibly through the modulation of the NogoA-NgR/Rho-ROCK signaling pathway and the promotion of synaptic plasticity in H/R CNCs.