Abstract: Objective: To investigate the protective effect of emodin on the focal cerebral ischemia in the rats, and to clarify its mechanism. Methods: Sixty healthy male SD rats were randomly divided into sham operation group(given saline), model group(given saline,modeling),positive control group(give 5 mg·kg^-1 dexamethasone, modeling), low, medium and high doses of emodin groups(given 10,20,and 40 mg·kg^-1 emodin,modeling)(n=10). The middle cerebral artery occlusion(MCAO) was used to establish the rat models of focal cerebral ischemia.The behavioral scores of the rats in various groups were detected,the percentages of cerebral infarction volumes of the rats in various groups were determined by TTC staining,the levels of tumor necrosis factor (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6(IL-6) in hippocampus tissue at ischemic side of the rats in various groups were measured by enzyme linked immunosorbent assay(ELISA) method,and the expression levels of nuclear transcription factor-κB (NF-κB) p65 protein and nuclear transcription factor κB inhibitor-α(IκBα) protein in hippocampus tissue at ischemic side of the rats in various groups were detected by Western blotting method. Results: No neurological defects or cerebral infarction of the rats in sham operation group was found. Compared with sham operation group, the levels of IL-6,IL-1β, and TNF-α in hippocampus tissue of the rats in model group were significantly increased (P<0.05), while the expression level of NF-κB p65 protein was significantly increased (P<0.05), and the expression level of IκBα protein was decreased significantly (P<0.05).Compared with model group, the behavioral scores of the rats in positive control group, medium and high doses of emodin groups were significantly decreased(P<0.05),the percentages of cerebral infarction volumes were decreased(P<0.05), the levels of IL-6,IL-1β,and TNF-α in hippocampus tissue at ischemic side of the rats were significantly decreased(P<0.05), the expression levels of NF-κB p65 protein were significantly decreased(P<0.05),and the expression levels of IκBα protein were significantly increased(P<0.05).Compared with low dose of emodin group, the behavioral scores and the percentages of cerebral infarction volumes of the rats in medium and high doses of emodin groups were significantly decreased (P<0.05), the levels of IL-6,IL-1β,and TNF-α in hippocampus tissue at ischemic side of the rats were significantly decreased (P<0.05), the expression levels of NF-κB p65 protein were significantly decreased(P<0.05), and the expression levels of IκBα protein were significantly increased(P<0.05). Conclusion: Emodin has the protective effect on the focal cerebral ischemia, and its mechanism may be related to the inhibition of NF-κB signaling pathway and the secretion of inflammatory factors.

Key words: emodin, cerebral ischemia, inflammatory cytokines, nuclear transcription factor-κB, cerebral infarction