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 SI) rats were randomly divided into sham operation group (given saline), model group (given saline∗ modeling), positive control group (give 5 mg • kg dexamethasone, modeling), low, medium and high doses of emodin groups (given 10, 20, and 40 mg • kg 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-a)» interleukin-1 beta (IL-lp) » 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-icB (NF-kB) p65 protein and nuclear transcription factor kB inhibitor-a (bcBa) 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-1|3∗ and TNF-a in hippocampus tissue of the rats in model group were significantly increased (P'<0. 05) ∗ while the expression level of NF-kB p65 protein was significantly increased ( P<∗0. 05)∗ and the expression level of IkBo 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-lp∗ and TNF-a in hippocampus tissue at ischemic side of the rats were significantly decreased (P<0.05)∗ the expression levels of NF-kB p65 protein were significantly decreased ( P
