| Background and objective: Cerebrovascular disease is nervous system frequently-occurring disease,which have high morbidity and high death rate. Ischemic cerebrovascular disease is more common in clinic. Ischemic cerebrovascular disease also bring heavy burden to society and the patient's family.According to the most related studies, Gadd45βpromote damaged tissue repair. Tissue damage was caused by oxidatie stress, ionizing radiation, infections. The upstream regulated gene of Gadd45βis NF-κB. According to the most related studies, Gadd45βplays an important role in regulating the neural progenitor cell proliferation of mature hippocampus and the new neurons dendritic growth. The neural progenitor cell proliferation and new neurons dendritic growth was induced by neural activity. Gadd45βlinks neuronal circuit activity to epigenetic DNA modification and expression of secreted factors in mature neurons for extrinsic modulation of neurogenesis in the adult brain. Gadd45βexpression changes and its function is not clear after brain ischemic damage. This experiment through observing the change of growth arrest and DNA-damage inducible(repair)geneβexpression in the rats brain after ischemia-reperfusion (I/R),in order to supply some experimant basis for clinical rehabilitation treatment of cerebral ischemia.Methods:The middle cerebral artery I/R model (MCAIR) was established by nylon monofilament occlusion method in rats. Rats were randomly assigned into normal group,sham group,I/R control group, intraperitoneal injection of PDTC group(PDTC group).Normal Saline was given by intraperitoneal injection into rats of sham group and I/R control group.The dose of normal saline was equal to the PDTC group.The expression of Gadd45βwere determined by RT-PCR,Western blot and immunohistochemistry. The behavioral scores of wounded limb were measured by Zea Longa standard.Result:The expression of Gadd45βprotein in I/R control group began to increase at 6h,increased significantly and reached the maximum at 24h after MCAIR,and decreased but was still higher than that of sham group at 48h and 72h (P<0.05). The expression of Gadd45βprotein in PDTC group was much lower than that of I/R control group,but much higher than that of sham group at any point (P<0.05).The expression of Gadd45βmRNA in I/R control group was much higher than that of sham group, increased significantly and reached the maximum at 24h after MCAIR, and decreased but still was higher than that of sham group at 72h (P<0.01). The expression of Gadd45βmRNA in PDTC group was much higher than that of sham group ,but much lower than that of I/R control group at any point (P<0.01). The expression of Gadd45βmRNA in PDTC group was reached the maximum at 24h after MCAIR. The neurological defct scores of I/R control and PDTC group at any time point had the same variation tendency and the score of PDTC group was much higher than that of I/R control group at 72h after MCAIR (P<0.05).Conclusion: (1) In around of rat ischemia brain tissue, Gadd45 beta expression was increased after cerebral ischemia reperfusion.(2)PDTC can restrain the expression of Gadd45βin rat brain after ischemia. (3)Gadd45βmight have nerve protective effect.
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