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@#Objective:To observe the interactive effects of early exercise and γ-aminobutyric acid (GABA) receptor antagonists on the neurologic function and brain-derived neurotrophic factor (BDNF) expression in the cerebral ischemia-reperfusion (I/R) rat model. Methods:Male Sprague-Dawley rats were divided into sham (<italic>n</italic> = 10), I/R (<italic>n</italic> = 10), exercise (EX) (<italic>n</italic> = 10), pentetrazol (PTZ) (<italic>n</italic> = 10) and pentetrazol plus exercise (PTZEX) (<italic>n</italic> = 10) groups. All the rats, except the sham group, accepted middle cerebral artery occlusion (MCAO) for one hour and reperfused. Since two days after reperfusion, PTZ and PTZEX groups accepted PTZ, a GABA receptor antagonist, 0.25 mg/kg peritoneal injection, once a day for five days; while EX and PTZEX groups ran on a treadmill, 30 minutes a day for five days. Seven days after reperfusion, all the rats were assessed with neurobehavioral score, the infarct volumes were assessed with TTC, and BDNF expression in ischemic penumbra was detected with reverse transcription polymerase chain reaction and ELISA. Results:Compared with I/R group, the neurobehavioral scores of EX group, PTZ group and PTZEX group improved, the volumes of cerebral infarction reduced (<italic>P </italic>< 0.05), and PTZEX group was the best (<italic>P </italic>< 0.05). The expression of BNDF was the most in PTZEX group (<italic>P </italic>< 0.05). Conclusion:Early exerxise combined with PTZ could promote the recovery of neurologic function in I/R rats, which may be related to the up-regulation of BDNF.
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Objective To explore the role of microRNA-181b (miR-181b) in cerebral ischemic injury in vivo and its mechanism. Methods Using middle cerebral artery occlusion (MCAO) model to mimic ischemic injury in vivo, the heat shock protein A5(HSPA5) protein level was determined by using Western blotting. The extent of neural cell loss in ischemic cortex after MCAO was assessed by Nissl staining. Neurological score was performed to evaluate the degree of cerebral ischemic injury after MCAO. Results We found that miR-181b antagomir down-regulated miR-181b expression levels in cerebral ischemic cortex of mice after MCA0(P <0.05, n =3). MiR-181 b antagomir improved neurological deficit of mice at 24 hours after transient MCAO (P < 0.05, n =6). HSPA5 protein levels were significantly up-regulated in ischemic cortex of mice after MCAO, and miR-181b antagomir further up-regulated HSPA5 (P < 0.05, n=3). Consequently, miR-181b antagonists attenuated neural cell loss in ischemic cortex after MCAO (P <0.05, n=3). Conclusion MiR-181 b plays an important role in ischemic injury of mice through regulating HSPA5 protein level.
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<p><b>AIM</b>To explore the effects of periphery injection of L-SOP on the activation of p38MAPK in spinal cord in formalin pain model in rats.</p><p><b>METHODS</b>Fourty-eight male Wistar rats were divided randomly into four groups (n=12): NS group and three different dose of L-SOP groups. For each group, 6 rats used to observe flinching and licking time every as nociception behavior 3 minutes in 1 hour after formalin injected and the other 6 rats used to observe the activation of p38(P-p38) by Western blotting.</p><p><b>RESULTS</b>All the three different groups of L-SOP could inhibit nociception behavior in the tonic phase,and 250 nmoVl/L and 500 nmol/L groups could suppress not only in the tonic phase but also in the acute phase. 250 nmol/L and 500 nmol/L groups could reduce activated or phosphorylated p38MAPK in spinal cord.</p><p><b>CONCLUSION</b>Periphery injection of L-SOP can reduce nociceptive behavior and phosphorylated p38MAPK in the spinal cord in formalin-induced hyperalgia, it is suggested that there is functional expression of mGluRs III in the periphery and is involved in the processing of peripheral noxious informations.</p>