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Objective: To determine the role of heat shock protein A5 (HSPA5) induced autophagy on cerebral ischemia/reperfusion in-jury in mice., Methods: Thirty-six BALB/c mice were randomly divided into sham group, ischcmia/reperfusion (I/R) group, vehicle + I/R group, 3-Methyladenine(3-MA) + I/R group, scramble siRNA group and HSPA5 siRNA + I/R group( n =6). In sham group, the operation was only performed, did not insert line switch. Focal cerebral ischemia was performed using the method of middle cerebral artery occlusion (MCAO) for 60 min and 24 h reperfusion. In vehicle + I/R group and 3-MA + I/R group, 2 μ l 0.9% NaCl or 3-MA(30 mg/ml) was admin-istered by intracerebroventricular injection 30 min before MCAO; In scramble siRNA + I/R group and HSPA5 siRNA + I/R group, 5 μ l scram-ble siRNA or HSPA5 siRNA(2 μ g/ μ l) was administered by intracerebroventricular injection 24 h before MCAO. Autophagosome in neuron, the expression of microtubule-associated protein light chain 3 (LC3)-Ⅱ/LC3-I in ischemic cortex, the degree of cerebral ischemic injury and neu-rological function score were detected., Results: Initial electron microscopy showed that neuronal morphology appeared to be normal in the sham group. At 24 h after I/R, cell shrinkage, loss of cellular organelles and formation of autophagosomes were observed in the ischemic cerebral cortex of I/R group. In addition, autophagosomes were less frequently observed than that in I/R group. The expressions of LC3-Ⅱ/LC3-I and Beclin-1 protein were increased significantly in I/R group compared with that in sham group( P < 0.05). Compare with I/R group, the LC3-Ⅱ/LC3-I protein levels induced by I/R in 3-MA + I/R group or HSPA5 siRNA + I/R group was decreased effectively ( P < 0.05). In addi-tion, the cerebral ischemic injury and neurological symptoms after I/R in 3-MA + I/R group or HSPA5 siRNA + I/R group were exacerbated significantly ( P < 0.05)., Conclusions: These results suggest that HSPA5 induced autophagy may play a protective role in focal I/R damage in mice.

Aim: To explore the effects of periphery injection of L-SOP on the activation of p38MAPK in spinal cord in formalin pain model in rats., Methods: 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., Results: 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., Conclusion: 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.