GYY4137 protects against MCAO via p38 MAPK mediated anti-apoptotic signaling pathways in rats.

摘要

Hydrogen sulfide (H2S) is a neuromodulator that protect the cerebral ischemia-reperfusion (I/R) injury. The present study aimed to investigate the possible mechanisms of GYY4137 (a slow-releasing donor of H2S) against cerebral I/R injury. GYY4137 significantly increased the level of H2S in rat brain cortex. Compared with the I/R group, the cerebral infarction volume in GYY4137 group (GYY) and SB203580 group (SB) were significantly decreased. Compared with SB group, the cerebral infarction volume in GYY group was significantly decreased. The brain edema in GYY group and SB group were significantly decreased than that in I/R group. Compared with I/R group, the Garcia score in GYY and SB group were significantly increased. Western blot analysis showed that the phosphorylation of p38 MAPK, ERK1/2 and JNK protein in GYY group was significantly increased compared with I/R group. Compared with I/R group, the expression of Bax protein in GYY and SB group were significantly decreased, while the expression of Bcl-2 protein was significantly increased. The activity of caspase-3 in GYY group and SB group were significantly decreased than that of I/R group. Our findings suggested that H2S slow-releasing agent GYY4137 improved the neurological function and reduced the infarct area after cerebral I/R injury. The protective effects were achieved by inhibiting apoptosis via regulating p38 MAPKERK1/2 and JNK signaling pathways.

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