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1.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-1039777

RESUMO

@#Objective To investigate the protective effect of dexmedetomidine (DEX) on apoptosis of hippocampal neurons in rats with status epilepticus (SE) by regulating MAPK/ERK-CREB pathway.Methods SE rat model was established by intraperitoneal injection of lithium pilocarpine,and was randomly divided into 4 groups,with 10 rats in each group.1 μmol/L of DEX was injected intraperitoneally in the SE+DEX group and 1 μmol/L of phenobarbital was injected intraperitoneally in the positive control group,after 24 hours of drug intervention,Nissl and TUNEL methods were used to detect the damage and apoptosis of hippocampal neurons,and Western blot was used to detect the expression of MAPK,p-ERK,p-CREB and caspase-3,Bcl-2,Bax in hippocampus of rats.Results Compared with the control group,the Racine scores of SE group,positive control group and SE+DEX group were significantly higher (P<0.05),the number of hippocampal neurons and the expression of Bcl-2 protein expressions were decreased significantly (P<0.05),and the number of sepia TUNEL positive cells,MAPK,p-ERK,p-CREB,caspase-3,Bax,Bax/Bcl-2 protein levels increased significantly (P<0.05).Compared with the SE group,the Racine scores of the positive control group and the SE+DEX group were significantly lower (P<0.05),the number of hippocampal neurons and the expression of Bcl-2 protein were significantly increased (P<0.05),and the number of sepia TUNEL positive cells,MAPK,p-ERK,p-CREB,caspase-3,Bax,Bax/Bcl-2 protein expressions decreased significantly (P<0.05).Conclusions DEX may inhibit apoptosis of hippocampal neurons by inhibiting MAPK/ERK-CREB pathway,and then improve epilepsy in rats.

2.
Chinese Journal of Anesthesiology ; (12): 1465-1467, 2016.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-514262

RESUMO

Objective To evaluate the effect of dezocine on the c-fos expression in neurons in the midbrain periaqueductal gray in a rat model of incisional pain.Methods Thirty-six pathogen-free healthy adult male Wistar rats,weighing 250-300 g,were divided into 3 groups (n =12 each) using a random number table:control group (group C),incisional pain group (group I) and dezocine group (group D).A 1 cm longitudinal incision was made through skin,fascia and muscle of the plantar aspect of the right hind paw in sevoflurane-anesthetized rats.In group C,the rats were only anesthetized and underwent no operation.In group I,0.9% sodium chloride solution 2 ml was injected via the caudal vein at 15 min before the model was established.In group D,dezocine 1 mg/kg (diluted to 2 ml in 0.9% sodium chloride solution) was injected via the caudal vein at 15 min before the model was established.At 24 h before operation (T0) and 2,6 and 24 h after operation (T1-3),the mechanical paw withdrawal threshold (MWT) and cumulative pain score were measured.After measurement of the pain threshold at T3,the whole brain was removed for determination of the c-fos expression in neurons in the midbrain periaqueductal gray by immunohistochemistry.Results Compared with group C,the MWT was significantly decreased,cumulative pain scores were increased,and the expression of c-fos in neurons in the midbrain periaqueductal gray was upregulated at T1-3 in I and D groups (P<0.05).Compared with group I,the MWT was significantly increased,the cumulative pain score was decreased,and the expression of c-fos protein in neurons in the midbrain periaqueductal gray was down-regulated at T1.3 in group D (P<0.05).Conclusion Dezocine mitigates incisional pain through inhibiting the expression of c-fos in neurons in the midbrain periaqueductal gray of rats.

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