| Abstrakt: |
Objective: To observe the effect of electroacupuncture at Jiaji (EX-B2) points on the expression of microRNA-21 and neuronal apoptosis in rats with acute spinal cord injury. Methods: SD rats were randomly divided into sham-operated group, model group, electroacupuncture group and methylprednisolone group. The model of acute spinal cord injury was reproduced by modified Allen's method. Each group was given corresponding intervention treatment 2 hours after modeling. The electroacupuncture group was treated with electroacupuncture at Jiaji (EX-B2) points in T8 to T12, the methylprednisolone group was given intraperitoneal injection of 30 mg/kg methylprednisolone sodium succinate, and the sham operation group and model group were not treated. After treatment, BBB scores were observed to evaluate the motor function of posterior limb in each group, and the injured spinal cord tissues were taken. The pathological changes of spinal cord neuropathy were observed by Nissl staining. The expression of microRNA-21 was detected by RT-qPCR, and the expression of apoptotic proteins (Bax, Bcl-2 and cleaved-Caspase-3) was detected by Western-Blot. Result: Compared with sham operation group, BBB, neuron survival rate and expression of microRNA-21 were significantly lower, apoptotic rate of neurons was significantly higher, expression of Bax, Bcl-2, cleaved Caspase-3 protein and Bax/Bcl-2 ratio were significantly increased in model group (P< 0.05). Electroacupuncture could significantly increase BBB score, neuron survival rate and expression of microRNA-21, reduce apoptotic rate of neurons and the ratio of Bax/Bcl-2, and inhibit the expression of Bax, Bcl-2 and cleaved Caspase-3 protein in tissues, which were significantly different from those of model group (P< 0.05). Conclusions: Electroacupuncture at Jiaji (EX-B2) points can significantly promote the recovery of neurological function in rats after ASCI, and its mechanism may be closely related to the up-regulation of the expression of microRNA-21 in tissues and the inhibition of the activation of Bax/Bcl-2/cleaved Caspase-3 signaling pathway. [ABSTRACT FROM AUTHOR] |
