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The Journal of Clinical Anesthesiology ; (12): 594-597, 2016.
Article in Chinese | WPRIM | ID: wpr-494510

ABSTRACT

Objective To investigate the effect of electroacupuncture on the expressions of in-terleukin(IL)-33 and ST2 in spinal cord and dorsal root ganglion in rats with neuropathic pain. Methods Forty adult female SD rats were randomly divided into sham operation group (group Sham),model group (group MC),ipsilateral electroacupuncture group (group SE)and contralateral electroacupuncture group (group VE).Each group had 10.The sciatic nerve injury models were es-tablished.The rats in group SE and group VE were respectively accepted electrical acupuncture treat-ment in Yanglingquan and Zusanli in the right and left limbs.Respectively,before treatment (T0 ), treated for 7 d (T1 ),3 d (T2 )and 7 d (T3 )after treatment,the MWT and TWL of rats in the four groups were measured.At T3 ,the expressions of IL-33 in spinal cord and dorsal root ganglion in rats were detected by using quantitative PCR.Results Compared with T0 ,MWT and TWL in group MC, group SE and group VE at T1-T3 were decreased significantly (P < 0.05).Compared with sham group,MWT in group SE and group VE,TWL in group MC,group SE and group VE at T1-T3 were decreased significantly (P <0.05).Compared with group MC,MWT and TWL in group SE and group VE at T2 ,T3 were increased significantly (P <0.05).Compared with sham group,the relative expression levels of IL-33 mRNA and ST2 mRNA in spinal cord and dorsal root ganglion in the group MC,group SE and group VE were elevated,the differences were statistically significant (P <0.05). Compared with group MC,the relative expression levels of IL-33 mRNA and ST2 mRNA in spinal cord and dorsal root ganglion group SE and group VE were decreased,the differences were statistical-ly significant (P <0.05).Conclusion The electroacupuncture treatment could significantly reduce the pain symptoms of neuropathic pain in rats,possibly via inhibiting the expressions of IL-33 and ST2 in spinal cord and dorsal root ganglion and blocking the IL-33/ST2 mediated inflammatory to play role.

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