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CN 13-1154/R

 
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Effects of Electroacupuncture on the Expression of Nogo-A/NgR in the Lateral Geniculate Nody of Rats with Monocular Deprivation Amblyopia
HU Chen-ying, YU Bo-yan, LI Qing-hong, JI Yang-bin, WU Feng, DING Jian
Abstract23)      PDF (7440KB)(0)      
Objective To investigate the effect of electroacupuncture on the expression of Nogo-A and NgR proteins in the lateral geniculate body of monocular deprivation amblyopia rats. Methods Twenty-eight out of 40 SPF-grade newborn SD rats were randomly selected to establish a monocular deprivation rat model by right eyelid suture at 14d of birth, and 24 rats with successful modelling were randomly divided into the model group and the electroacupuncture group. In the electroacupuncture group, electroacupuncture was applied to the left and right sides of the eye at "Cuanzhu" and "Fengchi". Differences in the amplitude and latency values of the P100 wave of the P-VEP of the rats in each group were detected by P-VEP; HE staining was used to observe the pathological morphological changes of neurons in LGN; immunohistochemistry and Western blot were used to detect the expression levels of Nogo-A and NgR proteins in the lateral geniculate body. Results Compared with the normal group, the cells of the model group were solidified; the P100 wave amplitude in the deprived eye was significantly decreased and the latency value was significantly increased, the mean cell number of Nogo-A and NgR proteins in LGN was increased, the average gray value was decreased, and the relative expression was increased (P<0.01). In the electroacupuncture group, compared with the model group, the cellular of the deprived eye morphology had a significantly improved; the P100 wave amplitude was significantly higher (P<0.05), and the latency value was significantly reduced (P<0.01); and the mean number of positive cells in LGN for Nogo-A and NgR proteins was reduced, with an increase in the mean gray value (P<0.05) and a decrease in the relative expression (P<0.01). Conclusion Electroacupuncture protects nerve cells damaged by monocular deprivation of the posterior LGN, and its mechanism of action may be associated with inhibition of the over expression of Nogo-A and NgR.
2024, 41 (4): 276-280.