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目的:探讨健脾益气明目胶囊对N-甲基-N-亚硝脲(MNU)诱导的大鼠视网膜光感受器细胞变性动物模型的治疗作用。方法:43天龄的雌性SD大鼠33只随机分为3组。健脾益气明目胶囊组以健脾益气明目胶囊溶解后灌胃,正常对照组和模型对照组以等量蒸馏水灌胃,2次/d,连续7 d。给药7 d后,健脾益气明目胶囊组和模型对照组大鼠予MNU40 mg/kg腹腔注射;正常对照组注射等量生理盐水。观察MNU处理后12、24、48、72 h各组大鼠视网膜电图a波及b波的变化,并于MNU作用后7 d处死大鼠,取眼球测定视网膜全层及外核层厚度。结果:正常对照组大鼠不同时间点视网膜电图(ERG)a波和b波的振幅差异无统计学意义(P>0.05);模型对照组在MNU处理后ERG a波和b波的振幅均呈持续性、进行性下降,健脾益气明目胶囊可明显抑制ERG a波b波振幅的降低(P<0.05)。眼病理结果显示,健脾益气明目胶囊组与模型组比较,MNU诱导的大鼠视网膜光感受器细胞损伤显著减轻(P<0.05)。结论:健脾益气明目胶囊可减轻MNU对大鼠视网膜光感受器细胞的损伤程度,促进MNU诱导的大鼠视网膜光感受器细胞损伤的功能恢复。
Objective: To investigate the therapeutic effect of Jianpi Yiqi Mingmu capsule on rat retinal photoreceptor cell degeneration induced by N-methyl-N-nitrosourea (MNU). Methods: Thirty-three 43-day-old female SD rats were randomly divided into three groups. The spleen and qi Mingmu Capsule group was treated with spleen and qi Mingmu Capsules, then the rats in the normal control group and the model control group were given gavage with equal volume of distilled water twice a day for 7 days. After 7 days of administration, the rats in the spleen and qi Mingmu capsule group and the model control group were intraperitoneally injected with MNU 40 mg / kg; the normal control group was injected with the same amount of normal saline. After 12, 24, 48 and 72 h MNU treatment, the changes of retinal wave a and b wave in each group were observed. The rats were sacrificed at 7 days after MNU treatment. The thickness of the whole retina and the outer nuclear layer were measured by eyeball. Results: There was no significant difference in amplitude of a-wave and b-wave of ERG at different time points in normal control group (P> 0.05). The amplitude of ERG a-wave and b-wave in model control group were The results showed that Jianpi Yiqi Mingmu capsule could significantly reduce the amplitude of b wave of ERG a wave (P <0.05). Eye pathology results showed that MNU-induced retinal photoreceptor cell injury in rats was significantly reduced compared with model group (P <0.05). Conclusion: Jianpi Yiqi Mingmu capsule can reduce the damage of retinal photoreceptor cells induced by MNU and promote the functional recovery of MNU-induced retinal photoreceptor cell injury in rats.