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目的探讨灵芝孢子油对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,为防治视网膜变性提供一种有价值的现代化中药。方法大鼠随机分为5组,对照组、灵芝孢子油治疗组、二十二碳六烯酸(DHA)治疗组、灵芝孢子油+DHA治疗组和模型组,在造模前2 d用不同的药物ig给药,第3天采用40 mg/kg MNU单次剂量ip造模,造模后继续ig给药至第10天,造模后1、3、5、7、10 d进行视网膜电图(ERG)检查,并取眼球进行眼病理检查。结果不同用药组各时间点的b波振幅明显高于模型组(P<0.05、0.01);灵芝孢子油组的a波振幅明显高于模型组(P<0.05),但与DHA组和灵芝孢子油+DHA组相比较,无明显差异(P>0.05)。眼病理结果,不同用药组在各个时间点与相应的模型组比较,MNU诱导的大鼠视网膜光感受器损伤均明显减轻(P<0.05)。结论灵芝孢子油和DHA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 ganoderma lucidum spore oil on N-methyl-N-nitrosourea (MNU) induced animal model of rat retinal photoreceptor cell degeneration and provide a valuable modern Chinese medicine for preventing and treating retinal degeneration. Methods Rats were randomly divided into 5 groups: control group, ganoderma lucidum spore oil treatment group, docosahexaenoic acid (DHA) treatment group, ganoderma lucidum spore oil + DHA treatment group, and model group. They were used 2 days before modeling. The drug ig was administered on the third day using a 40 mg/kg MNU single-dose ip model, continued ig administration to the 10th day after modeling, and electroretinex was performed 1, 3, 5, 7, and 10 days after the model was established. Figure (ERG) examination and eyeball examination of the eye. Results The b-wave amplitudes of different drug groups at each time point were significantly higher than those of the model group (P<0.05, 0.01). The a-wave amplitude of Ganoderma lucidum spore oil group was significantly higher than that of the model group (P<0.05), but with the DHA group and Ganoderma lucidum spores. There was no significant difference in the oil + DHA group (P>0.05). According to the pathological results of the eye, compared with the corresponding model group at different time points in the different drug groups, MNU-induced photoreceptor damage in the rat retina was significantly reduced (P<0.05). Conclusion Ganoderma lucidum spore oil and DHA can reduce the degree of damage of MNU on retinal photoreceptor cells in rats and promote the recovery of MNU-induced photoreceptor cell damage in rat retina.