杜柏荣, 许衍峰, 韦志强. 维生素C通过调节巨噬细胞功能缓解大鼠黄斑变性的研究[J]. 实用临床医药杂志, 2022, 26(17): 130-134. DOI: 10.7619/jcmp.20220296
引用本文: 杜柏荣, 许衍峰, 韦志强. 维生素C通过调节巨噬细胞功能缓解大鼠黄斑变性的研究[J]. 实用临床医药杂志, 2022, 26(17): 130-134. DOI: 10.7619/jcmp.20220296
DU Borong, XU Yanfeng, WEI Zhiqiang. Vitamin C alleviates macular degeneration in rats by regulating function of macrophages[J]. Journal of Clinical Medicine in Practice, 2022, 26(17): 130-134. DOI: 10.7619/jcmp.20220296
Citation: DU Borong, XU Yanfeng, WEI Zhiqiang. Vitamin C alleviates macular degeneration in rats by regulating function of macrophages[J]. Journal of Clinical Medicine in Practice, 2022, 26(17): 130-134. DOI: 10.7619/jcmp.20220296

维生素C通过调节巨噬细胞功能缓解大鼠黄斑变性的研究

Vitamin C alleviates macular degeneration in rats by regulating function of macrophages

  • 摘要:
    目的 探讨维生素C通过调节巨噬细胞功能缓解大鼠黄斑变性的可能机制。
    方法 应用尾静脉注射碘酸钠法建立黄斑变性SD大鼠模型,并灌胃维生素C对其进行治疗。30只SD大鼠适应性喂养1周后,随机分为正常组、模型组、治疗组,每组10只。正常组不给予处理;治疗组尾静脉注射40 mg/kg碘酸钠造模,实验开始后每天灌胃1次维生素C,灌胃剂量100 mg/kg; 模型组尾静脉注射40 mg/kg碘酸钠造模,实验开始后每天灌胃等体积生理盐水。治疗结束后,使用视网膜电图记录系统检测大鼠视网膜电位,使用苏木精-伊红染色法(HE染色法)对视网膜结构、视网膜外核层细胞数、视网膜色素细胞上皮层进行观察,使用流式细胞仪检测视网膜巨噬细胞的CD36和CD206。
    结果 维生素C能够减缓大鼠视网膜损伤。模型组视网膜外核层细胞数为(72.90±15.60)个/视野,低于治疗组的(126.40±13.60)个/视野,差异有统计学意义(P<0.01); 模型组视网膜色素上皮细胞层数为(1.56±0.93)层/视野,低于治疗组的(3.49±0.88)层/视野,差异有统计学意义(P<0.05)。维生素C能提高年龄相关性黄斑变性(AMD)大鼠视网膜电位,保护大鼠视网膜功能,缓解AMD进展。维生素C能够提高CD36阳性细胞比率,降低CD206阳性细胞比率,体现为模型组视网膜巨噬细胞CD36阳性细胞比率为(33.98±6.86)%, 低于治疗组的(46.86±3.83)%, 差异有统计学意义(P<0.01); 模型组视网膜巨噬细胞CD206阳性细胞比率为(43.59±6.51)%, 高于治疗组的(31.52±4.08)%, 差异有统计学意义(P<0.01)。
    结论 维生素C通过增强视网膜巨噬细胞吞噬能力、抑制巨噬细胞M2极化发挥缓解大鼠黄斑变性的功效。

     

    Abstract:
    Objective To explore the possible mechanism of vitamin C in alleviating macular degeneration in rats by regulating the function of macrophages.
    Methods SD rats were injected with sodium iodate into the tail vein to create a macular degeneration model, and vitamin C was given to the rats by gavage. Thirty SD rats were randomly divided into normal group, model group and treatment group after adaptive feeding for one week, with 10 rats in each group. The normal group was not given any treatment measures; in the treatment group, 40 mg/kg sodium iodate was injected into the tail vein to establish the model, and 100 mg/kg vitamin C was given by gavage once a day after the start of experiment; in the model group, 40 mg/kg sodium iodate was injected into the tail vein to establish the model, and the equal volume of normal saline was given by gavage every day after the start of experiment. After the treatment, the electroretinogram recording system was used to detect retinal potential of rats, the retinal structure, the number of retinal external nuclear cells and the epithelial layer of retinal pigment cells were detected by hematoxylin-eosin staining (HE staining), and flow cytometry was used to detect CD36 and CD206 in retinal macrophages.
    Results Vitamin C was able to alleviate the retinal damage in rats. The number of retinal external nuclear cells in the model group was (72.90±15.60) cells per field of vision, which was lower than (126.40±13.60) cells per field of vision in the treatment group (P < 0.01). The epithelial layer of retinal pigment cells in the model group was (1.56±0.93) layers per field of vision, which was significantly lower than (3.49±0.88) layers per field of vision in the treatment group (P < 0.05). Vitamin C was able to increase the retinal potential of age-related macular degeneration (AMD) rats, protect the retinal function of rats, and alleviate the progression of AMD. Vitamin C was able to increase the ratio of CD36 positive cells and reduce the ratio of CD206 positive cells, which was reflected as follows: the ratio of CD36 positive cells of retinal macrophages in the model group was (33.98±6.86)%, which was significantly lower than (46.86±3.83)% in the treatment group (P < 0.01). The ratio of CD206 positive cells of retinal macrophages in the model group was (43.59±6.51)%, which was significantly higher than (31.52±4.08)% in the treatment group (P < 0.01).
    Conclusion Vitamin C can alleviate macular degeneration in rats by enhancing phagocytic capacity of retinal macrophages and inhibiting M2 polarization of macrophages.

     

/

返回文章
返回