Kong Qihang, Han Xiu, Cheng Haiyang, Liu Jiayu, Zhang Huijun, Dong Tangrong, Chen Jiansu, So Kwok-Fai, Mi Xuesong, Xu Ying, Tang Shibo
Department of Ophthalmology, Aier Eye Hospital, Jinan University, Guangzhou, Guangdong Province, China.
Department of Ophthalmology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong Province, China.
Neural Regen Res. 2024 Oct 1;19(10):2290-2298. doi: 10.4103/1673-5374.390958. Epub 2023 Dec 15.
JOURNAL/nrgr/04.03/01300535-202410000-00030/figure1/v/2024-02-06T055622Z/r/image-tiff Photoreceptor cell degeneration leads to blindness, for which there is currently no effective treatment. Our previous studies have shown that Lycium barbarum (L. barbarum) polysaccharide (LBP) protects degenerated photoreceptors in rd1, a transgenic mouse model of retinitis pigmentosa. L. barbarum glycopeptide (LbGP) is an immunoreactive glycoprotein extracted from LBP. In this study, we investigated the potential protective effect of LbGP on a chemically induced photoreceptor-degenerative mouse model. Wild-type mice received the following: oral administration of LbGP as a protective pre-treatment on days 1-7; intraperitoneal administration of 40 mg/kg N-methyl-N-nitrosourea to induce photoreceptor injury on day 7; and continuation of orally administered LbGP on days 8-14. Treatment with LbGP increased photoreceptor survival and improved the structure of photoreceptors, retinal photoresponse, and visual behaviors of mice with photoreceptor degeneration. LbGP was also found to partially inhibit the activation of microglia in N-methyl-N-nitrosourea-injured retinas and significantly decreased the expression of two pro-inflammatory cytokines. In conclusion, LbGP effectively slowed the rate of photoreceptor degeneration in N-methyl-N-nitrosourea-injured mice, possibly through an anti-inflammatory mechanism, and has potential as a candidate drug for the clinical treatment of photoreceptor degeneration.
《期刊》/nrgr/04.03/01300535 - 202410000 - 00030/图1/v/2024 - 02 - 06T055622Z/图像 - tiff 光感受器细胞变性会导致失明,目前尚无有效的治疗方法。我们之前的研究表明,枸杞多糖(LBP)可保护视网膜色素变性转基因小鼠模型rd1中退化的光感受器。枸杞糖肽(LbGP)是从LBP中提取的一种免疫反应性糖蛋白。在本研究中,我们研究了LbGP对化学诱导的光感受器退行性变小鼠模型的潜在保护作用。野生型小鼠接受以下处理:在第1 - 7天口服LbGP作为保护性预处理;在第7天腹腔注射40 mg/kg N - 甲基 - N - 亚硝基脲以诱导光感受器损伤;在第8 - 14天继续口服LbGP。LbGP治疗可提高光感受器存活率,改善光感受器变性小鼠的光感受器结构、视网膜光反应和视觉行为。还发现LbGP可部分抑制N - 甲基 - N - 亚硝基脲损伤视网膜中小胶质细胞的激活,并显著降低两种促炎细胞因子的表达。总之,LbGP可能通过抗炎机制有效减缓了N - 甲基 - N - 亚硝基脲损伤小鼠的光感受器变性速度,具有作为光感受器变性临床治疗候选药物的潜力。