Sun Xiaowei, Sun Peng, Liu Limei, Jiang Pengfei, Li Yuanbin
Department of Ophthalmology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, 264000, People's Republic of China.
BMC Ophthalmol. 2021 Jan 6;21(1):13. doi: 10.1186/s12886-020-01765-7.
Retinal degeneration is often accompanied by microglia-mediated neuroinflammation. Ferulic acid (FA), an active ingredient of traditional Chinese medicines (TCMs), has been reported to have anti-inflammatory effects. This study explores the impact of FA on microglia-mediated neuroinflammation and associated retinal degeneration in rd10 mice.
Rd10 mice received different concentrations of FA every day from postnatal day (P)4 to P24. On P25, the visual function of the mice was evaluated by electroretinogram, and retinae were collected for further investigation. Microglial activation and the expression of relevant cytokines in the retina were evaluated by qPCR, western blotting and immunofluorescence staining. Retinal structure was assessed by haematoxylin and eosin (HE) staining.
Supplementation with 50 mg/kg FA provided optimal protection against retinal degeneration, with treated mice exhibiting more photoreceptor nuclei as well as greater wave amplitude amplification on electroretinogram than untreated mice. FA suppressed microglial activation both in vivo and in vitro, and inhibited the expression of pro-inflammatory factors Tnfα, IL1β, and Ccl2 in the retinae of rd10 mice. Furthermore, FA suppressed the activation of STAT1 and subsequently inhibited IRF8 expression, potentially highlighting a role for these pathways in FA-mediated immunomodulatory activity.
Attenuation of neuroinflammation by FA may be beneficial for retarding retinal degeneration.
视网膜变性常伴有小胶质细胞介导的神经炎症。阿魏酸(FA)是中药的一种活性成分,据报道具有抗炎作用。本研究探讨了FA对rd10小鼠小胶质细胞介导的神经炎症及相关视网膜变性的影响。
rd10小鼠从出生后第4天(P4)至第24天(P24)每天接受不同浓度的FA。在P25时,通过视网膜电图评估小鼠的视觉功能,并收集视网膜进行进一步研究。通过qPCR、蛋白质免疫印迹和免疫荧光染色评估视网膜中小胶质细胞的激活及相关细胞因子的表达。通过苏木精-伊红(HE)染色评估视网膜结构。
补充50mg/kg的FA可提供最佳的视网膜变性保护作用,与未处理的小鼠相比,处理后的小鼠视网膜电图显示出更多的光感受器细胞核以及更大的波幅放大。FA在体内和体外均抑制小胶质细胞的激活,并抑制rd10小鼠视网膜中促炎因子Tnfα、IL1β和Ccl2的表达。此外,FA抑制STAT1的激活,随后抑制IRF8的表达,这可能突出了这些信号通路在FA介导的免疫调节活性中的作用。
FA减轻神经炎症可能有助于延缓视网膜变性。