Exploring the protective effects of Qiju Granule in a rat model of dry age-related macular degeneration.

The aim of this study was to evaluate the potential protective effect of Qiju Granule in a rat model of age-related macular degeneration (AMD) and investigate the underlying mechanisms involved. Rats were injected intravenously with 40 mg/kg of sodium iodate (SI) to induce a dry AMD model. The rats in the treatment group received three different doses of Qiju Granule once a day via gavage, while the rats in the control group were given an equal volume of physiological saline. On day 14 and day 28 following the intervention, various methods were employed to evaluate retinal function and structure, including electroretinography (ERG), optical coherence tomography (OCT), and histological examination. The expression of glial fibrillary acidic protein (GFAP), basic fibroblast growth factor (bFGF), brain-derived neurotrophic factor (BDNF), and ciliary neurotrophic factor (CNTF) was assessed via immunofluorescence. Beyond immunofluorescence, the mRNA levels of bFGF, BDNF, and CNTF were quantitatively determined using real-time polymerase chain reaction (qRT-PCR). Rats treated with Qiju Granule exhibited significant improvements in both retinal function and structure compared to the model group. The most noteworthy effects were observed at a high dose of Qiju Granule. Furthermore, the expression levels of bFGF, BDNF, and CNTF were significantly unregulated in the treated groups compared to the model group. Qiju Granule demonstrated a protective effect on the retina in the SI-induced rat model of AMD. The protective mechanism may be attributed to the upregulation of retinal neurotrophic factors expression. • The etiology of age-related macular degeneration (AMD) is multifactorial, involving both genetic and environmental components. • Currently, there are no effective preventive measures or treatments available for dry AMD. • This study assesses the protective effects of Qiju Granule in a rat model of dry AMD and finds significant improvements in retinal function and structure, especially at higher doses. • The protective mechanism is associated with the upregulation of neurotrophic factors, including bFGF, BDNF, and CNTF, as demonstrated by immunofluorescence and qRT-PCR analyses. • These findings provide valuable insights into potential therapeutic approaches and highlight the importance of targeting these neurotrophic factors to enhance the treatment of AMD. [ABSTRACT FROM AUTHOR]