Chronic central serous chorioretinopathy (CSC) usually demonstrates frequent recurrence, diffuse leakage and persistent subretinal fluid, which cannot be absorbed, thus lead to photoreceptor damage and poor visual acuity. As glucocorticoids have been implicated in the pathogenesis of chronic CSC, various anti-glucocorticoids oral drugs were used in the clinic to promote retinal fluid absorption and reduce the central retinal thickness of the macula and improve the vision outcomes. In addition, the 5α-reductase-specific inhibitor finasteride, the P450-3A4 inducer rifampicin, circadian rhythmic regulator melatonin, and systemic anti-inflammatory drug methotrexate have also been put into clinical trials for chronic CSC, and achieved certain effects. However, most of the clinical studies on these oral drugs were case reports, but not multi-center randomized clinical trials. The long-term effects of these oral drugs need to be observed and studied further.
Objective To observe the expression of alpha;A-and alpha;B-in retina after blue-light exposure.Methods Forty female Wistar rats were divided randomly into 4 groups:control group,and blue-light exposure for 6,12,and 24 hours groups, with 10 rats in each group. The rats in the control group were not intervened.The other three groups of rats were exposed to blue fluorescent lights for 6,12,and 24 hours respcetively. Then the rats were kept in darkness for 12 hours. The globes were enucleated after anaesthesia.The immunohistochemistry and Western blot were performed to detect the expression of alpha;A and alpha;B-crystallin in retina.Results The absorbance value (A value) of retina alpha;A-crystallin was 1.40573plusmn;0.70748 in the control group, and were 4.317 51plusmn;0.412 97, 7.397 08plusmn;1.947 90, 9.634 32plusmn;2.377 61, respectively in the other 3 groups; the difference among the groups was significant (F=24.569，P＜0.001). The A value of retina alpha;B-crystallin is 0.129 36plusmn;0.033 93 in the control group, and were 0.507 17plusmn;0.117 55, 7.345 43plusmn;2.292 97, 4.042 26plusmn;3.890 23, respectively in the other 3 groups; the difference among the groups was significant（F=40.102，P＜0.001）. The results of Western blot showed that the expression of alpha;A and alpha;B crystallin in groups with bluelight exposure was obviously higher than that in the control group.Conclusions Blue light may up-regulate the expression of alpha;A-and alpha;B-crystallin in ratsprime; retina.
Age-related macular degeneration (AMD) is the third leading cause of irreversible blindness worldwide. Wet AMD (wAMD) is the primary type of AMD leading to blindness, characterized by rapid vision loss due to neovascularization. Currently, the primary treatment for wAMD relies on anti-vascular endothelial growth factor (VEGF) drugs. However, some patients respond poorly to this therapy, suggesting a complex pathogenesis that necessitates the exploration of multi-target therapeutic strategies. Recent studies have revealed that aberrant activation of the complement system plays a crucial role in the development of wAMD. Specifically, molecules such as C3, C5, C3a, C5a, and the membrane attack complex (MAC) are involved in the formation of choroidal neovascularization (CNV) by modulating VEGF and other inflammatory factors. Genetic studies have confirmed a strong association between mutations in complement-related genes and wAMD, such as CFH and C3. Furthermore, animal experiments support the therapeutic potential of complement inhibitors in treating CNV. Currently, clinical trials targeting complement components like C3, C5, and MAC are underway, with some drugs having advanced to phase II/III clinical studies. However, their efficacy requires further validation. In the future, complement-targeted therapy, particularly in combination with anti-VEGF treatment, is poised to become a new direction in wAMD management, potentially offering superior therapeutic options for patients.