Oxidative stress alters cellular microenvironment, facilitating cell apoptosis and inflammatory response, and oxidation of lens constituents may ultimately result in cataracts. Astragaloside IV (AS-IV) exhibits a variety of pharmacological activities, such as antioxidative and anti-inflammatory activity via regulating various signaling pathways. However, the effect of AS-IV on lens epithelial cells and its potential therapeutic role in cataracts remained to be investigated. In this study, AS-IV prevented H 2 O 2 -induced injury and inflammatory response in human lens epithelial cell line HLE-B3 through inhibiting NLRP3 inflammasome in a mitogen-activated protein kinase-dependent pathway, providing a potential novel therapeutic strategy for cataracts.

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Diabetic retinopathy (DR) is a microvascular lesion that occurs as a complication of diabetes mellitus. Many studies reveal that retinal neurodegeneration occurs early in its pathogenesis, and abnormal retinal function can occur in patients without any signs of microvascular abnormalities. The gut microbiota is a large, diverse colony of microorganisms that colonize the human intestine. Studies indicated that the gut microbiota is involved in the pathophysiological processes of DR and plays an important role in its development. On the one hand, numerous studies demonstrated the involvement of gut microbiota in retinal neurodegeneration. On the other hand, alterations in gut bacteria in RD patients can cause or exacerbate DR. The present review aims to underline the critical relationship between gut microbiota and DR. After a brief overview of the composition, function, and essential role of the gut microbiota in ocular health, and the review explores the concept of the gut-retina axis and the conditions of the gut-retina axis crosstalk. Because gut dysbiosis has been associated with DR, the review intends to determine changes in the gut microbiome in DR, the hypothesized mechanisms linking to the gut-retina axis, and its predictive potential.

Background: In the diabetic condition, damage of Müller cells contributes to the pathogenesis of diabetic retinopathy. Methods: Primary rat retinal Müller cells (RRMC) were isolated and cultured under high glucose (50 nmol/L). The advanced glycation end products (AGEs) and sodium dithionite were applied to treat high-glucose administrated RRMC to mimic diabetic retinopathological conditions. Effect of BHTCM on diabetic retinopathological RRMC were evaluated. The expressions of aquaporin-4 (AQP4) and Kir4.1 were determined by double-labeling immunofluorescence and ELISA. Levels of vascular endothelial growth factor (VEGF), interleukin-1β (IL-1β) and pigment epithelium-derived factor (PEDF) were examined with ELISA. Lactate dehydrogenase (LDH) activity was also evaluated. Results: Retinal Muller cells were successfully isolated and identified. RRMC treated with AGEs and sodium dithionite resulted in increase of AQP4 and decrease of Kir4.1 in RRMC, increase of VEGF and IL-1β secretion, increase of LDH activity, decrease of PEDF secretion in culture medium, all of which in a dose-dependent or time-dependent manner. Post treating RRMC with AGEs and dithionite, BHTCM reversed changes in expression of AQP4 and Kir4.1 in RRMC, and reversed VEGF levels, PEDF and IL-1β secretion in culture medium. Moreover, BHTCM reversed the decrease of RRMC cell membrane integrity after AGEs and dithionite treatment. Conclusions: BHTCM protected Müller cells from diabetic damage through reducing abnormal changes of Kir4.1 and AQP4, inhibiting VEGF and IL-1β, increasing PEDF production, and maintaining cell membrane integrity. Therefore, BHTCM is a potential drug for the treatment of diabetic retinopathy, which can correct the function of Müller cells.