Age‐related cataract (ARC) is caused by the exposure of the lens to UVB which promotes oxidative damage and cell death. This study aimed to explore the role of lncRNA H19 in oxidative damage repair in early ARC. lncRNAs sequencing technique was used to identify different lncRNAs in the lens of early ARC patients. Human lens epithelial cells (HLECs) were exposed to ultraviolet irradiation; and 8‐OHdG ELISA, Cell counting kit 8 (CCK8), EDU, flow cytometry and TUNEL assays were used to detect DNA damage, cell viability, proliferation and apoptosis. Luciferase assay was used to examine the interaction among H19, miR‐29a and thymine DNA glycosylase (TDG) 3'UTR. We found that lncRNA H19 and TDG were highly expressed while miR‐29a was down‐regulated in the three types of early ARC and HLECs exposed to ultraviolet irradiation, compared to respective controls. lncRNA H19 knockdown aggravated oxidative damage, reduced cell viability and proliferation, and promoted apoptosis in HLECs, while lncRNA H19 overexpression led to opposite effects in HLECs. Mechanistically, miR‐29a bound TDG 3'UTR to repress TDG expression. lncRNA H19 up‐regulated the expression of TDG by repressing miR‐29a because it acted as ceRNA through sponging miR‐29a. In conclusion, the interaction among lncRNA H19, miR‐29a and TDG is involved in early ARC. lncRNA H19 could be a useful marker of early ARC and oxidative damage repair pathway of lncRNA H19/miR‐29a/TDG may be a promising target for the treatment of ARC.

Background: Diabetic macular edema (DME) is a serious complication of diabetic retinopathy (DR).Recent studies have shown that inflammation is closely associated with the development of DME, and peripheral blood inflammatory markers [white blood cell (WBC) count and its subtypes] are relatively simple and easy to detect. Here, we investigated the relationship between peripheral blood inflammatory markers and macular edema in patients with severe DR (including both severe non-proliferative DR and proliferative DR).Methods: A total of 42 patients with severe DR were included in this study and divided into two groups: a severe DR with DME group (DME group, n=18) and a severe DR without DME group (non-DME group, n=24). Ophthalmologic findings and hematologic results were retrospectively retrieved from hospitalization records and databases.Results: The neutrophil percentage was significantly higher in the DME group (62.52%±8.21%) than in the non-DME group (57.30%±8.17%) (P<0.05); in contrast, the lymphocyte percentage was significantly lower in the DME group (28.09%±7.45%) than in the non-DME group (33.54%±7.29%) (P<0.05). Logistic regression analysis showed a significant correlation between lymphocyte percentage and DME [odds ratio (OR) =0.654, 95% CI: 0.436-0.851; P=0.011].Conclusions: Lymphocyte percentage can be used as an inflammatory marker for the development of DME in patients with severe DR.

Optic nerve injury is a type of neurodegenerative disease. Physcion is an anthraquinone that exerts a protective role against various diseases. However, its function in regulating optic nerve injury remains largely unknown. An in vitro model of optic nerve injury was established in HAPI cells treated with IFN-β. Functional assays were used to detect HAPI cell viability and apoptosis. The levels of inflammation and the expression levels of oxidative stress-related genes were measured in HAPI cells. In addition, western blot analysis was used to detect the expression levels of Janus kinase 2 (JAK2)/STAT3-linked genes in HAPI cells. Treatment of the cells with physcion prevented cells against IFN-β-induced neuronal injury. Physcion restrained IFN-β-induced inflammatory response and oxidative stress in HAPI cells. In addition, it improved IFN-β-induced injury in HAPI cells by suppressing the JAK2/STAT3 pathway. In conclusion, the present study revealed that physcion improved optic nerve injury in vitro by inhibiting the JAK2/STAT3 pathway. Physcion may be a promising therapeutic target for the treatment of this disease.

Background: Inflammation and immune dysregulation are involved in the pathogenesis of diabetic macular edema (DME). The progressive increase of neutrophils in peripheral blood can lead to the increase of the number of neutrophils in the retina, thus leading to the sustained damage of the retinal vascular system and the destruction of the blood retinal barrier (BRB); lymphocytes play a protective role in vascular diseases caused by type 2 diabetes mellitus (T2DM). The purpose of this study was to study the relationship between the changes of leukocytes and their classification in peripheral blood and the occurrence and progression of DME in patients with T2DM. Methods: A retrospective analysis was made on 81 patients with T2DM with DME (DME group) hospitalized in our hospital from January 2019 to December 2020. According to the morphological characteristics of macular edema in optical coherence tomography (OCT), they were divided into early DME group (n=33) and late DME group (n=48); 33 patients with diabetes retinopathy (DR) but without DME matched in age and course of disease served as the control group (NO-DME group). The clinical parameters assessed included eye examination, OCT results, WBCs and subtypes, blood glucose, and glycosylated hemoglobin.Results: Compared with NO-DME group (n=33), Neutrophils% in DME group (n=81) was higher (57.37±9.52 vs. 63.27±7.85; P=0.001); Monocyte% (7.63±1.77 vs. 6.88±1.83; P=0.047) and lymphocyte% (30.35±9.51 vs. 27.26±6.59; P=0.032) were decreased. The optimal model was obtained with R 4.0.5 software.With other relevant variables being the same, females had a significantly increased risk of DME (b=1.273, P=0.015), %neutrophils was significantly associated with increased risk of DME (b=0.152, P=0.0006), and %lymphocytes was significantly associated with a reduced risk of DME (b=−0.027, P=0.179). However, in the early and late DME groups, no significant differences in biological markers were found, and a high-quality model was not obtained.Conclusions: In this preliminary study, %neutrophils is associated with increased risk of DME, whereas %lymphocytes is associated with a reduced risk of DME.