Hispidin, a polyphenol compound isolated from Phellinus linteus, has been reported to possess antioxidant activities. In this study, we aimed to investigate the mechanisms underlying the protective effect of hispidin against hydrogen peroxide (H₂O₂)-induced oxidative stress on Adult Retinal Pigment Epithelial cell line-19 (ARPE-19) cells. Hispidin was not cytotoxic to ARPE-19 cells at concentrations of less than 50 μM. The levels of intracellular reactive oxygen species (ROS) were analyzed by dichlorofluorescin diacetate (DCFDA) staining. Hispidin significantly restored H₂O₂-induced cell death and reduced the levels of intracellular ROS. The expression levels of antioxidant enzymes, such as NAD(P)H:Quinine oxidoreductase-1 (NQO-1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and glutamate-cysteine ligase modifier subunit (GCLM) were examined using real-time PCR and Western blotting. Our results showed that hispidin markedly enhanced the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), HO-1, NQO-1, GCLM, and GCLC in a dose-dependent manner. Furthermore, knockdown experiments revealed that transfection with Nrf2 siRNA successfully suppresses the hispidin activated Nrf2 signaling in ARPE-19 cells. Moreover, activation of the c-Jun N-terminal kinase (JNK) pathway is involved in mediating the protective effects of hispidin on the ARPE-19 cells. Thus, the present study demonstrated that hispidin provides protection against H₂O₂-induced damage in ARPE-19 cells via activation of Nrf2 signaling and up-regulation of its downstream targets, including Phase II enzymes, which might be associated with the activation of the JNK pathway.

Background and objectives: We aimed to evaluate the correlation between periodontal disease (PD) and following ocular diseases via the National Health Insurance Research Database in Taiwan. Materials and Methods: A retrospective cohort study was conducted. Subjects were regarded as having PD according to the diagnostic codes. For comparison, each subject with PD was matched to one non-PD individual from the database after exclusion. The main outcome was defined as the development of infectious keratitis, endophthalmitis, orbital cellulitis, lacrimal duct infection, uveitis and infectious scleritis. Cox proportional hazard regression was used to yield the adjusted hazard ratios (aHR) of ocular diseases between the study and control groups. Results: A total of 426,594 subjects were enrolled in both the study and control groups. In the multivariable analysis, significantly higher rates of infectious keratitis (aHR: 1.094, 95% CI: 1.030–1.161), uveitis (aHR: 1.144, 95% CI: 1.074–1.218) and infectious scleritis (aHR: 1.270, 95% CI: 1.114–1.449) were found in the study group. Concerning the PD interval, infectious keratitis (aHR: 1.159, 95% CI: 1.041–1.291) and infectious scleritis (aHR: 1.345, 95% CI: 1.055–1.714) would significantly occur in PD patients with an interval shorter than two years, individuals with a PD interval that ranged from two to five years were under a higher risk of developing uveitis (aHR: 1.184, 95% CI: 1.065–1.315) and infectious scleritis (aHR: 1.386, 95% CI: 1.125–1.708), and the rate of uveitis (aHR: 1.149, 95% CI: 1.038–1.272) was significantly higher if PD persisted more than five years. Conclusions: The presence of PD was moderately associated with the risk of developing infectious keratitis, uveitis and infectious scleritis.

Sialidosis is a rare autosomal recessive lysosomal storage disorder caused by mutations in the NEU1 gene, resulting in deficient neuraminidase-1 activity and the subsequent accumulation of sialylated compounds in lysosomes. This review comprehensively analyzes the genetic and clinical heterogeneity associated with sialidosis, emphasizing the distinction between the milder type I form and the more severe type II form. Over 90 pathogenic NEU1 variants, predominantly missense mutations, have been identified, highlighting significant phenotypic diversity. Advancements in genomic sequencing technologies have facilitated the identification of known and novel mutations, with population-specific insights elucidating ethnic variability in symptomatology and genetic profiles. Recent case studies, including a novel compound heterozygous variant, further illustrate the complexity of the genotype–phenotype correlations. Emerging therapeutic approaches, such as enzyme replacement therapy and adeno-associated virus-mediated gene therapy, demonstrate promising potential for restoring neuraminidase-1 function and improving outcomes in preclinical models. This review emphasizes the critical role of genetic analysis in diagnosis and management while advocating for continued research into the molecular mechanisms underlying sialidosis to enable the development of targeted, personalized treatments.

This study investigates the development of glaucoma in subjects with surgery-indicated chronic rhinosinusitis (CRS) by the use of the National Health Insurance Research Database in Taiwan. Individuals that received the functional endoscopic sinus surgery (FESS) with a diagnostic code of CRS were regarded as surgery-indicated CRS and enrolled in the study group. Four non-CRS patients were age- and gender-matched to each patient in the study group. The exclusion criteria included legal blindness, ocular tumor, history of eyeball removal, and previous glaucoma. The outcome was regarded as the development of glaucoma, and conditional logistic regression was used for the statistical analysis, which involved multiple potential risk factors in the multivariate model. A total of 6506 patients with surgery-indicated CRS that received FESS and another 26,024 non-CRS individuals were enrolled after exclusion. The age and gender distributions were identical between the two groups due to matching. There were 108 and 294 glaucoma events in the study group and control group, respectively, during the follow-up period, and the study group had a significantly higher adjusted hazard ratio (1.291, 95% confidential interval: 1.031–1.615). The cumulative probability analysis also revealed a correlation between the occurrence of glaucoma and the CRS disease interval. In the subgroup analysis, the chance of developing open-angle glaucoma and normal-tension glaucoma was significantly higher in the study group than in the control group. In conclusion, the existence of surgery-indicated CRS is a significant risk factor for the development of glaucoma, which correlated with the disease interval.