Traumatic optic neuropathy (TON) is a significant cause of vision loss and irreversible blindness worldwide. It is defined as retinal ganglion cell death and axon degeneration caused by injury. Optic nerve crush (ONC), a well-validated model of TON, activates retinal microglia and initiates neuroinflammation. High-mobility group box 1 (HMGB1), a non-histone chromosomal binding protein in the nucleus of eukaryotic cells, is an important inducer of microglial activation and pro-inflammatory cytokine release. The purpose of this study was to examine the protective effects and mechanism of the HMGB1 inhibitor BoxA to neuroinflammation-induced retinal ganglion cells (RGCs) damage in traumatic optic neuropathy. For that purpose, an optic nerve crush model was established in C57BL/6J mice at 10–12 weeks. Model mice received an intravitreal injection of PBS and the HMGB1 inhibitor BoxA. Our data demonstrated that HMGB1 expression increased after optic nerve crush. Retinal ganglion cell function and morphology were damaged, and retinal ganglion cell numbers were reduced after optic nerve crush. Intravitreal injection of BoxA after ONC can alleviate damage. Furthermore, BoxA reduced microglial activation and expression levels of nuclear factor κB (NF-kB), nucleotide-binding domain, leucine-rich repeat containing protein 3 (NLRP3), and apoptosis-associated speck-like protein containing a CARD (ASC) in experimental ONC mice. In summary, HMGB1 mediates NLRP3 inflammasome via NF-kB to participate in retinal inflammatory injury after ONC. Thus, intravitreal injection of BoxA has potential therapeutic benefits for the effective treatment of RGC death to prevent TON.

Purpureocillium lilacinum is an emerging pathogen that can cause severe ocular infections. This study aimed to investigate the risk factors, clinical manifestations, antifungal susceptibilities, and outcomes of ocular infections caused by P. lilacinum at a large ophthalmic center in Southern China. This retrospective study reviewed the medical records of 34 patients with culture-proven P. lilacinum oculomycosis treated at the Zhongshan Ophthalmic Center from January 2020 to December 2024. The study included 34 patients (17 males, 17 females). The most common risk factor was ocular trauma (38.2%). In vitro susceptibility testing revealed high resistance to fluconazole and caspofungin, but general susceptibility to voriconazole (median MIC 0.25 mg/L). Despite 97.1% of patients receiving voriconazole therapy, outcomes were generally poor, with 54.5% of patients experiencing a poor outcome (vision worse than counting fingers). A significantly shorter time to microbiological diagnosis was associated with a favorable outcome (median 26 days vs. 65 days, p = 0.007). In conclusion, the visual outcomes of this infection remain generally poor, with the major clinical challenge being the delay in diagnosis. Therefore, prompt microbiological investigation is recommended for patients with suspected intraocular infection. Voriconazole remains the first-line therapeutic choice, the therapeutic potential of newer triazoles warrants further investigation.