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A retinal disorder known as age-related macular degeneration (AMD) can be very damaging, which may result in vision loss. Cordyceps militaris has antioxidant, anti-inflammatory, anticancer activity and immunomodulatory functions. carotenoids were considered potential therapeutic agents for the treatment of age-related macular degeneration. In this study, we evaluated for the first time the protective effect of purified carotenoids (CMCT) extracted from Cordyceps militaris on hydrogen peroxide (H2O2)-induced damage to human retinal pigment epithelial cells (ARPE-19). The pretreatment of ARPE-19 cells with CMCT (1, 2.5μg/ml) for 12h after exposure to H2O2 (400μM) greatly improved cell viability and injury tolerance. and reduced reactive oxygen species production (ROS) and decreased malondialdehyde (MDA) formation. Furthermore, Bax and Caspase-3 showed increased protein expression and less protein expression of Bcl-2 in cellular oxidative stress by flow cytometry analysis but showed the opposite expression by adding CMCT. Besides, cells were treated with H2O2 and then CMCT restored catalase (CAT), superoxide dismutase (SOD) and glutathione (GSH) enzyme activities to normal levels. Our results suggest that CMCT can protect RPE cells from oxidative stress damage by regulating oxidative activity and anti-apoptotic function. It indicates that CMCT has a potential therapeutic role in oxidative stress-directed protection and prevention of AMD.

Additional file 1: Fig. S1. The immune infiltration score in CD276hi/OLIG2lo and CD276lo/OLIG2hi groups. (p-value: *, < 0.05; **, < 0.01; ***, < 0.001).

Additional file 2: Fig. S2. The survival curve of TCGA, GSE84010, and Gravandeel’s dataset according to the three-subtype classifications (Proneural, Mesenchymal, and Classical).

Although the neuroprotective effects of hydrogen sulfide (H(2)S) have been demonstrated in several studies, whether H(2)S protects against early brain injury (EBI) and secondary cognitive dysfunction in subarachnoid hemorrhage (SAH) model remains unknown. This study was undertaken to evaluate the influence of H(2)S on both acute brain injury and neurobehavioral changes as well as the underlying mechanisms after SAH. The H(2)S donor, NaHS, was administered via an intraperitoneal injection at a dose of 5.6 mg/kg at 2 h, 6 h, 24 h, and 46 h after SAH in rat model. The results showed that NaHS treatment significantly improved brain edema and neurobehavioral function, and attenuated neuronal cell death in the prefrontal cortex, associated with a decrease in Bax/Bcl‐2 ratio and suppression of caspase‐3 activation at 48 h after SAH. NaHS also promoted phospho‐Akt and phospho‐ERK levels. Furthermore, NaHS treatment significantly enhanced the levels of brain‐derived neurotrophic factor (BDNF) and phospho‐CREB. Importantly, NaHS administration improved learning and memory performance in the Morris water maze test at 7 days post‐SAH in rats. These results demonstrated that NaHS, as an exogenous H(2)S donor, could significantly alleviate the development of EBI and cognitive dysfunction induced by SAH via Akt/ERK‐related antiapoptosis pathway, and upregulating BDNF‐CREB expression.