The excessive activation of glutamate in the brain is a factor in the development of vascular dementia. γ-Oryzanol is a natural compound that has been shown to enhance brain function, but more research is needed to determine its potential as a treatment for vascular dementia. This study investigated if γ-oryzanol can delay or improve glutamate neurotoxicity in an in vitro model of differentiated HT-22 cells and explored its neuroprotective mechanisms. The differentiated HT-22 cells were treated with 0.1 mmol/L glutamate for 24 h then given γ-oryzanol at appropriate concentrations or memantine (10 µmol/L) for another 24 h. Glutamate produced reactive oxygen species and depleted glutathione in the cells, which reduced their viability. Mitochondrial dysfunction was also observed, including the inhibition of mitochondrial respiratory chain complex I activity, the collapse of mitochondrial transmembrane potential, and the reduction of intracellular ATP levels in the HT-22 cells. Calcium influx triggered by glutamate subsequently activated type II calcium/calmodulin-dependent protein kinase (CaMKII) in the HT-22 cells. The activation of CaMKII-ASK1-JNK MAP kinase cascade, decreased Bcl-2/Bax ratio, and increased Apaf-1-dependent caspase-9 activation were also observed due to glutamate induction, which were associated with increased DNA fragmentation. These events were attenuated when the cells were treated with γ-oryzanol (0.4 mmol/L) or the N-methyl-D-aspartate receptor antagonist memantine. The results suggest that γ-oryzanol has potent neuroprotective properties against glutamate excitotoxicity in differentiated HT-22 cells. Therefore, γ-oryzanol could be a promising candidate for the development of therapies for glutamate excitotoxicity-associated neurodegenerative diseases, including vascular dementia.

Purpose: To evaluate the pharmacological effects of propranolol treatment of patients with central serous chorioretinopathy (CSCR) over 4 months. Results: Among the 89 male and 31 female patients, the mean BCVA decreased to 0.42 ± 0.08 logMAR during CSCR attacks. Oral propranolol showed good effectiveness in reducing CSCR signs after at least 4 months of treatment. The final BCVA of the patients in groups 1 and 2 was 0.09 ± 0.01 and 0.19 ± 0.03 logMAR, respectively (p < 0.05). Moreover, the mean complete remission time in groups 1 and 2 was 1.9 and 3.5 months, respectively (p < 0.05), while the “success” rate in groups 1 and 2 was 95.0% (57/60) and 78.3% (47/60), respectively (p < 0.05). The recurrence rate in groups 1 and 2 was 5.3% (3/57) and 25.5% (12/47) after a further 5 months of follow-up, respectively (p < 0.05). Materials and Methods: One hundred and twenty patients were enrolled and randomly divided into two groups that both underwent a visual acuity test and optical coherence tomography (OCT) scanning, between April and December 2017. The 60 patients in group 1 were requested to take propranolol for 4 months, while the other 60 subjects (group 2) received placebo therapy during the same period. The best-corrected visual acuity (BCVA) of every volunteer and an OCT image of each patient were checked and recorded at the beginning of the study and each week thereafter. If the signs of CSCR disappeared completely from the OCT scans, the case was considered a “success” and treatment stopped at once. However, the “success” subjects were further evaluated in follow-ups throughout the next 5 months to determine the rate of recurrence in groups 1 and 2. The time of total complete remission of CSCR from the OCT scans was also measured in groups 1 and 2. Conclusion: CSCR patients revealed an excellent prognosis and success rate of 95.0% after taking propranolol. The treatment was able to enhance subretinal fluid (SRF) absorption, shorten the time to total complete remission, and significantly decrease CSCR recurrence. As such, we suggest that taking propranolol may be an alternative and viable choice for CSCR patients, given that the new method was shown to be safe, cheap, effective, well tolerated and convenient.

Background and Objectives: This study aimed to illustrate a novel method for improving presbyopia by drinking cassiae tea. Materials and Methods: A total of 425 eyes from 425 participants (aged 52.5 ± 9.5 years) were recruited and divided into several experimental groups over a 6-month period. Participants consumed cassiae tea daily (10 g of cassiae semen brewed in 500 cc of water). Meanwhile, control group participants consumed 500 cc of plain water along with 1000 mg of vitamin C each day. Experiments 1 and 2: Participants with severe dry eye and intraocular pressure (IOP) > 30 mmHg were enrolled, and outcomes were assessed for these conditions, respectively. Experiments 3, 4, and 7: These experiments evaluated pupil size, near vision, and serum superoxide dismutase (SOD) levels in two groups of volunteers. Experiment 5: Different quantities of cassiae tea were prescribed to various groups, and near vision was measured. Experiment 6: Three questionnaires assessed presbyopic symptoms after cassiae tea consumption. Experiment 8: The antioxidant activity of cassiae tea compared with other bioactive compounds and Chinese herbs was evaluated using the DPPH test. Results: By the fourth month of the study, participants experienced increased tear volume and reduced IOP. Pupil size constricted, near vision improved, and serum SOD levels increased. Furthermore, greater consumption of cassiae tea was correlated with better near vision. The antioxidant activity of cassiae tea was found to surpass that of anthocyanins, wolfberry, and vitamin C. Conclusions: Drinking cassiae tea improves dry eye symptoms, reduces IOP, regulates pupil size, and enhances near vision due to its excellent antioxidant and pharmacological properties. These benefits may particularly aid individuals with presbyopia and those engaged in near-distance activities, such as smartphone use.