The study exists, is peer reviewed, is open access, and the figure in the post is its genuine Figure 2. The figure caption text in the post matches the published caption verbatim.

The paper reports: mice were given regular drinking water or drinking water containing 150 mM NaHCO3 for one week before treatment with paraquat (15 mg/kg), an oxidative stress inducer, and under oxidative stress the researchers observed a decline in visual acuity indicated by reduced spatial frequency and reduced visual evoked potential P1-N1 amplitudes, along with increased latency, measured by optomotor response and VEP . Bicarbonate administration restored spatial frequency and VEP P1-N1 potentials in the oxidatively stressed mice, although there were no statistically significant differences in latency .

The broader findings the post lists in its caption are also in the paper: using mouse models of oxidative stress induced by ischemic injury and paraquat administration, the authors found that administration of bicarbonate, as an activator of sAC, protected retinal ganglion cells, blocked AMP-activated protein kinase activation, inhibited glial activation, and improved visual function . The paper further reports that bicarbonate ameliorated mitochondrial dysfunction in RGCs by enhancing mitochondrial biogenesis, preserving mitochondrial structure, and increasing ATP production .

No human study of ingested bicarbonate for vision, visual acuity, or glaucoma was found. The largest randomised human trial of oral sodium bicarbonate located (a different clinical question, kidney disease) found no significant treatment effect on the primary physical function outcome, no significant benefit on any secondary outcome, and more frequent adverse events in the bicarbonate arm (457 vs 400) , with the authors concluding oral sodium bicarbonate did not improve physical function or renal function, increased adverse events, and is unlikely to be cost-effective for that patient group .