Ocular neurodegeneration comprises a group of complex processes that severely affect visual function and is recognized as a key pathogenetic process in a variety of blinding ocular diseases, including glaucoma, diabetic retinopathy, age-related macular degeneration and retinitis pigmentosa. Although these diseases have different etiologies and mechanisms, apoptosis, metabolic disorders and oxidative damage are common features shared by all of them. Increasing evidence indicates that gut microbiota regulates distant organs by engaging in the host's neural, endocrine, immune regulation and even intercellular information. However，in ocular degenerative diseases, specific gut microbiota and their metabolites play an important role in ocular degenerative diseases. Therefore, in this review, we summarize the pathways through which the "gut-eye axis" functions and the mechanisms by which it interacts with ocular degenerative diseases, as well as the alterations in gut microbiota profiles observed in several common ocular degenerative diseases. Additionally, we provide an outlook on the clinical application of the "gut-eye axis", including its potential diagnostic, therapeutic, and adjunctive therapies.

Ischemic stroke is characterized by cute onset and high mortality. The suppression of neuroinflammation is crucial in the treatment of ischemic stroke. Exosomes derived from mesenchymal stem cell (MSC) have attracted extensive research attention due to their wide origin, small size, and containing large number of active components. Recent studies have shown that MSC-derived exosomes can inhibit the proinflammatory activity of microglia and astrocytes and stimulate their neuroprotective activity; also can inhibit neuroinflammation by regulating immune cells and inflammatory mediators. This article reviews the roles and related mechanism of MSC-derived exosomes in neuroinflammation after ischemic stroke, hoping to provide ideas and references for the development of a novel approach for the treatment of ischemic stroke diseases.