Lycii Fructus, a medicine food homology material, attenuates retinal damage in sodium iodate-induced retinal degeneration mice and inhibits oxidation-induced apoptosis of Müller cells via regulating Nrf2-HO1 signaling pathway.

[Display omitted] • Antioxidative effects of Lycii Fructus on Müller glia cells during AMD. • Mechanism of Lycii Fructus on relieving apoptosis of Müller cells was explored. • The aqueous extracts of Lycii Fructus protect Müller glia from oxidative injury. • Mechanism of Lycii Fructus protect Müller glia via Nrf2/HO-1 signaling pathway. Lycii Fructus (LF) is a medicinal-edible homology material frequently used for treating age-related macular degeneration (AMD) in Chinese medicine. Abundant of literatures verified the retina protection effect of LF on AMD-like animal models. However, previous studies on LF attenuating retinal damage mainly focused on its protection effect on pigment epithelial cells and optic ganglion cells while few reports on Müller cells. In the current study, we found that LF extracts attenuated oxidation damages and inhibited cell apoptosis of retina on a mouse retinal injury model induced by sodium iodate. LF extracts also increased expressions of Müller cell biomarker glutamine synthetase of eyeballs of model mice, which indicated that LF extract protected Müller cell from oxidation injury induced by sodium iodate. In Müller cell MIO-M1 cultures, LF also significantly inhibited cellular apoptosis induced by NaIO 3 by regulating Nrf2/HO-1 signaling pathway and the aqueous extracts exerted better active tendency than ethanol extracts. These data implied that the antioxidant effect of LF on protecting Müller cell might contribute to its retina repair function, thereby providing more scientific evidences for the development of LF as an alternative therapy or preventive measures for AMD. [ABSTRACT FROM AUTHOR]