胃泌素在体外和体内氧化应激诱导的老年性黄斑变性中的保护作用

IF 6 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Medicine Pub Date : 2024-09-09 DOI:10.1186/s10020-024-00920-w

Jie Bai, Yanqing Wang, Yanze Li, Yan Liu, Shan Wang

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引用次数: 0

摘要

人类视网膜色素上皮（RPE）细胞的氧化损伤是老年性黄斑变性（AMD）的主要病因，在我们之前的研究中，我们发现胃泌素对人类晶状体上皮（HLE）细胞具有抗氧化作用，然而，利用胃泌素治疗视网膜退行性疾病的研究却鲜有报道。本文评估了胃泌素对防止过氧化氢（H2O2）诱导的 ARPE-19 细胞氧化应激的作用及其机制。我们观察到，预处理胃泌素能保护ARPE-19细胞免受H2O2诱导的细胞氧化损伤和凋亡反应。此外，通过向小鼠尾静脉注射碘酸钠（NaIO3），建立了氧化应激诱导的小鼠老年性视网膜病变模型。首次报道了胃泌素对 H2O2 诱导的 RPE 细胞的保护作用。使用胃泌素可抑制 NaIO3 诱导的体内视网膜细胞凋亡。结合体外和体内实验，结果全面可靠。

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Protective effect of ghrelin in oxidative stress-induced age-related macular degeneration in vitro and in vivo

Oxidative damage to human retinal pigment epithelial (RPE) cells is the main cause of age-related macular degeneration (AMD), in our previous work, we showed that ghrelin has an antioxidative effect on human lens epithelium (HLE) cells, however, the studies of using ghrelin in treating the degenerative diseases of the retina have rarely been reported. In this article, we assessed the effect of ghrelin on preventing oxidative stress induced by hydrogen peroxide (H2O2) in ARPE-19 cells and its mechanism. We observed that pretreatment with ghrelin protected ARPE-19 cells from H2O2-induced cell oxidative injuries and apoptosis responses. Furthermore, an oxidative stress-induced mouse model of AMD was established via injection of sodium iodate (NaIO3) to tail veins, and treatment with ghrelin preserved retinal function, and protected photoreceptors. The first to report ghrelin’ protective effect on H2O2-induced RPE cells. Treatment with ghrelin inhibits NaIO3-induced retinal cell apoptosis in vivo. Combined with in vitro and in vivo experiments, the results are comprehensive and reliable.

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来源期刊

Molecular Medicine 医学-生化与分子生物学

CiteScore

8.60

自引率

0.00%

发文量

137

审稿时长

1 months

期刊介绍： Molecular Medicine is an open access journal that focuses on publishing recent findings related to disease pathogenesis at the molecular or physiological level. These insights can potentially contribute to the development of specific tools for disease diagnosis, treatment, or prevention. The journal considers manuscripts that present material pertinent to the genetic, molecular, or cellular underpinnings of critical physiological or disease processes. Submissions to Molecular Medicine are expected to elucidate the broader implications of the research findings for human disease and medicine in a manner that is accessible to a wide audience.