Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Salidroside ameliorated high-altitude exposure induced retinal ganglion cell death by activating HIF-1α/BNIP3 signaling mediated mitophagy and inhibiting ferroptosis.
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Han Cong, Li Yuting, Qiao Junyi, Zheng Xingxing, Liu Qian, Wang Zhaoxiong, Yang Rui, Meng Yaping, Zhang Wenfang, Yang Yi
Аннотация
BACKGROUND: The mechanism of retinal ganglion cells (RGCs) injury induced by high-altitude hypobaric hypoxic conditions remains unclear, and there are no effective treatment methods available. Salidroside (SAL) is an antioxidant drug, but its protective effect on hypobaric hypoxia induced RGCs injury remains unclear.
OBJECTIVE: This study investigated the mechanisms underlying RGCs injury following acute high-altitude exposure (HAE) and the protective effects of SAL on RGCs, along with its underlying mechanisms.
METHODS: We established a high-altitude hypobaric hypoxia exposure mouse model to evaluate the protective effect of SAL on RGCs. RNA sequencing and bioinformatics analysis were used for injury mechanism prediction and pathway enrichment. Western blot (WB), immunofluorescence (IF), optical coherence tomography (OCT), scotopic threshold reaction (STR) and transmission electron microscopy (TEM) were used to elucidate the protective effect of SAL.
RESULTS: SAL treatment significantly improved the damage to RGCs caused by HAE. Mechanistically, SAL treatment significantly activated the mitophagy mediated by the HIF-1α/BNIP3 pathway, reduced the levels of Fe²⁺ and reactive oxygen species (ROS), and enhanced the expression of GPX4. Thus, it alleviated the ferroptosis caused by HAE in RGCs, maintaining the structure and function of RGCs.
CONCLUSION: SAL demonstrates significant promise as a therapeutic agent for RGCs damage by enhancing protective mitophagy, reducing oxidative stress responses, and inhibiting ferroptosis in RGCs caused by HAE.
OBJECTIVE: This study investigated the mechanisms underlying RGCs injury following acute high-altitude exposure (HAE) and the protective effects of SAL on RGCs, along with its underlying mechanisms.
METHODS: We established a high-altitude hypobaric hypoxia exposure mouse model to evaluate the protective effect of SAL on RGCs. RNA sequencing and bioinformatics analysis were used for injury mechanism prediction and pathway enrichment. Western blot (WB), immunofluorescence (IF), optical coherence tomography (OCT), scotopic threshold reaction (STR) and transmission electron microscopy (TEM) were used to elucidate the protective effect of SAL.
RESULTS: SAL treatment significantly improved the damage to RGCs caused by HAE. Mechanistically, SAL treatment significantly activated the mitophagy mediated by the HIF-1α/BNIP3 pathway, reduced the levels of Fe²⁺ and reactive oxygen species (ROS), and enhanced the expression of GPX4. Thus, it alleviated the ferroptosis caused by HAE in RGCs, maintaining the structure and function of RGCs.
CONCLUSION: SAL demonstrates significant promise as a therapeutic agent for RGCs damage by enhancing protective mitophagy, reducing oxidative stress responses, and inhibiting ferroptosis in RGCs caused by HAE.