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<p>This study evaluates the protective effects of Sanggenol L (SL), a flavonoid from Morus alba root bark, against retinal ischemia/reperfusion injury (RI/RI)-induced retinal ganglion cell (RGC) damage in an oxygen and glucose deprivation/reoxygenation (OGD/R) model. SL (5–30 µM) significantly improved R28 cell viability, upregulated anti-apoptotic gene expression, and restored antioxidant status. Furthermore, SL reduced pro-inflammatory cytokines, lactate dehydrogenase (LDH), reactive oxygen species (ROS), malondialdehyde (MDA), and pro-apoptotic gene expression in a dose-dependent manner. SL treatment (30 µM) activated the PI3K/Akt/Nrf2 signaling pathway, providing neuroprotection. In silico molecular docking revealed strong binding affinities between SL and key inflammatory and apoptotic markers (cyt-c, cleaved caspase-9, cleaved PARP, Nrf2, PI3K, Akt), suggesting its mechanism of action. These results indicate that SL may serve as a potential therapeutic agent for glaucomatous neurodegeneration by targeting oxidative stress, inflammation, and apoptosis via the PI3K/Akt/Nrf2 pathway.</p>

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Sanggenol L attenuates inflammation and apoptosis via Nrf2/PI3K/Akt signaling in retinal ganglion cells: an in vitro and in silico study on OGD/R-induced retinal ischemia–reperfusion injury

  • 期刊论文

  • 发表日期：

    2026年5月25日

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  • Bing Xu,
  • Periyannan Velu,
  • June Fan,
  • Vijayapoopathi Singaravel

摘要

This study evaluates the protective effects of Sanggenol L (SL), a flavonoid from Morus alba root bark, against retinal ischemia/reperfusion injury (RI/RI)-induced retinal ganglion cell (RGC) damage in an oxygen and glucose deprivation/reoxygenation (OGD/R) model. SL (5–30 µM) significantly improved R28 cell viability, upregulated anti-apoptotic gene expression, and restored antioxidant status. Furthermore, SL reduced pro-inflammatory cytokines, lactate dehydrogenase (LDH), reactive oxygen species (ROS), malondialdehyde (MDA), and pro-apoptotic gene expression in a dose-dependent manner. SL treatment (30 µM) activated the PI3K/Akt/Nrf2 signaling pathway, providing neuroprotection. In silico molecular docking revealed strong binding affinities between SL and key inflammatory and apoptotic markers (cyt-c, cleaved caspase-9, cleaved PARP, Nrf2, PI3K, Akt), suggesting its mechanism of action. These results indicate that SL may serve as a potential therapeutic agent for glaucomatous neurodegeneration by targeting oxidative stress, inflammation, and apoptosis via the PI3K/Akt/Nrf2 pathway.