Protective effects of Gentiana macrophylla Pall. against blue light-induced retinal injury associated with of antioxidant defense, mitochondrial dysfunction, apoptosis, and inflammatory responses
Abstract
BackgroundThis study aimed to investigate the protective effects of the methanol extract of Gentiana macrophylla Pall. (MEG) against acute blue light (BL)-induced retinal injury and to characterize the associated changes in antioxidant defense, mitochondrial status, apoptosis, and inflammatory responses.MethodsThe phytochemical profile of MEG was characterized using high-performance liquid chromatograph (HPLC), and its chemical radical-scavenging properties were evaluated using cell-free assays. The protective effects of MEG were investigated in A2E/BL-exposed ARPE-19 cells and BL-exposed BALB/c mice following MEG pretreatment. Oxidative stress, mitochondrial membrane potential and morphology, apoptosis- and inflammation-related markers, and retinal histopathological changes were evaluated using biochemical, molecular, imaging, and histological analyses.ResultsEighteen metabolites were tentatively annotated in MEG. MEG pretreatment significantly reduced intracellular reactive oxygen species (ROS) by 31% and 48% at 100 and 200 μg/mL, respectively, compared with the Vehicle-treated group (p < 0.05). MEG also reduced nitric oxide production and was associated with increased superoxide dismutase expression and Nrf2 phosphorylation in age-related macular degeneration (AMD)-mimicking cells. MEG attenuated mitochondrial structural abnormalities, and was accompanied by changes in mitochondrial biogenesis-related gene expression. Consistently, TMRM fluorescence was increased by 20%–85% following MEG pretreatment (p < 0.05), indicating attenuation of mitochondrial membrane depolarization. In addition, MEG attenuated apoptosis-associated alterations and inflammatory responses involving NF-κB, iNOS, COX-2, and TNF-α. Consistent protective responses were observed in vivo, where MEG pretreatment attenuated BL-induced retinal thinning, increasing whole retinal thickness from 132 ± 4 μm to 187 ± 16 μm at 200 mg/kg (p < 0.05), together with attenuation of associated molecular alterations. Ursolic acid, a selected metabolite detected in MEG, reproduced several cellular responses observed following MEG treatment.ConclusionMEG pretreatment attenuated acute BL-induced retinal injury, accompanied by changes in antioxidant defense-related markers, mitochondrial status, apoptosis-associated alterations, and inflammatory responses. These findings provide experimental evidence supporting further investigation of MEG as a potential protective botanical preparation against oxidative and phototoxic retinal injury.
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BibTeX
@article{wang2026protective,
title = {{Protective effects of Gentiana macrophylla Pall. against blue light-induced retinal injury associated with of antioxidant defense, mitochondrial dysfunction, apoptosis, and inflammatory responses}},
author = {Su Ha Wang and Ji Eun Kim and Hee Jin Song and Ayun Seol and Su Jeong Lim and Ye Eun Ryu and Ye Ryeong Kim and So Hae Park and Gantuya Batdelger and Soo-Yong Kim and Dae Youn Hwang},
journal = {Frontiers in Pharmacology},
year = {2026},
month = nov,
doi = {10.3389/fphar.2026.1958175},
url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1958175},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Protective effects of Gentiana macrophylla Pall. against blue light-induced retinal injury associated with of antioxidant defense, mitochondrial dysfunction, apoptosis, and inflammatory responses
AU - Su Ha Wang
AU - Ji Eun Kim
AU - Hee Jin Song
AU - Ayun Seol
AU - Su Jeong Lim
AU - Ye Eun Ryu
AU - Ye Ryeong Kim
AU - So Hae Park
AU - Gantuya Batdelger
AU - Soo-Yong Kim
AU - Dae Youn Hwang
PY - 2026
DA - 2026/11/05
JO - Frontiers in Pharmacology
DO - 10.3389/fphar.2026.1958175
UR - https://www.frontiersin.org/articles/10.3389/fphar.2026.1958175
AB - BackgroundThis study aimed to investigate the protective effects of the methanol extract of Gentiana macrophylla Pall. (MEG) against acute blue light (BL)-induced retinal injury and to characterize the associated changes in antioxidant defense, mitochondrial status, apoptosis, and inflammatory responses.MethodsThe phytochemical profile of MEG was characterized using high-performance liquid chromatograph (HPLC), and its chemical radical-scavenging properties were evaluated using cell-free assays. The protective effects of MEG were investigated in A2E/BL-exposed ARPE-19 cells and BL-exposed BALB/c mice following MEG pretreatment. Oxidative stress, mitochondrial membrane potential and morphology, apoptosis- and inflammation-related markers, and retinal histopathological changes were evaluated using biochemical, molecular, imaging, and histological analyses.ResultsEighteen metabolites were tentatively annotated in MEG. MEG pretreatment significantly reduced intracellular reactive oxygen species (ROS) by 31% and 48% at 100 and 200 μg/mL, respectively, compared with the Vehicle-treated group (p < 0.05). MEG also reduced nitric oxide production and was associated with increased superoxide dismutase expression and Nrf2 phosphorylation in age-related macular degeneration (AMD)-mimicking cells. MEG attenuated mitochondrial structural abnormalities, and was accompanied by changes in mitochondrial biogenesis-related gene expression. Consistently, TMRM fluorescence was increased by 20%–85% following MEG pretreatment (p < 0.05), indicating attenuation of mitochondrial membrane depolarization. In addition, MEG attenuated apoptosis-associated alterations and inflammatory responses involving NF-κB, iNOS, COX-2, and TNF-α. Consistent protective responses were observed in vivo, where MEG pretreatment attenuated BL-induced retinal thinning, increasing whole retinal thickness from 132 ± 4 μm to 187 ± 16 μm at 200 mg/kg (p < 0.05), together with attenuation of associated molecular alterations. Ursolic acid, a selected metabolite detected in MEG, reproduced several cellular responses observed following MEG treatment.ConclusionMEG pretreatment attenuated acute BL-induced retinal injury, accompanied by changes in antioxidant defense-related markers, mitochondrial status, apoptosis-associated alterations, and inflammatory responses. These findings provide experimental evidence supporting further investigation of MEG as a potential protective botanical preparation against oxidative and phototoxic retinal injury.
SN - 1663-9812
ER -