# BlingLife®-Marigold Extract Alleviates Blue Light-Induced Retinal Mitochondria Oxidative Stress and Senescence by Activating NRF2/HO-1 Signaling

**Authors:** Zixiu Zhou, Sizhen Li, Qingsong Yang, Pengjie Zheng, Kexin Xie

PMC · DOI: 10.4014/jmb.2411.11037 · Journal of Microbiology and Biotechnology · 2025-02-24

## TL;DR

BlingLife®-marigold extract protects the retina from blue light damage by reducing oxidative stress and cell aging through a specific signaling pathway.

## Contribution

The study demonstrates that BLM protects retinal cells from blue light-induced damage via NRF2/HO-1 signaling activation.

## Key findings

- BlingLife®-marigold extract reduces blue light-induced retinal tissue and cell damage.
- BLM alleviates mitochondrial oxidative stress and cell senescence in retinal cells.
- NRF2/HO-1 signaling activation is crucial for BLM's protective effects.

## Abstract

Blue light poses a risk of retinal damage with excessive exposure. BlingLife®-marigold extract (BLM) is an alcohol extract of magrigold, which contains abundant lutein, zeaxanthin and meso-zeaxanthin. This study aimed to explore the role and potential mechanisms of BLM in blue light-induced retinal damage both in vivo and in vitro. Rats or human retinal pigment epithelial cell line (ARPE-19) were exposed to blue LED light with or without BLM treatment. The retinal morphology changes of rat were evaluated by H&E staining. Mitochondrial morphology was examined by using a transmission electron microscope. Besides, mitochondria oxidative stress was evaluated by detecting mitochondrial membrane potential, ROS, MDA and SOD levels. By measuring γH2AX expression and performing SA-β-galactosidase (gal) staining, cell senescence was assessed. Additionally, cell cycle was detected using flow cytometry. Western blot was employed to examine the expression of NRF2 and HO-1. Results indicated that BLM could protect against blue light-induced damage of rat retinal tissues and ARPE-19 cells, as evidenced by the improved histopathological changes, alleviated mitochondria oxidative stress and attenuated senescence of tissues and cells. More importantly, BLM activated NRF2/HO-1 signaling, and addition of NRF2 inhibitor ML385 significantly blocked the protective effects of BLM on ARPE-19 cells exposed to blue light. In conclusion, BLM can provide an effective protection against blue light-induced retinal damage at least partly by activating NRF2/HO-1 signaling, suggesting that BLM may be useful for the prevention of blue light-induced retinal injury.

## Linked entities

- **Genes:** GABPA (GA binding protein transcription factor subunit alpha) [NCBI Gene 2551], HMOX1 (heme oxygenase 1) [NCBI Gene 3162], H2AXA (Histone superfamily protein) [NCBI Gene 837409]
- **Chemicals:** lutein (PubChem CID 181579), zeaxanthin (PubChem CID 5280899), meso-zeaxanthin (PubChem CID 6442658), MDA (PubChem CID 1614)
- **Species:** Rattus norvegicus (taxon 10116), Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** Glb1 (galactosidase, beta 1) [NCBI Gene 316033], Nfe2l2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 83619], HMOX1 (heme oxygenase 1) [NCBI Gene 3162] {aka HMOX1D, HO-1, HSP32, bK286B10}, NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}
- **Diseases:** retinal injury (MESH:D012173), retinal damage (MESH:D012164)
- **Chemicals:** alcohol (MESH:D000438), BLM (-), MDA (MESH:D015104), H&amp;E (MESH:D006371), zeaxanthin (MESH:D065146), meso-zeaxanthin (MESH:C584722), lutein (MESH:D014975)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** Retinal — Rattus norvegicus (Rat), Transformed cell line (CVCL_8140), ARPE-19 — Homo sapiens (Human), Spontaneously immortalized cell line (CVCL_0145)

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11896799/full.md

## References

47 references — full list in the complete paper: https://tomesphere.com/paper/PMC11896799/full.md

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Source: https://tomesphere.com/paper/PMC11896799