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Journals / Journal of Cellular Neuroscience and Oxidative Stress / 2026 / Volume: 18 Issue: 1

Glutathione Protects Human Retinal Pigment Epithelial Cells From Lipopolysaccharide-Induced Apoptosis and Oxidative Stress by Inhibiting The TRPM2 Channel

Anıl Selim Apa
Pages
1292–1301
Publication Date
2026-04-02
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AI Summary & Key Takeaways

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⚡ TL;DR(Too Long; Didn't Read)

In conclusion, GSH decreased the levels of LPS caused oxidative stress and apoptosis via suppressing TRPM2 in the ARPE-19.

📌 3 Key Takeaways

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Objective & Hypothesis:Gram-negative bacteria's outer membranes include lipopolysaccharides (LPS), which are a major contributor to inflammatory eye disorders.
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Key Findings & Data:In microglia, LPS-induced ROS stimulates transient receptor melastatin 2 (TRPM2), whereas glutathione (GSH) and N-(p-amylcinnamoyl) anthranilic acid (ACA) decrease their activation.
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Conclusion & Impact:In conclusion, GSH decreased the levels of LPS caused oxidative stress and apoptosis via suppressing TRPM2 in the ARPE-19.
🔬Design:Text.Serial.Journal
📍Scope:Comprehensive Sample
⚙️Variables:Apoptosis · ARPE-19 · lipopolysaccharide

Abstract

Gram-negative bacteria's outer membranes include lipopolysaccharides (LPS), which are a major contributor to inflammatory eye disorders. LPS cause apoptosis induction and produce reactive free radicals of oxygen (ROS). In microglia, LPS-induced ROS stimulates transient receptor melastatin 2 (TRPM2), whereas glutathione (GSH) and N-(p-amylcinnamoyl) anthranilic acid (ACA) decrease their activation. Anti-apoptotic and antioxidant properties of GSH through TRPM2 inhibition were not reported in human retinal pigment epithelial (ARPE-19) cells. Therefore, the modulator action of GSH on the TRPM2-mediated molecular oxidant and apoptotic pathways in ARPE-19 was investigated. Five main groups were generated in the ARPE-19: Control, GSH (10 mM for 2 h), LPS (1 μg/ml for 24 h), LPS + GSH, and LPS + ACA (25 μM for 30 min). The amounts of ROS, mitochondrial dysfunction, apoptosis, caspases (caspase-3, -8, and -9), and cytosolic free Ca2+ were increased by the LPS incubation, while the incubations of GSH and ACA reduced their amounts. The viable cell number and viability percentage were decreased by LPS, but their viability and number were increased by the incubations of GSH and ACA. In conclusion, GSH decreased the levels of LPS caused oxidative stress and apoptosis via suppressing TRPM2 in the ARPE-19. One possible treatment agent for oxidative retinal injury and inflammatory eye diseases induced by LPS could be the GSH treatment.

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Cite This Article

Apa, A. S. (2026). Glutathione Protects Human Retinal Pigment Epithelial Cells From Lipopolysaccharide-Induced Apoptosis and Oxidative Stress by Inhibiting The TRPM2 Channel. Journal of Cellular Neuroscience and Oxidative Stress, Volume: 18 Issue: 1, 1292–1301. https://doi.org/10.37212/jcnos.1872386

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References (11)

  1. Akpınar O, Nazıroğlu M. (2026). Glutathione and TRPM2 Inhibition Reduce Amyloid-Beta and Lipopolysaccharide-Induced Apoptosis, Inflammation, and Oxidative Stress in Microglial Cells. Cell Biol Int. 50(1):e70109. https://doi.org/10.1002/cbin.70109
  2. Ana RD, Gliszczyńska A, Sanchez-Lopez E, et al. (2023). Precision Medicines for Retinal Lipid Metabolism-Related Pathologies. J Pers Med. 13(4):635. https://doi.org/10.3390/jpm13040635
  3. Bardak H, Uğuz AC, Bardak Y, et al. (2023). Selenium Protects ARPE-19 and ACBRI 181 Cells against High Glucose-Induced Oxidative Stress. Molecules. 28(16):5961. https://doi.org/10.3390/molecules28165961
  4. Böhm EW, Buonfiglio F, Voigt AM, et al. (2023). Oxidative stress in the eye and its role in the pathophysiology of ocular diseases. Redox Biol. 68:102967. https://doi.org/10.1016/j.redox.2023.102967
  5. Cao F, Liang K, Tang WW, et al. (2024). Polyvinylpyrrolidone-curcumin nanoparticles with immune regulatory and metabolism regulatory effects for the treatment of experimental autoimmune uveitis. J Control Release. 372:551-570. https://doi.org/10.1016/j.jconrel.2024.06.047
  6. Chistyakov DV, Tiulina VV, Gancharova OS, et al. (2024) Targeting Oxidative Stress and Inflammation in the Eye: Insights from a New Model of Experimental Autoimmune Uveitis. Int J Mol Sci. 25(23):12910. https://doi.org/10.3390/ijms252312910
  7. Çınar R, Nazıroğlu M. (2023). TRPM2 Channel Inhibition Attenuates Amyloid β42-Induced Apoptosis and Oxidative Stress in the Hippocampus of Mice. Cell Mol Neurobiol. 43(3):1335-1353. https://doi.org/10.1007/s10571-022-01253-0
  8. Daldal H, Nazıroğlu M. (2022) Rituximab Attenuated Lipopolysaccharide-Induced Oxidative Cytotoxicity, Apoptosis, and Inflammation in the Human Retina Cells via Modulating the TRPM2 Signaling Pathways. Ocul Immunol Inflamm. 30(6):1315-1328. https://doi.org/10.1080/09273948.2022.2075400
  9. Ertuğrul A, Özkaya D, Nazıroğlu M. (2023) Curcumin attenuates hydroxychloroquine-mediated apoptosis and oxidative stress via the inhibition of TRPM2 channel signalling pathways in a retinal pigment epithelium cell line. Graefes Arch Clin Exp Ophthalmol. 261(10):2829-2844. https://doi.org/10.1007/s00417-023-06082-5
  10. Ertuğrul A. (2024). Lipopolysaccharide induces apoptosis and oxidative cytotoxicity through stimulation of the TRPV1 channel in retinal pigment epithelium cell line. J Cell Neurosci Oxid Stress. 16(3): 1229-1236. https://doi.org/10.37212/jcnos.1609591
  11. Huster D, Hjelle OP, Haug FM, Nagelhus EA, Reichelt W, Ottersen OP. (1998