Neuroprotective effect of chrysin in PTZ-induced neurotoxicity in SH-SY5Ycells: Role of TRPM2 channel


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Ahlatcı A., Yıldızhan K., Tülüce Y., Bektaş M.

8th World Congress of Oxidative Stress, Calcium Signaling and TRP Channels, Isparta, Turkey, 5 - 08 September 2023, vol.15, no.3, pp.43

  • Publication Type: Conference Paper / Summary Text
  • Volume: 15
  • City: Isparta
  • Country: Turkey
  • Page Numbers: pp.43
  • Van Yüzüncü Yıl University Affiliated: Yes

Abstract

Chrysin (CHR) is a promising phytochemical that belongs to the flavonoid class based on its chemical structure. Experimental studies have shown that CHR has various biological effects, including anti-cancer, antioxidant, hepatoprotective, antiviral, neuroprotective, and anti-anxiety properties (Stompor-Goracy et al., 2021). In recent years, transient receptor potential (TRP) ion channels have been reported to play an important role in the pathology of neurological disorders (Yıldızhan et al., 2020). TRP Melastatin 2 (TRPM2) are oxidative stress-dependent active cation channels within the TRP superfamily and are widely expressed, including in the brain, immune system, endocrine cells, and endothelium. This study examined the protective role of CHR against neurotoxicity induced via the TRPM2 channel in SH-SY5Y cells exposed to pentylenetetrazol (PTZ). For the study, control, CHR (50 μM, 24 h) (Darendelioglu 2020), PTZ (30 μM, 24 h) (Ahlatci et al., 2022), and PTZ+CHR (CHR treatment was administered 30 minutes before PTZ incubation) groups were formed from SH-SY5Y cells. The study measured the levels of MDA, GSH, ROS, PARP-1, and TRPM2 channels in the cells using ELISA kits. The study found that administering PTZ to the human neuroblastoma cell line SH-SY5Y resulted in neurotoxicity demonstrated by decreased GSH levels and increased MDA, ROS, PARP-1, and TRPM2 (p < 0.05). In SH-SY5Y cells treated with CHR prior to PTZ incubation, levels of MDA, ROS, PARP-1, and TRPM2 decreased, and levels of GSH increased, compared to the PTZ group (p < 0.05). Consequently, we found that CHR treatment may effectively reduce PTZ-induced neurotoxicity in SH-SY5Y cells by inhibiting the activation of TRPM2 channels.