1. Academic Validation
  2. Gastrodia protects HT22 cells from damage caused by oxygen glucose deprivation and reperfusion through inhibiting ferroptosis

Gastrodia protects HT22 cells from damage caused by oxygen glucose deprivation and reperfusion through inhibiting ferroptosis

  • Sci Rep. 2025 May 27;15(1):18470. doi: 10.1038/s41598-025-03404-x.
Dongyue Zhou 1 2 Zhixuan Huang 1 2 Jian Liu 1 2 Jinlong Tan 1 2 Hui Li 1 2 3 Yangwen Ai 4 5
Affiliations

Affiliations

  • 1 Jiangxi Province Key Laboratory of Traditional Chinese Medicine Pharmacology, Institute of Traditional Chinese Medicine Health Industry, China Academy of Chinese Medical Sciences, Nanchang, 330115, China.
  • 2 Jiangxi Health Industry Institute of Traditional Chinese Medicine, Nanchang, 330115, China.
  • 3 Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, 100700, China.
  • 4 Jiangxi Province Key Laboratory of Traditional Chinese Medicine Pharmacology, Institute of Traditional Chinese Medicine Health Industry, China Academy of Chinese Medical Sciences, Nanchang, 330115, China. 13260568664@163.com.
  • 5 Jiangxi Health Industry Institute of Traditional Chinese Medicine, Nanchang, 330115, China. 13260568664@163.com.
Abstract

Gastrodin (Gas) is a key active ingredients of Gastrodia elata Bl., with applications in treating cardiovascular and neurodegenerative conditions. However, the impact of Gas on neuronal damage caused by cerebral ischemia/reperfusion remains uncertain. A cell model of oxygen-glucose deprivation/reoxygenation (OGD/R) was established and the viability and Apoptosis of HT22 cells were measured using the CCK-8 assay and TUNEL staining. Different kits detected the levels of LDH, Fe2+ and MDA. The levels of ferroptosis-related genes and proteins were evaluated utilizing RT-qPCR and Western blotting. Following OGD/R, there was a decrease in HT22 cell viability and an increase in LDH level and Apoptosis rate. Gas (25µM) increased cell viability, decreased LDH, Fe2+, MDA and ACSL4 levels, up-regulated SLC7A11 and GPX4 and ameliorated OGD/R-induced Apoptosis (P < 0.01). Ferroptosis inducer Erastin (Era, 10µM) successfully induced Ferroptosis in HT22 cells, while Gas treatment attenuated the effect of Era. Era further promoted OGD/R-induced damage and Ferroptosis in HT22 cells, whereas Gas inhibited the effect of Era. In conclusion, Gas might provide protection against induced HT22 cell injury caused by OGD/R through inhibiting Ferroptosis, shows promising potential for clinical treatment of cerebral ischemia/reperfusion.

Keywords

Cerebral ischemia-reperfusion; Ferroptosis; Gastrodia; Neuronal damage; Oxygen-glucose deprivation/Reoxygenation.

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