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CC BY 4.0 · Chinese medicine and natural products 2025; 05(04): e235-e241
DOI: 10.1055/s-0045-1814092
Original Article

Senkyunolide A Attenuates OGD/R-Induced HT22 Cell Injury by Inhibiting Oxidative Stress and Apoptosis

Authors

  • Roujia Guo

    1   School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, Henan, China

  • Yufang Zhao

    1   School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, Henan, China

  • Zhouli Yue

    1   School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, Henan, China

  • Yucheng Li

    2   Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, Henan, China

Funding This study was supported by the National Natural Science Foundation of China (82574916) and the Joint Fund of Henan Province (232301420018).
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Abstract

Objective

This study aimed to investigate the protective effect and mechanism of Senkyunolide A (SenA) on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury in mouse hippocampal neuronal HT22 cells, providing experimental evidence for elucidating the application of SenA in the prevention and treatment of cerebral ischemia–reperfusion injury.

Methods

An HT22 cell injury model was established using the OGD/R method and divided into the Control group, Model (OGD/R) group, Edaravone (EDA) group (OGD/R + EDA), and SenA group (OGD/R + SenA). Cell viability was detected by Cell counting kit-8 (CCK-8) assay; live and dead cells were observed by Calcein AM/PI cell viability assay kit (Calcein-AM/PI) double staining; intracellular reactive oxygen species (ROS) levels were measured using the H2DCFDA (DCFH-DA) fluorescent probe; levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) were determined by biochemical kits; apoptosis rate was detected by flow cytometry; protein expression levels of Bcl-2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), and Cysteine-dependent aspartate-specific protease-3 (Caspase-3) were measured by Western blot.

Results

Compared with the Control group, the OGD/R group showed significantly reduced cell viability (p < 0.001), increased proportions of dead cells, ROS and MDA levels, and apoptosis rate (p < 0.001), decreased SOD activity and GSH levels (p < 0.05; p < 0.001), significantly upregulated protein expression of Bax and Caspase-3 (p < 0.01; p < 0.001), and downregulated Bcl-2 expression (p < 0.001). Compared with the OGD/R group, both SenA and EDA significantly increased cell viability (p < 0.001), reduced the proportion of dead cells, ROS and MDA levels, and apoptosis rate (p < 0.001), upregulated SOD activity and GSH levels (p < 0.01; p < 0.001), downregulated protein expression of Bax and Caspase-3 (p < 0.01; p < 0.001), and upregulated Bcl-2 expression (p < 0.001).

Conclusion

SenA can alleviate OGD/R-induced neuronal injury by mitigating oxidative stress and inhibiting cell apoptosis. This study provides modern experimental evidence for the traditional theory of Chuanxiong in “promoting blood circulation, removing blood stasis, and unblocking brain collaterals,” and offers new insights for the prevention and treatment of ischemia–reperfusion brain injury with traditional Chinese medicine.

Keywords

ischemic stroke - senkyunolide A - oxygen-glucose deprivation/reoxygenation - oxidative stress - apoptosis

CRediT Authorship Contribution Statement

Roujia Guo: Methodology, investigation, visualization, and writing original draft. Yufang Zhao: Investigation, and data curation. Zhouli Yue: Conceptualization, investigation, formal analysis, and visualization. Yucheng Li: Project administration, supervision, conceptualization, funding acquisition, and writing-review & editing.




Publication History

Received: 21 July 2025

Accepted: 17 September 2025

Article published online:
30 December 2025

© 2025. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

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