ArticleNeurotoxicity research2022
Pratensein Mitigates Oxidative Stress and NLRP3 Inflammasome Activation in OGD/R-Injured HT22 Cells by Activating Nrf2-Anti-oxidant Signaling.
Article in Neurotoxicity research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Danggui Buxue Tang, a Traditional Chinese Herbal Formula, Potentiates Paclitaxel Efficacy in Non-Small-Cell Lung Cancer by Inducing Ferroptosis via the Nrf2/GPX4 Axis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Evaluation of anti-cancer and Immunomodulatory effects of Globe Thistle (Echinops Shakrokii S.A. Ahmad) extracts: an in vitro and in vivo study.Scientific reports · 2025Article
- Network pharmacological analysis, Mendelian randomization analysis and animal experimental reveal the mechanism of Wenxin Granules in inhibiting heart failure after myocardial infarction: apoptosis and inflammation.Frontiers in cardiovascular medicine · 2025Article
- Neuroprotective Effects of Metformin on Cerebral Ischemia-Reperfusion Injury: Modulation of JNK and p38 MAP Kinase Signaling Pathways.Cell biochemistry and biophysics · 2024Article
- Article
- Neurotrophic Natural Products.Progress in the chemistry of organic natural products · 2024Article
- Anti-apoptosis effect of traditional Chinese medicine in the treatment of cerebral ischemia-reperfusion injury.Apoptosis : an international journal on programmed cell death · 2023Review
- Anti-Inflammatory Effects of Flavonoids in Common Neurological Disorders Associated with Aging.International journal of molecular sciences · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The current investigation seeks to uncover the neuroprotective effects and mechanisms of pratensein (Pra) against cerebral ischemia-reperfusion (CI/R) injury. An in vitro model was created by subjecting HT22 cells to oxygen-glucose deprivation/reoxygenation (OGD/R) injury. Various doses of Pra were administered to HT22 cells during the process of OGD/R. Nrf2 knockdown was achieved by siRNA transfection. Pra antagonized OGD/R-triggered HT22 cell damage, as suggested by increased cell viability and reduced levels of LDH secretion. Additionally, Pra reversed OGD/R-induced cell apoptosis, oxidative stress, and inflammatory injury. Transfection of Nrf2 siRNA partially ameliorated the protective effects of Pra on the OGD/R-stimulated increase in cell apoptosis, oxidative stress, and inflammatory response in HT22 cells. Pra significantly inhibited the expression of nod-like-receptor-protein-3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, and cleaved caspase-1 protein in OGD/R-induced cells. Nrf2 knockdown reversed the benefits of Pra on NLRP3 inflammasome activation. Besides, Pra administration mitigated middle cerebral artery occlusion/reperfusion-induced cerebral infarction, neurological deficits, and neuronal apoptosis in vivo. This study found that Pra suppresses NLRP3 inflammasome activation through Nrf2 activation, resulting in reduced inflammatory responses and rates of apoptosis in OGD/R-stimulated HT22 cells, highlighting the neuroprotective properties of Pra in CI/R.
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