Evidence map›Paper›PMID 42920030›Full record

ArticleMolecular neurobiology2026

β-Asarone Alleviates Post-stroke Neuroinflammation and Improves Mitochondrial Quality Via the BNIP3/BNIP3L-dependent Mitophagy Pathway.

Yujiao Wang, Daojun Xie, Yuhe Wang, Chengcheng Zhang, Zhuyue Chen

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In one paragraph

Article in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Yujiao WangThe First Clinical Medical College, Anhui University of Chinese Medicine, Hefei, 230036, Anhui, China.
Daojun XieEncephalopathy Center, The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, 230036, Anhui, China. daojunxie187@163.com.
Yuhe WangThe First Clinical Medical College, Anhui University of Chinese Medicine, Hefei, 230036, Anhui, China.
Chengcheng ZhangThe First Clinical Medical College, Anhui University of Chinese Medicine, Hefei, 230036, Anhui, China.
Zhuyue ChenThe First Clinical Medical College, Anhui University of Chinese Medicine, Hefei, 230036, Anhui, China.

Funding

National Natural Science Foundation of China No. 81874389
6 · The paper itself

Abstract

Ischemic stroke (IS) is a leading cause of death and disability worldwide, with mitophagy playing a central role in post-stroke neurological dysfunction. β-Asarone, a major bioactive component derived from the traditional herb Acorus tatarinowii, possesses antioxidant, anti-inflammatory, and neuroprotective properties. However, whether β-asarone ameliorates IS by regulating mitophagy and its underlying mechanisms remains unclear. This study aimed to investigate whether β-asarone exerts neuroprotective effects against IS by modulating BNIP3/BNIP3L-mediated mitophagy. A middle cerebral artery occlusion (MCAO) rat model and an oxygen-glucose deprivation/reperfusion (OGD/R) cell model were established. Neuroprotective effects were evaluated using neurological behavioral scores, 2,3,5-triphenyltetrazolium chloride (TTC) staining, hematoxylin-eosin (H&E) staining, and Nissl staining. Mitochondrial function was assessed by measuring reactive oxygen species (ROS) levels and mitochondrial membrane potential (MMP). Mitophagy was observed via transmission electron microscopy (TEM) and fluorescence microscopy. Western blot (WB) analysis was performed to detect BNIP3/BNIP3L pathway proteins. Results showed that β-asarone enhanced mitophagy, improved mitochondrial function, and alleviated post-stroke neuroinflammation. Conversely, the autophagy inhibitor 3-methyladenine (3-MA) impaired mitophagic function, exacerbating ischemia-induced brain injury and inflammation, while β-asarone treatment reversed these detrimental effects. In summary, β-asarone mitigates neuroinflammation and neuronal injury after IS, at least partly through promoting BNIP3/BNIP3L-mediated mitophagy, highlighting this pathway as a promising therapeutic target for IS.

Indexed as

AnisolesMembrane ProteinsMitochondriaMitochondrial ProteinsMitophagyNeuroinflammatory DiseasesStrokeAllylbenzene DerivativesAnimalsInfarction, Middle Cerebral ArteryMaleMembrane Potential, MitochondrialNeuroprotective AgentsProto-Oncogene ProteinsRatsRats, Sprague-DawleyAllylbenzene DerivativesAnisolesasaroneBNIP3L protein, ratBNIP3 protein, ratMembrane ProteinsMitochondrial ProteinsNeuroprotective AgentsProto-Oncogene ProteinsReactive Oxygen SpeciesBNIP3/BNIP3LIschemic strokeMitophagyNeuroinflammationβ-asarone

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.