Honokiol alleviated neurodegeneration by reducing oxidative stress and improving mitochondrial function in mutant SOD1 cellular and mouse models of amyotrophic lateral sclerosis
Open accessAbstract
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting both upper and lower motor neurons (MNs) with large unmet medical needs. Multiple pathological mechanisms are considered to contribute to the progression of ALS, including neuronal oxidative stress and mitochondrial dysfunction. Honokiol (HNK) has been reported to exert therapeutic effects in several neurologic disease models including ischemia stroke, Alzheimer's disease and Parkinson's disease. Here we found that honokiol also exhibited protective effects in ALS disease models both in vitro and in vivo. Honokiol improved the viability of NSC-34 motor neuron-like cells that expressed the mutant G93A SOD1 proteins (SOD1-G93A cells for short). Mechanistical studies revealed that honokiol alleviated cellular oxidative stress by enhancing glutathione (GSH) synthesis and activating the nuclear factor erythroid 2-related factor 2 (NRF2)-antioxidant response element (ARE) pathway. Also, honokiol improved both mitochondrial function and morphology via fine-tuning mitochondrial dynamics in SOD1-G93A cells. Importantly, honokiol extended the lifespan of the SOD1-G93A transgenic mice and improved the motor function. The improvement of antioxidant capacity and mitochondrial function was further confirmed in the spinal cord and gastrocnemius muscle in mice. Overall, honokiol showed promising preclinical potential as a multiple target drug for ALS treatment.
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Honokiol extends the lifespan of SOD1-G93A transgenic mice and improves their motor function and the viability of neuroblastoma/spinal cord NSC-34 hybrid cell lines and the morphology of mitochondria in SOD1-G93A cells.
“Honokiol has been shown to extend the lifespan of SOD1-G93A transgenic mice and improve their motor function and the viability of neuroblastoma/spinal cord NSC-34 hybrid cell lines and the morphology of mitochondria in SOD1-G93A cells (Zhou et al. 2023).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Zhou et al. 2023
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Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging
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- Authors
- Zhou, Y., Tang, J., Lan, J., Zhang, Y., Wang, H., Chen, Q., Kang, Y., Sun, Y., Feng, X., Wu, L., Jin, H., Chen, S., & Peng, Y.
- Affiliations
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Peking University (CN)
- Beijing Tsinghua Chang Gung Hospital (CN)
- Corresponding author
- Jin, Hongtao
- Chen, Shizhong
- Peng, Ying
- ORCID
- Venue
- Acta Pharmaceutica Sinica B
- Publisher
- Elsevier BV
- Published
- 2023-02
- Volume
- 13
- Issue
- 2
- Pages
- 577-597
- ISSN
- 2211-3835 (ISSN-L)
- PMC
- PMC9979194
- OpenAlex
- W4292551363
- Cited by
- 80
- References
- 91
- Citations by year
- 2026: 23 · 2025: 22 · 2024: 23 · 2023: 10 · 2022: 2
- FWCI
- 7.50
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Acta Pharmaceutica Sinica B (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81872855, 82073835)
- Chinese Academy of Meteorological Sciences (2021-I2M-1-028)
- National Key Research and Development Program of China (2019YFC1708901)
- Topics
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Health Sciences › Medicine › Rehabilitation › Magnolia and Illicium research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- honokiol, amyotrophic lateral sclerosis, oxidative stress, mitochondrial dysfunction, mitochondrial dynamics, Nrf2/ARE pathway, glutathione synthesis, motor neuron-like cells, transgenic mouse model, neuroprotection, lifespan extension, motor function
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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