Journal
ACTA PHARMACOLOGICA SINICA
Volume 42, Issue 9, Pages 1409-1421Publisher
NATURE PUBL GROUP
DOI: 10.1038/s41401-020-00558-4
Keywords
Huntington’ s disease; ginsenoside Rg1; 3-nitropropionic acid; striatum; neuroprotective effects; MAPKs; NF-κ B
Funding
- National Natural Science Foundation of China [81773924, 81873026, 81973499]
- CAMS Innovation Fund for Medical Sciences (CIFMS) [2016-I2M-1-004]
- Drug Innovation Major Project [2018ZX09711001-003-005, 2018ZX09711001-009-013]
- Beijing Key Laboratory of New Drug Mechanisms and Pharmacological Evaluation Study [BZ0150]
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Ginsenoside Rg1 shows potential neuroprotective effects in a mouse model of Huntington's disease, alleviating weight loss, behavioral defects, and neuronal loss, possibly through inhibiting the activation of MAPKs and NF-kappa Beta signaling pathways. It may serve as a novel therapeutic option for Huntington's disease.
Huntington's disease (HD) is one of main neurodegenerative diseases, characterized by striatal atrophy, involuntary movements, and motor incoordination. Ginsenoside Rg1 (Rg1), an active ingredient in ginseng, possesses a variety of neuroprotective effects with low toxicity and side effects. In this study, we investigated the potential therapeutic effects of Rg1 in a mouse model of HD and explored the underlying mechanisms. HD was induced in mice by injection of 3-nitropropionic acid (3-NP, i.p.) for 4 days. From the first day of 3-NP injection, the mice were administered Rg1 (10, 20, 40 mg center dot kg(-1), p.o.) for 5 days. We showed that oral pretreatment with Rg1 alleviated 3-NP-induced body weight loss and behavioral defects. Furthermore, pretreatment with Rg1 ameliorated 3-NP-induced neuronal loss and ultrastructural morphological damage in the striatum. Moreover, pretreatment with Rg1 reduced 3-NP-induced apoptosis and inhibited the activation of microglia, inflammatory mediators in the striatum. We revealed that Rg1 exerted neuroprotective effects by suppressing 3-NP-induced activation of the MAPKs and NF-kappa Beta signaling pathways in the striatum. Thus, our results suggest that Rg1 exerts therapeutic effects on 3-NP-induced HD mouse model via suppressing MAPKs and NF-kappa Beta signaling pathways. Rg1 may be served as a novel therapeutic option for HD.
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