Abstract | BACKGROUND: METHODS: The G93A-SOD1 transgenic mouse ALS model was used. Gintonin (50 or 100 mg/kg/day, p.o.) administration started from week seven. We performed histological analyses, immunoblot assays, and behavioral tests. RESULTS:
Gintonin extended mouse survival and relieved motor dysfunctions. Histological analyses of spinal cords revealed that gintonin increased the survival of motor neurons, expression of brain-derived neurotrophic factors, choline acetyltransferase, NeuN, and Nissl bodies compared with the vehicle control. Gintonin attenuated elevated spinal NAD(P) quinone oxidoreductase 1 expression and decreased oxidative stress-related ferritin, ionized calcium-binding adapter molecule 1-immunoreactive microglia, S100β-immunoreactive astrocyte, and Olig2-immunoreactive oligodendrocytes compared with the control vehicle. Interestingly, we found that the spinal LPA1 receptor level was decreased, whereas gintonin treatment restored decreased LPA1 receptor expression levels in the G93A-SOD1 transgenic mouse, thereby attenuating neurological symptoms and histological deficits. CONCLUSION:
Gintonin-mediated symptomatic improvements of ALS might be associated with the attenuations of neuronal loss and oxidative stress via the spinal LPA1 receptor regulations. The present results suggest that the spinal LPA1 receptor is engaged in ALS, and gintonin may be useful for relieving ALS symptoms.
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Authors | Sung Min Nam, Jong Hee Choi, Sun-Hye Choi, Hee-Jung Cho, Yeon-Jin Cho, Hyewhon Rhim, Hyoung-Chun Kim, Ik-Hyun Cho, Do-Geun Kim, Seung-Yeol Nah |
Journal | Journal of ginseng research
(J Ginseng Res)
Vol. 45
Issue 3
Pg. 390-400
(May 2021)
ISSN: 1226-8453 [Print] Korea (South) |
PMID | 34025132
(Publication Type: Journal Article)
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Copyright | © 2020 The Korean Society of Ginseng. Publishing services by Elsevier B.V. |