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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2021.5
- 수록면
- 390 - 400 (11page)
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초록· 키워드
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Background: We recently showed that gintonin, an active ginseng ingredient, exhibits antibrain neurodegenerative disease effects including multiple target mechanisms such as antioxidative stress and antiinflammation via the lysophosphatidic acid (LPA) receptors. Amyotrophic lateral sclerosis (ALS) is a spinal disease characterized by neurodegenerative changes in motor neurons with subsequent skeletal muscle paralysis and death. However, pathophysiological mechanisms of ALS are still elusive, and therapeutic drugs have not yet been developed. We investigate the putative alleviating effects of gintonin in ALS.
Methods: The G93A-SOD1 transgenic mouse ALS model was used. Gintonin (50 or 100 ㎎/㎏/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, S100b-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.
Methods: The G93A-SOD1 transgenic mouse ALS model was used. Gintonin (50 or 100 ㎎/㎏/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, S100b-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.
목차
ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
5. Conclusion
References
참고문헌 (43)
참고문헌 신청
Bucchia M / 2015 / Therapeutic development in amyotrophic lateral sclerosis / Clin Ther 37:668~680
Pasinelli P / 2006 / Molecular biology of amyotrophic lateral sclerosis : insights from genetics / Nat Rev Neurosci 7:710~723
Rosen DR / 1993 / Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis / Nature 362:59~62
Boillée S / 2008 / Revisiting oxidative damage in ALS : microglia, Nox, and mutant SOD1 / J Clin Invest 118:474~478
Bordt EA / 2014 / NADPH oxidase-and mitochondria-derived reactive oxygen species in proinflammatory microglial activation : a bipartisan affair / Free Radic Biol Med 76:34~46
Pasinelli P / 2006 / Molecular biology of amyotrophic lateral sclerosis : insights from genetics / Nat Rev Neurosci 7:710~723
Rosen DR / 1993 / Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis / Nature 362:59~62
Boillée S / 2008 / Revisiting oxidative damage in ALS : microglia, Nox, and mutant SOD1 / J Clin Invest 118:474~478
Bordt EA / 2014 / NADPH oxidase-and mitochondria-derived reactive oxygen species in proinflammatory microglial activation : a bipartisan affair / Free Radic Biol Med 76:34~46
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