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자료유형
학술저널
저자정보
Yin Cao (Shanghai University of Traditional Chinese Medicine) Yingbo Yang (Shanghai University of Traditional Chinese Medicine) Hui Wu (Shanghai University of Traditional Chinese Medicine) Yi Lu (Shanghai University of Traditional Chinese Medicine) Shuang Wu (Shanghai University of Traditional Chinese Medicine) Lulu Liu (Shanghai University of Traditional Chinese Medicine) Changhong Wang (Shanghai University of Traditional Chinese Medicine) Fei Huang (Shanghai University of Traditional Chinese Medicine) Hailian Shi (Shanghai University of Traditional Chinese Medicine) Beibei Zhang (Shanghai University of Traditional Chinese Medicine) Xiaojun Wu (Shanghai University of Traditional Chinese Medicine) Zhengtao Wang (Shanghai University of Traditional Chinese Medicine)
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.44 No.3
발행연도
2020.5
수록면
442 - 452 (11page)

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Backgroud: Sleep deprivation (SD) impairs learning and memory by inhibiting hippocampal functioning at molecular and cellular levels. Abnormal autophagy and apoptosis are closely associated with neurodegeneration in the central nervous system. This study is aimed to explore the alleviative effect and the underlying molecular mechanism of stemeleaf saponins of Panax notoginseng (SLSP) on the abnormal neuronal autophagy and apoptosis in hippocampus of mice with impaired learning and memory induced by SD.
Methods: Mouse spatial learning and memory were assessed by Morris water maze test. Neuronal morphological changes were observed by Nissl staining. Autophagosome formation was examined by transmission electron microscopy, immunofluorescent staining, acridine orange staining, and transient transfection of the tf-LC3 plasmid. Apoptotic event was analyzed by flow cytometry after PI/annexin V staining. The expression or activation of autophagy and apoptosis-related proteins were detected by Western blotting assay.
Results: SLSP was shown to improve the spatial learning and memory of mice after SD for 48 h, accomanied with restrained excessive autophage and apoptosis, whereas enhanced activation of phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway in hippocampal neurons. Meanwhile, it improved the aberrant autophagy and apoptosis induced by rapamycin and re-activated phosphoinositide 3-kinase/Akt/mammalian target of rapamycin signaling transduction in HT-22 cells, a hippocampal neuronal cell line.
Conclusion: SLSP could alleviate cognitive impairment induced by SD, which was achieved probably through suppressing the abnormal autophagy and apoptosis of hippocampal neurons. The findings may contribute to the clinical application of SLSP in the prevention or therapy of neurological disorders associated with SD.

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ABSTRACT
1. Materials and methods
2. Results
3. Discussions
References

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UCI(KEPA) : I410-ECN-0101-2020-524-000843073