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        Stem-leaf saponins from Panax notoginseng counteract aberrant autophagy and apoptosis in hippocampal neurons of mice with cognitive impairment induced by sleep deprivation

        Yin Cao,Yingbo Yang,Hui Wu,Yi Lu,Shuang Wu,Lulu Liu,Changhong Wang,Fei Huang,Hailian Shi,Beibei Zhang,Xiaojun Wu,Zhengtao Wang 고려인삼학회 2020 Journal of Ginseng Research Vol.44 No.3

        Backgroud: Sleep deprivation (SD) impairs learning and memory by inhibiting hippocampal functioningat molecular and cellular levels. Abnormal autophagy and apoptosis are closely associated with neurodegenerationin the central nervous system. This study is aimed to explore the alleviative effect and theunderlying molecular mechanism of stemeleaf saponins of Panax notoginseng (SLSP) on the abnormalneuronal autophagy and apoptosis in hippocampus of mice with impaired learning and memory inducedby SD. Methods: Mouse spatial learning and memory were assessed by Morris water maze test. Neuronalmorphological changes were observed by Nissl staining. Autophagosome formation was examined bytransmission electron microscopy, immunofluorescent staining, acridine orange staining, and transienttransfection of the tf-LC3 plasmid. Apoptotic event was analyzed by flow cytometry after PI/annexin Vstaining. The expression or activation of autophagy and apoptosis-related proteins were detected byWestern 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 phosphoinositide3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway in hippocampalneurons. Meanwhile, it improved the aberrant autophagy and apoptosis induced by rapamycinand re-activated phosphoinositide 3-kinase/Akt/mammalian target of rapamycin signaling transductionin HT-22 cells, a hippocampal neuronal cell line. Conclusion: SLSP could alleviate cognitive impairment induced by SD, which was achieved probablythrough suppressing the abnormal autophagy and apoptosis of hippocampal neurons. The findings maycontribute to the clinical application of SLSP in the prevention or therapy of neurological disordersassociated with SD.

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        Stem-leaf saponins from Panax notoginseng counteract aberrant autophagy and apoptosis in hippocampal neurons of mice with cognitive impairment induced by sleep deprivation

        Cao, Yin,Yang, Yingbo,Wu, Hui,Lu, Yi,Wu, Shuang,Liu, Lulu,Wang, Changhong,Huang, Fei,Shi, Hailian,Zhang, Beibei,Wu, Xiaojun,Wang, Zhengtao The Korean Society of Ginseng 2020 Journal of Ginseng Research Vol.44 No.3

        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 stem-leaf 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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