Lycium barbarum polysaccharide protects against oxygen glucose deprivation/reoxygenation-induced apoptosis and autophagic cell death via the PI3K/Akt/mTOR signaling pathway in primary cultured hippocampal neurons

Yu, Yang; Wu, Xiuquan; Pu, Jingnan; Luo, Peng; Ma, Wenke; Wang, Jiu; Wei, Jialiang; Wang, Yuanxin; Fei, Zhou

doi:10.1016/j.bbrc.2017.11.165

Cited by 61 publications

(45 citation statements)

References 33 publications

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“…Shi et al displayed LBPs enhanced cell viability in OGD-treated primary cultured cortical neurons [23]. In addition, Yu et al have detected the functions of LBPs in OGD/reperfusion-treated primary hippocampal neuron cells and the results revealed the pretreatment of LBPs obviously enhanced cell viability, reduced cell apoptosis, cell autophagy and ROS [24]. Together with these findings, our results suggested LBPs could remit OGD-induced damage in PC-12 cells.…”

Section: Discussionsupporting

confidence: 80%

RETRACTED ARTICLE: Lycium barbarum polysaccharide alleviates oxygen glucose deprivation-induced PC-12 cells damage by up-regulating miR-24

Song

Lin

Zhu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Objective: This research was aimed to detect the functions of Lycium barbarum polysaccharides (LBPs) on oxygen and glucose deprivation (OGD) injury and potential mechanisms at PC-12 cells. Methods: CCK-8, flow cytometry and reactive oxygen species (ROS) assays were used to detect OGD, LBPs and miR-24 effects on cell viability, apoptosis, and oxidative stress. MiR-24 was transfected and texted by transfection and qRT-PCR. Moreover, the related-protein levels of apoptosis, autophagy and pathways were tested by Western blotting. Results: LBPs significantly enhanced cell viability , inhibited cell apoptosis, autophagy and ROS level in OGD injury. In addition, miR-24 expression was declined in OGD-treated cells, while it was elevated when added LBPs. The preventive effects of LBPs on PC-12 cell damage induced by OGD were reversed by down-regulating miR-24. Furthermore, miR-24 inhibitor declined LBPs-induced change in Wnt/b-catenin and JAK1/STAT3 pathways in OGD-injuried cells. Conclusions: LBPs exhibited preventive effects via up-regulating miR-122 and activating Wnt/b-catenin and JAK1/STAT3 pathways in OGD-induced PC-12 cells. ARTICLE HISTORY

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Section: Discussionsupporting

confidence: 80%

RETRACTED ARTICLE: Lycium barbarum polysaccharide alleviates oxygen glucose deprivation-induced PC-12 cells damage by up-regulating miR-24

Song

Lin

Zhu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…A number of reports have indicated that abnormal autophagy promotes the activation of apoptotic cascades, ultimately leading to neuronal death, which can be alleviated by autophagy inhibitors, such as 3-methyladenine (3-MA) and DL-3-n-butylphthalide (Sun et al, 2018;Yu et al, 2018;Zhang, Wang, Li, Huang, & Sun, 2014). A number of reports have indicated that abnormal autophagy promotes the activation of apoptotic cascades, ultimately leading to neuronal death, which can be alleviated by autophagy inhibitors, such as 3-methyladenine (3-MA) and DL-3-n-butylphthalide (Sun et al, 2018;Yu et al, 2018;Zhang, Wang, Li, Huang, & Sun, 2014).…”

Section: Introductionmentioning

confidence: 99%

“…Autophagy is closely associated with apoptosis in neuronal cells. A number of reports have indicated that abnormal autophagy promotes the activation of apoptotic cascades, ultimately leading to neuronal death, which can be alleviated by autophagy inhibitors, such as 3-methyladenine (3-MA) and DL-3-n-butylphthalide (Sun et al, 2018;Yu et al, 2018;Zhang, Wang, Li, Huang, & Sun, 2014). However, contradictory results also demonstrated that autophagy is likely to play a protective role in neuronal injury, and activation of autophagy inhibits neuronal apoptosis in neurodegenerative disorders Qiao et al, 2018;Wu et al, 2018;Xiao et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Modafinil protects hippocampal neurons by suppressing excessive autophagy and apoptosis in mice with sleep deprivation

Cao

Liu

et al. 2019

British J Pharmacology

113

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Background and Purpose: Sleep deprivation compromises learning and memory in both humans and animals, and can be reversed by administration of modafinil, a drug promoting wakefulness. Dysfunctional autophagy increases activation of apoptotic cascades, ultimately leading to increased neuronal death, which can be alleviated by autophagy inhibitors. This study aimed to investigate the alleviative effect and mechanism of modafinil on the excessive autophagy occurring in the hippocampus of mice with deficiency of learning and memory induced by sleep deprivation. Experimental Approach: The Morris water maze was used to assess the effects of modafinil on male C57BL/6Slac mice after 48-hr sleep deprivation. The HT-22 hippocampal neuronal cell line was also used. Nissl staining, transmission electron microscope, immunofluorescence, Western blot, transient transfection, and autophagy inducer were used to study the effect and mechanism of modafinil on hippocampal neurons with excessive autophagy and apoptosis. Key Results: Modafinil improved learning and memory in sleep-deprived mice, associated with the inhibition of excessive autophage and apoptosis and an enhanced activation of the PI3K/Akt/mTOR/P70S6K signalling pathway in hippocampal neurons. These effects of modafinil were abolished by rapamycin. In addition, modafinil suppressed the aberrant autophagy and apoptosis induced by rapamycin and reactivated PI3K/Akt/mTOR/P70S6K signals in HT-22 cells. Conclusions and Implications: These results suggested that modafinil alleviated impaired learning and memory of sleep-deprived mice potentially by suppressing excessive autophagy and apoptosis of hippocampal neurons. This novel mechanism may add to our knowledge of modafinil in the clinical treatment of impaired memory caused by sleep loss.Abbreviations: DG, dentate gyrus; 3-MA, 3-methyladenine; mTOR, mammalian target of rapamycin; MWM, Morris water maze; p62, ubiquitin-binding protein p62 or sequestosome-1; P70S6K, ribosomal protein S6 kinase; p-Akt, phosphorylated PKB; p-P70S6K, phosphorylated ribosomal protein S6 kinase; p-PI3K, phosphorylated PI3K

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“…In recent years, autophagy is emerging as a new strategy for cancer prevention and treatment and has been proven to be closely related to tumor cell growth and proliferation, as well as malignant metastasis [13]. In addition, studies have shown that LBP can protect against cell injury by regulating autophagy and apoptosis [14][15][16][17][18][19]. The study was aimed at investigating the regulatory effect of LBP on autophagy, and its effect on the proliferation, apoptosis of squamous cells The occurrence of cancer is often associated with abnormal proliferation and apoptosis resistance of tumor cells.…”

Section: Discussionmentioning

confidence: 99%

The Anticancer Activity of Lycium barbarum Polysaccharide by Inhibiting Autophagy in Human Skin Squamous Cell Carcinoma Cells In Vitro and In Vivo

Zeng

Kong

Liu

et al. 2019

International Journal of Polymer Science

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Objective. This study is aimed at investigating the effects of Lycium barbarum polysaccharide (LBP) on the proliferation and apoptosis of human cutaneous squamous cell carcinoma A431 cells in vitro and in vivo via its regulation on autophagy. Methods. In vitro experiment: A431 cells were treated with different concentrations of LBP, and cell viability was measured by the CCK8 method. Flow cytometry was used to detect the cell apoptosis rate. The expression of Ki67, PCNA, cl-caspase-3, Bcl-2, and LC3II and the phosphorylation status of JNK and ERK1/2, as well as the effect of SP600125 cotreatment on the expression of autophagy and apoptosis-associated proteins, were determined via Western blot. In vivo experiment: a transplanted tumor model was established by subcutaneous injection of A431 cells to the nude mice. 50 mg/kg LBP was injected into the mice intraperitoneally; the survival rate of mice, volume, and weight of tumor were determined on the 30th day. The expression of Ki67 and MMP-2 proteins was measured by immunohistochemistry. Results. LBP at concentrations of 400 μg/ml and above was significantly cytotoxic to A431 cells, whereas, within the dose range of 50 μg/ml~200 μg/ml, LBP significantly inhibited the expression of Ki67 and PCNA proteins, promoted the expression of cl-caspase-3, inhibited the expression of Bcl-2 protein, downregulated the expression of autophagy marker LC3II, and reduced the phosphorylation of ERK1/2, whereas the level of JNK phosphorylation was upregulated. At the same time, the regulation of Beclin1, LC3II, Bcl-2, and cl-caspase-3 by LBP was effectively reversed by the cotreatment of SP600125. In addition, LBP increased the survival rate of transplanted nude mice, reduced tumor volume and weight, and downregulated the expression of Ki67 and MMP-2. Conclusion. LBP can induce apoptosis of A431 cells by inhibiting autophagy and can inhibit tumor growth in vivo.

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Lycium barbarum polysaccharide protects against oxygen glucose deprivation/reoxygenation-induced apoptosis and autophagic cell death via the PI3K/Akt/mTOR signaling pathway in primary cultured hippocampal neurons

Cited by 61 publications

References 33 publications

RETRACTED ARTICLE: Lycium barbarum polysaccharide alleviates oxygen glucose deprivation-induced PC-12 cells damage by up-regulating miR-24

RETRACTED ARTICLE: Lycium barbarum polysaccharide alleviates oxygen glucose deprivation-induced PC-12 cells damage by up-regulating miR-24

Modafinil protects hippocampal neurons by suppressing excessive autophagy and apoptosis in mice with sleep deprivation

The Anticancer Activity of Lycium barbarum Polysaccharide by Inhibiting Autophagy in Human Skin Squamous Cell Carcinoma Cells In Vitro and In Vivo

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