Activation of HSP70 impedes tert-butyl hydroperoxide (t-BHP)-induced apoptosis and senescence of human nucleus pulposus stem cells via inhibiting the JNK/c-Jun pathway

Neural stem cells (NSCs) transplanted is one of the hottest research to treat Alzheimer’s disease (AD), but cholinergic neurons from stem cells were also susceptible to cell death which Heat shock protein 70 (HSP70) was affirmed to reverse. Related to cognitive impairment, cholinergic nervous cells should be investigated and ginsenoside Rg1 (G-Rg1) was considered to increase them. We chose tert-butyl hydroperoxide (t-BHP) damage model to study in vitro. Functional properties of our recombination plasmid pEGFP-C2-HSP70 were affirmed by SH-SY5Y cells. To opposite the transitory appearance of HSP70, NSCs used as the vectors of HSP70 gene overexpressed HSP70 for at least 7 days in vitro. After transfection for 3 days, G-Rg1 pretreatment for 4 hours, and coculture for 3 days, the expression of acetylcholinesterase (ChAT), synaptophysin, and the ratio of NeuN and GFAP were assessed by western blot; Morphological properties were detected by 3D reconstruction and immunofluorescence. ChAT was markedly improved in the groups contained G-Rg1. In coculture system, the ratio of neurons/astrocytes and the filaments of neurons were increased; apoptosis cells were decreased, compared to monotherapy (P<0.05). In conclusion, we demonstrated that, as a safe cotreatment affirmed in vitro, overexpression of HSP70 in NSCs plus G-Rg1 promoted nervous cells regeneration from chronic oxidative damage.

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Role of Ca2+ influx in the tert-butyl hydroperoxide-induced apoptosis of HepG2 human hepatoblastoma cellse

Experimental & Molecular Medicine ◽

10.1038/emm.1998.20 ◽

1998 ◽

Vol 30 (3) ◽

pp. 137-144 ◽

Cited By ~ 23

Author(s):

Jung-Ae Kim ◽

Young Shin Kang ◽

Young Ok Kim ◽

Sun Hee Lee ◽

Yong Soo Lee

Keyword(s):

Butyl Hydroperoxide ◽

Tert Butyl ◽

Tert Butyl Hydroperoxide ◽

Induced Apoptosis

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Osthole Delays Tert-Butyl Hydroperoxide-Induced Premature Senescence in Neural Stem Cells

Cellular Reprogramming ◽

10.1089/cell.2018.0010 ◽

2018 ◽

Vol 20 (4) ◽

pp. 268-274

Author(s):

Yingjia Yao ◽

Xicai Liang ◽

Yue Shi ◽

Ying Lin ◽

Jingxian Yang

Keyword(s):

Stem Cells ◽

Neural Stem Cells ◽

Premature Senescence ◽

Butyl Hydroperoxide ◽

Tert Butyl ◽

Tert Butyl Hydroperoxide

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CpG-Oligodeoxynucleotides Alleviate Tert-Butyl Hydroperoxide-Induced Macrophage Apoptosis by Regulating Mitochondrial Function and Suppressing ROS Production

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/1714352 ◽

2020 ◽

Vol 2020 ◽

pp. 1-19

Author(s):

Yibai Qu ◽

Chunxiu Yang ◽

Xueyang Li ◽

Haihua Luo ◽

Shan Li ◽

...

Keyword(s):

Oxidative Stress ◽

Underlying Mechanism ◽

Ros Production ◽

Cpg Odn ◽

Butyl Hydroperoxide ◽

Tert Butyl ◽

Cpg Oligodeoxynucleotides ◽

Tert Butyl Hydroperoxide ◽

Induced Apoptosis ◽

Related Proteins

Oxidative stress and mitochondrial dysfunction are related to disease pathogenesis. Oligodeoxynucleotide containing CpG motifs (CpG ODN) demonstrate possibilities for immunotherapy applications. The aim of the present work is to explore the underlying mechanism of the cytoprotective function of CpG ODN by employing the oxidative stress modulation in immune cells. We used the imaging flow cytometry to demonstrate that tert-butyl hydroperoxide (t-BHP) induces mitochondrial-mediated apoptosis and ROS production in RAW264.7 cells. After pretreatment with CpG ODN, the percentage of apoptotic cells and ROS production was both markedly reduced. The decrease in mitochondrial membrane potential (MMP) induced by t-BHP was partially reversed by CpG ODN. The t-BHP induced upregulation of the expression of apoptosis-related proteins (cleaved-caspase 3, cleaved-caspase 9, cleaved-PARP, and bax) was notably decreased in the presence of CpG ODN. Furthermore, we found that CpG ODN enhanced phosphorylation of ERK1/2 and Akt to inhibit ROS production. In conclusion, the protective effect of CpG ODN in mitigation of t-BHP-induced apoptosis is dependent on the reduction of ROS.

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