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Bone mesenchymal stem cell-conditioned medium attenuates the effect of oxidative stress injury on NSCs by inhibiting the Notch1 signaling pathway.

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Bone mesenchymal stem cell-conditioned medium attenuates the effect of oxidative stress injury on NSCs by inhibiting the Notch1 signaling pathway.

Cell Biol Int. 2019 Mar 06;:

Authors: Niu Y, Xia X, Song P, Fang H, Dong F, Tao H, Yang C, Shen C

Numerous studies have demonstrated the therapeutic effect of bone mesenchymal stem cells on Spinal cord injury (SCI), especially on neural stem cells (NSCs). However, the predominant mechanisms of bone mesenchymal stem cell (BMSCs) are unclear. Recently, some researchers have found that paracrine signaling plays a key role in the therapeutic capacity of BMSCs and emphasized that the protective effect of BMSCs may be due to paracrine factors. In this study, we aimed to investigate the potential mechanisms of BMSCs recover function to NSCs.NSCs were identified by immunocytochemistry. The oxidative stress environment was simulated by H2O2(50µM, 100µM, 200µM) for 2h. The apoptotic rate of the NSCs was detected via flow cytometry. Lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) activity were evaluated via corresponding assay kits. Western blot were used to detect the expressions of Notch1, HES1, Caspase-3, cleave Caspase-3, Bax and Bcl-2. We found that H2O2 could significantly induce the apoptosis of NSCs, increase LDH, MDA levels and decrease SOD activity by activating the Notch1 signaling pathway. DAPT (the specific blocker of Notch1) and BMSC-CM could significantly prevent the apoptotic effect and oxidative stress injury on NSCs that were treated with H2O2. We also revealed that BMSC-CM could decrease the expression of Notch1, Hes1, cleave Caspase-3, Bax and increases the expression of Bcl-2 in NSCs which was induced by H2O2. These results have revealed that BMSC-CM can neutralize the effect against oxidative stress injury on the apoptosis of NSCs by inhibiting the Notch1 signaling pathway.

PMID: 30839137 [PubMed – as supplied by publisher]

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