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Hydrogen-rich saline protects rat from oxygen glucose deprivation and reperusion-induced apoptosis through VDAC1 via Bcl-2.
Brain Res. 2019 03 01; 1706:110-115.BR

Abstract

BACKGROUND

Hydrogen is received as an inert gas that thought to be non-functional in vivo previously. Recently, emerging evidences showed that in ischemia/reperfusion (IR) condition, hydrogen reduced cellular reactive oxygen species (ROS) production and ameliorated cell apoptosis. However, the underlying mechanism of hydrogen on IR-induced apoptosis remains elusive. Here we tried to unravel the mode of action of hydrogen with rat adrenal medulla cell line PC-12 in vitro.

METHODS

The mitochondrial functions before and after oxygen glucose deprivation and reperfusion (OGD/RP) were determined with corresponding dyes. The expression of Bcl-2, Bax, VDAC1, cytochrome c and caspase 9 was detected using qRT-PCR and Western Blotting method. Then Bcl-2 inhibitor, AB-199, was applied to investigate the role of Bcl-2 in OGD/RP-induced cell apoptosis. Finally, we manipulated the expression of VDAC1 with plasmids transfection to understand the effects of VDAC1 on Bcl-2-mediated anti-apoptosis in OGD/RP.

RESULTS

In this study, we demonstrated that hydrogen-rich saline (HRS) reduced OGD/RP-mediated neuronal loss by stimulating the expression of Bcl-2, which suppressed the activity of VDAC1. Consequently, HRS maintained the mitochondrial functions, restrained the release of cytochrome c and caspase 9 activation, resulting in ameliorated cell viability.

CONCLUSIONS

HRS ameliorated OGD/RP-induced PC-12 cell apoptosis and provided a novel treatment option for ischemia.

Authors+Show Affiliations

Department of Emergency, Xiangya Hospital of Central South University, Changsha 410008, PR China.Department of Emergency, Xiangya Hospital of Central South University, Changsha 410008, PR China.Department of Emergency, Xiangya Hospital of Central South University, Changsha 410008, PR China.Department of Emergency, Xiangya Hospital of Central South University, Changsha 410008, PR China.Department of Emergency, Xiangya Hospital of Central South University, Changsha 410008, PR China.Department of Emergency, Xiangya Hospital of Central South University, Changsha 410008, PR China.Department of Emergency, Xiangya Hospital of Central South University, Changsha 410008, PR China. Electronic address: huangguoqing2222@sina.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

30287344

Citation

Mo, Xiao-Ye, et al. "Hydrogen-rich Saline Protects Rat From Oxygen Glucose Deprivation and Reperusion-induced Apoptosis Through VDAC1 Via Bcl-2." Brain Research, vol. 1706, 2019, pp. 110-115.
Mo XY, Li XM, She CS, et al. Hydrogen-rich saline protects rat from oxygen glucose deprivation and reperusion-induced apoptosis through VDAC1 via Bcl-2. Brain Res. 2019;1706:110-115.
Mo, X. Y., Li, X. M., She, C. S., Lu, X. Q., Xiao, C. G., Wang, S. H., & Huang, G. Q. (2019). Hydrogen-rich saline protects rat from oxygen glucose deprivation and reperusion-induced apoptosis through VDAC1 via Bcl-2. Brain Research, 1706, 110-115. https://doi.org/10.1016/j.brainres.2018.09.037
Mo XY, et al. Hydrogen-rich Saline Protects Rat From Oxygen Glucose Deprivation and Reperusion-induced Apoptosis Through VDAC1 Via Bcl-2. Brain Res. 2019 03 1;1706:110-115. PubMed PMID: 30287344.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hydrogen-rich saline protects rat from oxygen glucose deprivation and reperusion-induced apoptosis through VDAC1 via Bcl-2. AU - Mo,Xiao-Ye, AU - Li,Xiang-Min, AU - She,Chang-Shou, AU - Lu,Xiao-Qin, AU - Xiao,Cheng-Gen, AU - Wang,Shi-Hai, AU - Huang,Guo-Qing, Y1 - 2018/10/02/ PY - 2018/06/08/received PY - 2018/08/31/revised PY - 2018/09/30/accepted PY - 2018/10/6/pubmed PY - 2020/5/30/medline PY - 2018/10/6/entrez KW - Mitochondrial apoptosis KW - OGD/RP KW - Saturated hydrogen-rich saline KW - VDAC1 SP - 110 EP - 115 JF - Brain research JO - Brain Res. VL - 1706 N2 - BACKGROUND: Hydrogen is received as an inert gas that thought to be non-functional in vivo previously. Recently, emerging evidences showed that in ischemia/reperfusion (IR) condition, hydrogen reduced cellular reactive oxygen species (ROS) production and ameliorated cell apoptosis. However, the underlying mechanism of hydrogen on IR-induced apoptosis remains elusive. Here we tried to unravel the mode of action of hydrogen with rat adrenal medulla cell line PC-12 in vitro. METHODS: The mitochondrial functions before and after oxygen glucose deprivation and reperfusion (OGD/RP) were determined with corresponding dyes. The expression of Bcl-2, Bax, VDAC1, cytochrome c and caspase 9 was detected using qRT-PCR and Western Blotting method. Then Bcl-2 inhibitor, AB-199, was applied to investigate the role of Bcl-2 in OGD/RP-induced cell apoptosis. Finally, we manipulated the expression of VDAC1 with plasmids transfection to understand the effects of VDAC1 on Bcl-2-mediated anti-apoptosis in OGD/RP. RESULTS: In this study, we demonstrated that hydrogen-rich saline (HRS) reduced OGD/RP-mediated neuronal loss by stimulating the expression of Bcl-2, which suppressed the activity of VDAC1. Consequently, HRS maintained the mitochondrial functions, restrained the release of cytochrome c and caspase 9 activation, resulting in ameliorated cell viability. CONCLUSIONS: HRS ameliorated OGD/RP-induced PC-12 cell apoptosis and provided a novel treatment option for ischemia. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/30287344/Hydrogen_rich_saline_protects_rat_from_oxygen_glucose_deprivation_and_reperusion_induced_apoptosis_through_VDAC1_via_Bcl_2_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(18)30503-1 DB - PRIME DP - Unbound Medicine ER -