TY - JOUR
T1 - Atmospheric pressure plasma treatments protect neural cells from ischemic stroke-relevant injuries by targeting mitochondria
AU - Yan, Xu
AU - Zhang, Chenyang
AU - Ouyang, Jiting
AU - Shi, Zhongfang
AU - Chen, Ye
AU - Han, Ruoyu
AU - Zhang, Wei
AU - Yuan, Fang
AU - Ostrikov, Kostya
N1 - Publisher Copyright:
© 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
PY - 2020/10/1
Y1 - 2020/10/1
N2 - Most studies regarding plasma biomedicine applications mainly focus on the oxidative and/or nitrative stress on bacteria, cancer cells, and other treatment objects. In this study, we evaluate the protective effect of appropriate atmospheric pressure plasma jet (APPJ) treatments on oxygen and glucose deprivation (OGD)-induced neural cell apoptosis, which is a major pathological process during ischemic stroke, based on the physiological functions of NO. Results show that APPJ treatment reduces the OGD-induced apoptosis by weakening typical OGD injury consequences including loss of mitochondrial membrane potential, the release of cytochrome c from the mitochondria into the cytoplasm, lower antiapoptotic Bcl-2 expression, and upregulating the proapoptotic protein Bax. Furthermore, APPJ increased intracellular NO production, which is closely related to the cytoprotective effect of APPJ.
AB - Most studies regarding plasma biomedicine applications mainly focus on the oxidative and/or nitrative stress on bacteria, cancer cells, and other treatment objects. In this study, we evaluate the protective effect of appropriate atmospheric pressure plasma jet (APPJ) treatments on oxygen and glucose deprivation (OGD)-induced neural cell apoptosis, which is a major pathological process during ischemic stroke, based on the physiological functions of NO. Results show that APPJ treatment reduces the OGD-induced apoptosis by weakening typical OGD injury consequences including loss of mitochondrial membrane potential, the release of cytochrome c from the mitochondria into the cytoplasm, lower antiapoptotic Bcl-2 expression, and upregulating the proapoptotic protein Bax. Furthermore, APPJ increased intracellular NO production, which is closely related to the cytoprotective effect of APPJ.
KW - ischemic stroke
KW - mitochondrial apoptosis pathway
KW - neuroprotection
KW - nonthermal plasma
KW - plasma treatment
UR - http://www.scopus.com/inward/record.url?scp=85085935745&partnerID=8YFLogxK
U2 - 10.1002/ppap.202000063
DO - 10.1002/ppap.202000063
M3 - Article
AN - SCOPUS:85085935745
SN - 1612-8850
VL - 17
JO - Plasma Processes and Polymers
JF - Plasma Processes and Polymers
IS - 10
M1 - 2000063
ER -