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Propofol Suppressed HypoxiaReoxygenation-Induced Apoptosis in HBVSMC by Regulation of the Expression of Bcl-2, Bax, Caspase3, Kir6.1, and p-JNK
Joint Authors
Deng, Xiaoming
Zhang, Jianhai
Xia, Yunfei
Xu, Zifeng
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2016, Issue 2016 (31 Dec. 2016), pp.1-11, 11 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2016-01-05
Country of Publication
Egypt
No. of Pages
11
Main Subjects
Abstract EN
Recent studies have found that propofol may protect brain from cerebral ischemic-reperfusion injury.
However, the underlying mechanism remains unclear.
The effects of propofol were evaluated in HBVSMC after hypoxia/reoxygenation (H/R).
Cell viability and levels of SOD, LDH, and MDA were measured.
Apoptosis was detected by flow cytometry.
The levels of Bax, Bcl-2, Caspase3, Sur2b, Kir6.1, JNK, p-JNK, mTOR, and p-mTOR proteins were measured by western blotting.
H/R decreased cell viability and SOD activity and increased LDH leakage and MDA content in HBVSMC, all of which were significantly reversed by propofol.
Propofol suppressed the levels of H/R-induced apoptosis.
The expression of Bcl-2 and p-mTOR was significantly downregulated and the expression levels of Bax, Caspase3, Kir6.1, and p-JNK were upregulated following H/R injury.
The ratio of p-JNK/JNK was increased; however, that of p-mTOR/mTOR decreased correspondingly.
The effects on the expression of these proteins were reversed by propofol treatment.
SP600125 enhanced and Everolimus attenuated the effect of propofol.
These findings suggested that the protective effect of propofol against H/R injury in the HBVSMC was through the inhibition of apoptosis by inducing the expression of Bcl-2 and p-mTOR as well as inhibiting the expression levels of Bax, Caspase3, Kir6.1, and p-JNK.
American Psychological Association (APA)
Zhang, Jianhai& Xia, Yunfei& Xu, Zifeng& Deng, Xiaoming. 2016. Propofol Suppressed HypoxiaReoxygenation-Induced Apoptosis in HBVSMC by Regulation of the Expression of Bcl-2, Bax, Caspase3, Kir6.1, and p-JNK. Oxidative Medicine and Cellular Longevity،Vol. 2016, no. 2016, pp.1-11.
https://search.emarefa.net/detail/BIM-1113618
Modern Language Association (MLA)
Zhang, Jianhai…[et al.]. Propofol Suppressed HypoxiaReoxygenation-Induced Apoptosis in HBVSMC by Regulation of the Expression of Bcl-2, Bax, Caspase3, Kir6.1, and p-JNK. Oxidative Medicine and Cellular Longevity No. 2016 (2016), pp.1-11.
https://search.emarefa.net/detail/BIM-1113618
American Medical Association (AMA)
Zhang, Jianhai& Xia, Yunfei& Xu, Zifeng& Deng, Xiaoming. Propofol Suppressed HypoxiaReoxygenation-Induced Apoptosis in HBVSMC by Regulation of the Expression of Bcl-2, Bax, Caspase3, Kir6.1, and p-JNK. Oxidative Medicine and Cellular Longevity. 2016. Vol. 2016, no. 2016, pp.1-11.
https://search.emarefa.net/detail/BIM-1113618
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1113618