Propofol Suppressed HypoxiaReoxygenation-Induced Apoptosis in HBVSMC by Regulation of the Expression of Bcl-2, Bax, Caspase3, Kir6.1, and p-JNK
المؤلفون المشاركون
Deng, Xiaoming
Zhang, Jianhai
Xia, Yunfei
Xu, Zifeng
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2016، العدد 2016 (31 ديسمبر/كانون الأول 2016)، ص ص. 1-11، 11ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2016-01-05
دولة النشر
مصر
عدد الصفحات
11
التخصصات الرئيسية
الملخص 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.
نمط استشهاد جمعية علماء النفس الأمريكية (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
نمط استشهاد الجمعية الأمريكية للغات الحديثة (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
نمط استشهاد الجمعية الطبية الأمريكية (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
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1113618
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر