N-n-Butyl Haloperidol Iodide Ameliorates Oxidative Stress in Mitochondria Induced by HypoxiaReoxygenation through the Mitochondrial c-Jun N-Terminal KinaseSabSrcReactive Oxygen Species Pathway in H9c2 Cells
المؤلفون المشاركون
Gao, Fenfei
Zhong, Shuping
Chu, Qianwen
Wang, Bin
Zhang, Zhaojing
Cai, Wenfeng
Zheng, Fuchun
Zhang, Yanmei
Shi, Ganggang
Li, Weiqiu
Chen, Yicun
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-14، 14ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-05-08
دولة النشر
مصر
عدد الصفحات
14
التخصصات الرئيسية
الملخص EN
Both c-Jun N-terminal kinase (JNK) and reactive oxygen species (ROS) play important roles in myocardial ischemia/reperfusion (I/R) injury.
Our previous studies suggest that N-n-butyl haloperidol iodide (F2) exerts cardioprotection by reducing ROS production and JNK activation caused by I/R.
In this study, we hypothesized that there is a JNK/Sab/Src/ROS pathway in the mitochondria in H9c2 cells following hypoxia/reoxygenation (H/R) that induces oxidative stress in the mitochondria and that F2 exerts mitochondrial protective effects during H/R injury by modulating this pathway.
The results showed that H/R induced higher-level ROS in the cytoplasm on the one hand and JNK activation and translocation to the mitochondria by colocalization with Sab on the other.
Moreover, H/R resulted in mitochondrial Src dephosphorylation, and subsequently, oxidative stress evidenced by the increase in ROS generation and oxidized cardiolipin in the mitochondrial membranes and by the decrease in mitochondrial superoxide dismutase activity and membrane potential.
Furthermore, treatment with a JNK inhibitor or Sab small interfering RNA inhibited the mitochondrial translocation of p-JNK, decreased colocalization of p-JNK and Sab on the mitochondria, and reduced Src dephosphorylation and mitochondrial oxidative stress during H/R.
In addition, Src dephosphorylation by inhibitor PP2 increased mitochondrial ROS production.
F2, like inhibitors of the JNK/Sab/Src/ROS pathway, downregulated the H/R-induced mitochondrial translocation of p-JNK and the colocalization of p-JNK and Sab on the mitochondria, increased Src phosphorylation, and alleviated the above-mentioned mitochondrial oxidative stress.
In conclusion, F2 could ameliorate H/R-associated oxidative stress in mitochondria in H9c2 cells through the mitochondrial JNK/Sab/Src/ROS pathway.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Chu, Qianwen& Zhang, Yanmei& Zhong, Shuping& Gao, Fenfei& Chen, Yicun& Wang, Bin…[et al.]. 2019. N-n-Butyl Haloperidol Iodide Ameliorates Oxidative Stress in Mitochondria Induced by HypoxiaReoxygenation through the Mitochondrial c-Jun N-Terminal KinaseSabSrcReactive Oxygen Species Pathway in H9c2 Cells. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-14.
https://search.emarefa.net/detail/BIM-1205142
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Chu, Qianwen…[et al.]. N-n-Butyl Haloperidol Iodide Ameliorates Oxidative Stress in Mitochondria Induced by HypoxiaReoxygenation through the Mitochondrial c-Jun N-Terminal KinaseSabSrcReactive Oxygen Species Pathway in H9c2 Cells. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-14.
https://search.emarefa.net/detail/BIM-1205142
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Chu, Qianwen& Zhang, Yanmei& Zhong, Shuping& Gao, Fenfei& Chen, Yicun& Wang, Bin…[et al.]. N-n-Butyl Haloperidol Iodide Ameliorates Oxidative Stress in Mitochondria Induced by HypoxiaReoxygenation through the Mitochondrial c-Jun N-Terminal KinaseSabSrcReactive Oxygen Species Pathway in H9c2 Cells. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-14.
https://search.emarefa.net/detail/BIM-1205142
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1205142
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