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Prokineticin 2 (PK2) Rescues Cardiomyocytes from High GlucoseHigh Palmitic Acid-Induced Damage by Regulating the AKTGSK3β Pathway In Vitro
المؤلفون المشاركون
Yu, Wei
Zha, Wenliang
Yang, Zhen
Wu, Yin
Wang, Linge
Qiu, Peng
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-17، 17ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-05-18
دولة النشر
مصر
عدد الصفحات
17
التخصصات الرئيسية
الملخص EN
Prokineticin 2 (PK2) is a small 8 kDa protein that participates in many physiological processes, such as angiogenesis, inflammation, and neurogenesis.
This experiment investigated the effect of PK2 on high glucose/high palmitic acid-induced oxidative stress, apoptosis, and autophagy in cardiomyocytes and the AKT/GSK3β signalling pathway.
H9c2 cells were exposed to normal and high concentrations (33 mM) of glucose and palmitic acid (150 μM) with or without PK2 (10 nM) for 48 h.
Reactive oxygen species were detected using the fluorescent probes DCFH-DA and DHE.
Changes in apoptosis were assessed using flow cytometry, and autophagosomes were detected using Ad-GFP-LC3.
Apoptotic proteins, such as Cleaved Caspase3, Bax, and Bcl-2; autophagy proteins, including Beclin-1 and LC3B; and PK2/PKR/AKT/GSK3β signals were evaluated using western blotting.
Cardiomyocytes exposed to high glucose/high palmitic acid exhibited increases in intracellular ROS, apoptosis, and autophagosomes, and these increases were robustly prevented by PK2.
In addition, high glucose/high palmitic acid remarkably suppressed PK2, PKR1, and PKR2 expression and p-AKT/AKT and p-GSK3β/GSK3β ratios, and these effects were significantly prevented by PK2.
Moreover, an AKT1/2 kinase inhibitor (AKT inhibitor, 10 μM) blocked the effects of PK2 on the changes in cardiomyocyte exposure to high glucose/high palmitic acid.
These results suggest that PK2 attenuates high glucose/high palmitic acid-induced cardiomyocyte apoptosis by inhibiting oxidative stress and autophagosome accumulation and that this protective effect is most likely mediated by the AKT-related signalling pathway.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Yang, Zhen& Wu, Yin& Wang, Linge& Qiu, Peng& Zha, Wenliang& Yu, Wei. 2020. Prokineticin 2 (PK2) Rescues Cardiomyocytes from High GlucoseHigh Palmitic Acid-Induced Damage by Regulating the AKTGSK3β Pathway In Vitro. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-17.
https://search.emarefa.net/detail/BIM-1204181
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Yang, Zhen…[et al.]. Prokineticin 2 (PK2) Rescues Cardiomyocytes from High GlucoseHigh Palmitic Acid-Induced Damage by Regulating the AKTGSK3β Pathway In Vitro. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-17.
https://search.emarefa.net/detail/BIM-1204181
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Yang, Zhen& Wu, Yin& Wang, Linge& Qiu, Peng& Zha, Wenliang& Yu, Wei. Prokineticin 2 (PK2) Rescues Cardiomyocytes from High GlucoseHigh Palmitic Acid-Induced Damage by Regulating the AKTGSK3β Pathway In Vitro. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-17.
https://search.emarefa.net/detail/BIM-1204181
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1204181
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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