Carvedilol Inhibits Angiotensin II-Induced Proliferation and Contraction in Hepatic Stellate Cells through the RhoARho-Kinase Pathway
المؤلفون المشاركون
Zhang, Chunqing
Wu, Ying
Li, Zhen
Wang, Sining
Xiu, Aiyuan
المصدر
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-15، 15ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-11-07
دولة النشر
مصر
عدد الصفحات
15
التخصصات الرئيسية
الملخص EN
Aim.
Carvedilol is a nonselective beta-blocker used to reduce portal hypertension.
This study investigated the effects and potential mechanisms of carvedilol in angiotensin II- (Ang II-) induced hepatic stellate cell (HSC) proliferation and contraction.
Methods.
The effect of carvedilol on HSC proliferation was measured by Cell Counting Kit-8 (CCK-8).
Cell cycle progression and apoptosis in HSCs were determined by flow cytometry.
A collagen gel assay was used to confirm HSC contraction.
The extent of liver fibrosis in mice was evaluated by hematoxylin-eosin (H&E) and Sirius Red staining.
Western blot analyses were performed to detect the expression of collagen I, collagen III, α-smooth muscle actin (α-SMA), Ang II type I receptor (AT1R), RhoA, Rho-kinase 2 (ROCK2), and others.
Results.
The results showed that carvedilol inhibited HSC proliferation and arrested the cell cycle at the G0/G1 phase in a dose-dependent manner.
Carvedilol also modulated Bcl-2 family proteins and increased apoptosis in Ang II-treated HSCs.
Furthermore, carvedilol inhibited HSC contraction induced by Ang II, an effect that was associated with AT1R-mediated RhoA/ROCK2 pathway interference.
In addition, carvedilol reduced α-SMA expression and collagen deposition and attenuated liver fibrosis in carbon tetrachloride (CCl4)-treated mice.
The in vivo data further confirmed that carvedilol inhibited the expression of angiotensin-converting enzyme (ACE), AT1R, RhoA, and ROCK2.
Conclusions.
The results indicated that carvedilol dose-dependently inhibited Ang II-induced HSC proliferation by impeding cell cycle progression, thus alleviating hepatic fibrosis.
Furthermore, carvedilol could inhibit Ang II-induced HSC contraction by interfering with the AT1R-mediated RhoA/ROCK2 pathway.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Wu, Ying& Li, Zhen& Wang, Sining& Xiu, Aiyuan& Zhang, Chunqing. 2019. Carvedilol Inhibits Angiotensin II-Induced Proliferation and Contraction in Hepatic Stellate Cells through the RhoARho-Kinase Pathway. BioMed Research International،Vol. 2019, no. 2019, pp.1-15.
https://search.emarefa.net/detail/BIM-1127621
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Wu, Ying…[et al.]. Carvedilol Inhibits Angiotensin II-Induced Proliferation and Contraction in Hepatic Stellate Cells through the RhoARho-Kinase Pathway. BioMed Research International No. 2019 (2019), pp.1-15.
https://search.emarefa.net/detail/BIM-1127621
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Wu, Ying& Li, Zhen& Wang, Sining& Xiu, Aiyuan& Zhang, Chunqing. Carvedilol Inhibits Angiotensin II-Induced Proliferation and Contraction in Hepatic Stellate Cells through the RhoARho-Kinase Pathway. BioMed Research International. 2019. Vol. 2019, no. 2019, pp.1-15.
https://search.emarefa.net/detail/BIM-1127621
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1127621
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