Astragaloside IV Suppresses High Glucose-Induced NLRP3 Inflammasome Activation by Inhibiting TLR4NF-κB and CaSR
المؤلفون المشاركون
Leng, Bin
Zhang, Yingjie
Liu, Xinran
Zhang, Zhen
Liu, Yang
Wang, Hongxin
Lu, Meili
المصدر
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-16، 16ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-02-18
دولة النشر
مصر
عدد الصفحات
16
التخصصات الرئيسية
الملخص EN
Long-term exposure to high glucose induces vascular endothelial inflammation that can result in cardiovascular disease.
Astragaloside IV (As-IV) is widely used for anti-inflammatory treatment of cardiovascular diseases.
However, its mechanism of action is still not fully understood.
In this study, we investigated the effect of As-IV on high glucose-induced endothelial inflammation and explored its possible mechanisms.
In vivo, As-IV (40 and 80 mg/kg/d) was orally administered to rats for 8 weeks after a single intraperitoneal injection of streptozotocin (STZ, 65 mg/kg).
In vitro, human umbilical vein endothelial cells (HUVECs) were treated with high glucose (33 mM glucose) in the presence or absence of As-IV, NPS2143 (CaSR inhibitor), BAY 11-7082 (NF-κB p65 inhibitor), and INF39 (NLRP3 inhibitor), and overexpression of CaSR was induced by infection of CaSR-overexpressing lentiviral vectors to further discuss the anti-inflammatory property of As-IV.
The results showed that high glucose increased the expression of interleukin-18 (IL-18), interleukin-1β (IL-1β), NLRP3, caspase-1, and ASC, as well as the protein level of TLR4, nucleus p65, and CaSR.
As-IV can reverse these changes in vivo and in vitro.
Meanwhile, NPS2143, BAY 11-7082, and INF39 could significantly abolish the high glucose-enhanced NLRP3, ASC, caspase-1, IL-18, and IL-1β expression in vitro.
In addition, both NPS2143 and BAY 11-7082 attenuated high glucose-induced upregulation of NLRP3, ASC, caspase-1, IL-18, and IL-1β expression.
In conclusion, this study suggested that As-IV could inhibit high glucose-induced NLRP3 inflammasome activation and subsequent secretion of proinflammatory cytokines via inhibiting TLR4/NF-κB signaling pathway and CaSR, which provides new insights into the anti-inflammatory activity of As-IV.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Leng, Bin& Zhang, Yingjie& Liu, Xinran& Zhang, Zhen& Liu, Yang& Wang, Hongxin…[et al.]. 2019. Astragaloside IV Suppresses High Glucose-Induced NLRP3 Inflammasome Activation by Inhibiting TLR4NF-κB and CaSR. Mediators of Inflammation،Vol. 2019, no. 2019, pp.1-16.
https://search.emarefa.net/detail/BIM-1192549
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Leng, Bin…[et al.]. Astragaloside IV Suppresses High Glucose-Induced NLRP3 Inflammasome Activation by Inhibiting TLR4NF-κB and CaSR. Mediators of Inflammation No. 2019 (2019), pp.1-16.
https://search.emarefa.net/detail/BIM-1192549
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Leng, Bin& Zhang, Yingjie& Liu, Xinran& Zhang, Zhen& Liu, Yang& Wang, Hongxin…[et al.]. Astragaloside IV Suppresses High Glucose-Induced NLRP3 Inflammasome Activation by Inhibiting TLR4NF-κB and CaSR. Mediators of Inflammation. 2019. Vol. 2019, no. 2019, pp.1-16.
https://search.emarefa.net/detail/BIM-1192549
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1192549
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