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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
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