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The Role of TLR4 on PGC-1α-Mediated Oxidative Stress in Tubular Cell in Diabetic Kidney Disease
المؤلفون المشاركون
Shuguang, Yuan
Yuan, Shuguang
Liu, Xuemei
Qu, Zhong
Gong, Zailiang
Li, Jun
Xiao, Li
Yang, Yuan
Liu, Hong
Liu, Fuyou
Sun, Lin
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-14، 14ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2018-05-16
دولة النشر
مصر
عدد الصفحات
14
التخصصات الرئيسية
الملخص EN
The role and precise mechanism of TLR4 in mitochondria-related oxidative damage and apoptosis of renal tubules in diabetic kidney disease (DKD) remain unclear.
We examined the expression of TLR4 in renal biopsy tissues.
Db/db diabetic mice and HK-2 cells cultured under high glucose (HG) were used as in vivo and vitro models.
Real-time RT-PCR, Western blot, and immunohistochemistry were performed to examine the mRNA and protein levels of TLR4, NF-κΒ, PGC-1α, cytochrome C, and cleaved caspase-3.
ATP level, activity of electron transport chain complex III, and antioxidant enzymes were investigated for mitochondrial function.
Electron microscopy (EM) and MitoTracker Red CMXRos were used for mitochondrial morphology alteration.
DHE staining and TUNEL assay were detected for ROS accumulation and apoptosis.
PGC-1α plasmids were used for the overexpression of PGC-1α in HK-2.
TAK242 and parthenolide were used as TLR4 and NF-κB blockers, respectively.
Results showed that TLR4 was extensively expressed in the renal tubules of DKD patients and db/db diabetic mice, which was positively related to the tubular interstitial damage score and urinary β-NAG levels.
In diabetic mice, inhibition of TLR4 could reverse the decreased expression of PGC-1α, increased expression of cytochrome C and cleaved caspase-3, mitochondrial dysfunction and deformation, increased accumulation of ROS, and activation of tubular cell apoptosis.
In vitro, inhibition of TLR4 or NF-κB showed consistent results.
PGC-1α overexpression could reverse the mitochondrial dysfunction, increased cleaved caspase-3, and apoptosis in HK-2 cells treated with HG.
Data indicated that the TLR4/NF-κB signaling pathway might be the upstream pathway of PGC-1α and promote the tubular damage of DKD by modulating the mitochondria-related oxidative damage and apoptosis.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Yuan, Shuguang& Liu, Xuemei& Shuguang, Yuan& Qu, Zhong& Gong, Zailiang& Li, Jun…[et al.]. 2018. The Role of TLR4 on PGC-1α-Mediated Oxidative Stress in Tubular Cell in Diabetic Kidney Disease. Oxidative Medicine and Cellular Longevity،Vol. 2018, no. 2018, pp.1-14.
https://search.emarefa.net/detail/BIM-1211783
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Yuan, Shuguang…[et al.]. The Role of TLR4 on PGC-1α-Mediated Oxidative Stress in Tubular Cell in Diabetic Kidney Disease. Oxidative Medicine and Cellular Longevity No. 2018 (2018), pp.1-14.
https://search.emarefa.net/detail/BIM-1211783
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Yuan, Shuguang& Liu, Xuemei& Shuguang, Yuan& Qu, Zhong& Gong, Zailiang& Li, Jun…[et al.]. The Role of TLR4 on PGC-1α-Mediated Oxidative Stress in Tubular Cell in Diabetic Kidney Disease. Oxidative Medicine and Cellular Longevity. 2018. Vol. 2018, no. 2018, pp.1-14.
https://search.emarefa.net/detail/BIM-1211783
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1211783
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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