کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8259780 | 1534645 | 2015 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Blockage of ROS and NF-κB-mediated inflammation by a new chalcone L6H9 protects cardiomyocytes from hyperglycemia-induced injuries
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کلمات کلیدی
NF-κBMMPcox2CK-MBCURGCLCCTGFDCMHO-1Nrf2NQO-1Heme oxygenase-1ROS - ROSinflammation - التهاب( توروم) Oxidative stress - تنش اکسیداتیوdihydroethidium - دی هیدروتیدیمcyclooxygenase 2 - سیکلوکوکسیژناز 2antioxidant-responsive element - عنصر پاسخ دهنده آنتی اکسیدانConnective tissue growth factor - فاکتور رشد بافت همبندChalcone derivative - مشتق شده کلکونARE - هستندDHE - وMitochondrial membrane potential - پتانسیل غشای میتوکندریdiabetic cardiomyopathy - کاردیومیوپاتی دیابتی یا بیماری قلبی دیابتیGlutamate cysteine ligase catalytic subunit - کلوتامین کاتالیزوری لیستاز سیستئین گلوتاماتCurcumin - کورکومینhigh glucose - گلوکز بالا یا قند بالاReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Increased oxidative stress and cardiac inflammation have been implicated in the pathogenesis of diabetic cardiomyopathy (DCM). We previously found that a novel chalcone derivative, L6H9, was able to reduce LPS-induced inflammatory response in macrophages. This study was designed to investigate its protective effects on DCM and the underlying mechanisms. H9C2 cells were cultured with DMEM containing 33 mmol/L of glucose in the presence or absence of L6H9. Pretreatment with L6H9 significantly reduced high glucose-induced inflammatory cytokine expression, ROS level increase, mitochondrial dysfunction, cell apoptosis, fibrosis, and hypertrophy in H9c2 cells, which may be mediated by NF-κB inhibition and Nrf2 activation. In mice with STZ-induced diabetes, oral administration of L6H9 at 20 mg/kg/day for 8 weeks significantly decreased the cardiac cytokine and ROS level, accompanied by decreasing cardiac apoptosis and hypertrophy, and, finally, improved histological abnormalities and fibrosis, without affecting the hyperglycemia. L6H9 also attenuated the diabetes-induced NF-κB activation and Nrf2 decrease in diabetic hearts. These results strongly suggest that L6H9 may have great therapeutic potential in the treatment of DCM via blockage of inflammation and oxidative stress. This study also provides a deeper understanding of the regulatory role of Nrf2 and NF-κB in DCM, indicating that they may be important therapeutic targets for diabetic complications.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1852, Issue 7, July 2015, Pages 1230-1241
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1852, Issue 7, July 2015, Pages 1230-1241
نویسندگان
Peng Zhong, Lianpin Wu, Yuanyuan Qian, Qilu Fang, Dandan Liang, Jingying Wang, Chunlai Zeng, Yi Wang, Guang Liang,