Ibuprofen Attenuates Cardiac Fibrosis in Streptozotocin-Induced Diabetic Rats

Cardiology - Tập 131 Số 2 - Trang 97-106 - 2015
Wei‐Li Qiao1, Cheng Wang2, Bing Chen3, Fan Zhang4, Yao‐Wu Liu4, Qian Lü4, Hao Guo4, Caixia Yan3, Hong Sun3, Gang Hu5, Xiaoxing Yin5
1Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, China
2Department of Cardiology, Affiliated Hospital of XuZhou Medical College, Xuzhou, China
3Department of Physiology, Xuzhou Medical College, and
4Key Laboratory of New Drugs and Clinical Application and
5Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, and

Tóm tắt

<b><i>Objective:</i></b> To investigate the effects of ibuprofen on cardiac fibrosis in a rat model of type 1 diabetes. <b><i>Methods:</i></b> The diabetic model was established by injecting streptozotocin into the rats. Then, ibuprofen or pioglitazone was given by gavage for 8 weeks. The cardiac fibrosis was assessed, and the major components of the renin-angiotensin system, the transforming growth factor β<sub>1</sub> (TGF-β<sub>1</sub>) and the mammalian target of rapamycin (mTOR), were evaluated by histopathological, immunohistochemical, Western blot analysis or ELISA assay. <b><i>Results:</i></b> Obvious cardiac fibrosis was detected in the diabetic group and was alleviated by ibuprofen treatment. Angiotensin-converting enzyme (ACE), angiotensin (Ang) II and AngII type 1 receptor (AT1-R) levels were higher, and ACE2, Ang(1-7) and Mas receptor (Mas-R) were lower in the diabetic group. The ratio of ACE to ACE2 was raised in the diabetic group. All these changes were ameliorated by ibuprofen. TGF-β<sub>1</sub> and mTOR were raised in the hearts of the diabetic group and were attenuated by ibuprofen treatment. There was no significant difference between the ibuprofen and the pioglitazone groups. <b><i>Conclusion:</i></b> Ibuprofen could ameliorate the cardiac fibrosis in diabetic rats by reduction of the ACE/AngII/AT1-R axis and enhancement of the ACE2/Ang(1-7)/Mas-R axis, leading to a decrease in TGF-β<sub>1</sub> and mTOR.

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Thông tin
Thông tin xuất bản

Cardiology

Tập 131 Số 2

97-106

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