Tetramethylpyrazine Protects Retinal Capillary Endothelial Cells (TR-iBRB2) against IL-1β-Induced Nitrative/Oxidative Stress

International Journal of Molecular Sciences

Xue Zhu²  Ke Wang²  Kai Zhang²  Xuhua Tan⁴  Zhifeng Wu⁴  Song Sun⁴  Fanfan Zhou³  Ling Zhu¹ 

[1] Save Sight Institute, University of Sydney, New South Wales 2000, Australia; E-Mail:;Key Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi 214063, China; E-Mails:;Faculty of Pharmacy, University of Sydney, New South Wales 2006, Australia; E-Mail:;Department of Ophthalmology, Wuxi No. 2 People’s Hospital, Nanjing Medical University, Wuxi 214002, China; E-Mail:

关键词: tetramethylpyrazine;    TR-iBRB2 cells;    nitrosative stress;    oxidative stress;   

DOI  :  10.3390/ijms160921775

来源: mdpi

【 摘 要 】

Blood-retinal barrier (BRB) breakdown is one of the primary causes of diabetic retinopathy (DR). The pro-inflammatory factor interleukin-1β (IL-1β) was reported to be involved in the induction of BRB breakdown during the pathogenesis of DR. In the present study, we investigated the protective effect of tetramethylpyrazine (TMP), a major active component of the traditional herb Ligusticum chuanxiong, on IL-1β-induced cell death of the rat retinal capillary endothelial TR-iBRB2 cells. Our results showed that IL-1β-induced cell dysfunction in TR-iBRB2 cells via inducing nitrative/oxidative stress; however, such effect was attenuated with the pre-treatment of TMP. The cellular protective effect of TMP was likely to be mediated through the inhibition of inducible nitric oxide synthase (iNOS) expression and leukostasis as well as suppression of reactive oxygen species (ROS) generation, mitochondrial dysfunction and MAPKs activation. These findings significantly contribute to a better understanding of the protective effect of TMP in DR and form the basis of the therapeutic development of TMP in treating such disease in the future.

【 授权许可】

CC BY   
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