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J Neuroimmunol. 2016 Jun 15;295-296:47-53. doi: 10.1016/j.jneuroim.2016.04.002. Epub 2016 Apr 12.

Anti-inflammatory role of sesamin in STZ induced mice model of diabetic retinopathy.

Author information

1
Department of Biological Sciences, Rabigh College of Science and Arts, King Abdulaziz University (Jeddah), Rabigh Branch, Rabigh 21911, Saudi Arabia; Department of Ophthalmology, School of Medicine, Georgia Regents University, Augusta, GA, USA. Electronic address: asaif77@yahoo.com.
2
Department of Ophthalmology, School of Medicine, Georgia Regents University, Augusta, GA, USA; Department of Biochemistry, Mansoura University, Mansoura, Egypt.
3
King Fahd Medical Research Center (KFMRC), King Abdulaziz University, Jeddah, Saudi Arabia.
4
Department of Biological Sciences, Rabigh College of Science and Arts, King Abdulaziz University (Jeddah), Rabigh Branch, Rabigh 21911, Saudi Arabia.
5
Centre for Biological Science (Biotechnology), Central University of South Bihar, Patna, India.
6
Center of Excellence in Genomic Medicine Research (CEGMR), King Abdulaziz University, Jeddah, Saudi Arabia.
7
Department of Ophthalmology, School of Medicine, Georgia Regents University, Augusta, GA, USA.
8
Department of Biological Sciences, Rabigh College of Science and Arts, King Abdulaziz University (Jeddah), Rabigh Branch, Rabigh 21911, Saudi Arabia. Electronic address: kanchan1980@gmail.com.

Abstract

Diabetic retinopathy (DR) is the common cause of diabetic vascular complications that leads to the blindness in the working age population throughout the world. Free radicals mediated oxidative stress and inflammation play a significant role in pathophysiology of DR. To find a new and safe drug to treat DR is still challenging and for that purpose the natural compounds may be therapeutic agents. Here we show that sesamin (SES), which is the main component of sesame seed and its oil, and has been reported as potent antioxidant and neuroprotective, could be a therapeutic agent in DR. In the present study, we investigated protective effect of SES in Streptozotocin (STZ) induced DR in mice. The mice were divided into three groups (Control, DR and DR+SES) for the study. After two weeks post-diabetic establishment, mice were treated with SES (30mg/kg BW, i.p, alternate day) for four weeks. Mice body weight and blood glucose level were measured from each group. The microglial activation of retina was determined by immunohistochemistry analysis by using Iba-1 as a microglia marker. Retinal mRNA levels of Iba-1, tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS) and Intercellular Adhesion Molecule 1 (ICAM-1) were examined by qRT-PCR. The level of iNOS protein expression was examined by immunoblotting. Together these data demonstrate that SES treatment lowered the progression of diabetic retinal injury by: 1) decreasing blood glucose level, 2) suppressing microglia activation, 3) reducing retinal TNF-α and ICAM-1 levels and 4) quenching iNOS expression. In conclusion, the results suggest that SES treatment may be of therapeutic benefit in reducing the progression of DR by ameliorating hyperglycemia and inflammation in diabetic retina.

KEYWORDS:

Anti-inflammation; Cytokines; Diabetic retinopathy; Microglia; Sesamin

PMID:
27235348
DOI:
10.1016/j.jneuroim.2016.04.002
[Indexed for MEDLINE]

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