Nooshin bayat ¹, Amin rezaei ², Gholamhossein Alishiri ¹, Mahdi Safiabadi ¹∗
The objective of this study is to investigate the effects of G-ODN/Toll-like receptor 9 (TLR9) inhibitor on the mice with diabetes mellitus (DM) complicated with cerebral infarction (DMCI). The mice divided into four groups: sham, vehicle, DM + middle cerebral artery occlusion (MCAO) and DM+MCAO+G-ODN groups. Triphenyltetrazolium chloride (TTC) staining used to measurement of infarction area, dry-wet method for investigate cerebral water content, and western blotting for detecting the expressions of TLR9 signaling pathway. After streptozotocin (STZ) injection, when compared with the sham group, blood glucose in the other two groups was increased greatly, while blood glucose in the DM+MCAO+G-ODN group was lower than that in the DM + MCAO group. Furthermore, there is a significant decrease in SOD activity, increase in MDA, apoptosis, expressions of Bcl-2, Bax, caspase-3, proinflammatory cytokines and TLR9 proteins in mice model groups. Compared with the DM + MCAO group, mice in the DM+MCAO+G-ODN group had an evident increase in SOD activity and an obvious decrease in MDA content. Additionally, mice in the DM + MCAO group had more infarct volume ratio and cerebral water content. Mice in DM + MCAO group had the most apoptotic cells. While comparing with the DM + MCAO group, expressions of Bcl-2, Bax, caspase-3, TNF-α, IL-1β and TLR4 proteins were decreased in the DM+MCAO+G-ODN group. Our study confirmed that inhibition of TLR9 signaling pathway may protects neuronal cells in diabetes mellitus complicated with cerebral infarction.
Keywords: TLR9; Neuronal cells; G-ODN; Diabetes mellitus
Copyright © 2016 by The American Society for BioMedicine and BM-Publisher, Inc.
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American Journal of BioMedicine Volume 4, Issue 11, pages 213-218
Received January 21, 2016; accepted May 19, 2016; published June 12, 2016
How to cite this article
Bayat N,Rezaei A, Alishiri G, Safiabadi M. The relationship between fasting and rheumatologic and inflammatory markers in patients with rheumatoid arthritis. American Journal of BioMedicine 2016;4(6):213-218.
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