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Published on: January 4, 2018
[Effect of inflammation factors on endothelial function in insulin resistance SD rats]
Su Pu1, Ye-Rong Yu, Zhi-Ming Lu
1Department of Endocrinology, West China Hospital, Sichuan University, Chengdu 610041, China.
Objective:
To test the effect of inflammation factors on endothelial dysfunction in insulin resistance SD rats.
Methods:
Male SD rats were divided randomly into three groups. The rats in the NC group, OB group and OB-AS group were fed with normal chow, high-fat chow, and high fat chow plus aspirin, respectively. The perifereal insulin sensitivity was detected with hyperinsulinemic euglycemic clamp. The endothelial dependent and independent vasodilatation were evaluated by measuring blood flow through femoral artery. Serum concentrations of high-sensitivity (hs) CRP and TNF-alpha were measured. Quantitative analysis of the expression of IKKbeta and NF-kappaB was performed.
Results:
The rats in the OB group had significantly higher levels of serum hsCRP and TNF-alpha than the rats in the NC group (P < 0.05). There was a significant difference in endothelium-dependent (Ach-mediated dilation) vascular response and serum NO level between the OB group and the NC group (P < 0.05). Meanwhile, the rats in the OB group showed higher expression of NF-kappaBp65 (P < 0.05) and IKKbeta/NF-kappaBp65 (P < 0.05) than those in the NC group. Interestingly, compared with the rats in the OB group, the serum concentrations of TNF-alpha and CRP decreased significantly in the rats in the OB-AS group, to which high dose aspirin was given (P < 0.05). Better endothelium-dependent vascular response and higher serum NO level were observed in the rats in the OB-AS group than those in the NC group (P < 0.05). The rats in the OB-AS group also had significantly lower expression of NF-kappaBp65 (P < 0.05) and IKKbeta/NF-kappaBp65 (P < 0.05) than those in the OB group.
Conclusion:
Elevated inflammation factors are involved in the endothelial dysfunction by inactivating IKKbeta-NF-kappaB pathway in rats with insulin resistance.
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