Vascular inflammation, insulin resistance, and endothelial dysfunction in salt-sensitive hypertension: role of nuclear factor kappa B activation

2010 ◽  
Vol 28 (3) ◽  
pp. 527-535 ◽  
Author(s):  
Ming-Sheng Zhou ◽  
Ivonne Hernandez Schulman ◽  
Leopoldo Raij
2001 ◽  
Vol 28 (6) ◽  
pp. 626-633 ◽  
Author(s):  
James R. Berenson ◽  
Hongjin M. Ma ◽  
Robert Vescio

Oral Diseases ◽  
2013 ◽  
Vol 20 (3) ◽  
pp. 294-300 ◽  
Author(s):  
T Arabaci ◽  
O Köse ◽  
A Kizildağ ◽  
M Albayrak ◽  
Y Çiçek ◽  
...  

2021 ◽  
Vol 20 (1) ◽  
pp. 169-176
Author(s):  
Jingfang Hu ◽  
Jie Jin ◽  
Yan Chen ◽  
Jinyi Wei ◽  
Hanbei Chen

Diabetes mellitus is a metabolic disorder characterized by inflammation, abnormal glycolipid metabolism, insulin resistance, and mitochondrial dysfunction leading to hyperglycemia. The aim of the present investigation was to determine the efficacy of lycopsamine in a rat model of diabetes mellitus to understand its mechanism. Lycopsamine treatment markedly lowered the level of total cholesterol, triglyceride, nonesterified fatty acids, and low-density lipoprotein in diabetic rats. There was also a reduction in interleukin-6, interleukin-10, C-reactive protein, and tumor necrosis factor-α levels. Lycopsamine treatment normalized the metabolism of lipid and glucose, insulin resistance, and body weight of diabetic rats. Findings of immunohistochemical analyses exhibited rise in precipitation of immunocytes in renal cells. Results potentially demonstrated that lycopsamine treatment remarkably reduced the nuclear factor-kappa B level and enhanced the 5′ adenosine monophosphate-activated protein kinase expression. Altogether, administration of lycopsamine suppressed the expression of inflammatory cytokines and attenuated the metabolic symptoms in diabetes mellitus experimental rats.


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