Ellagic acid protects against carrageenan-induced acute inflammation through inhibition of nuclear factor kappa B, inducible cyclooxygenase and proinflammatory cytokines and enhancement of interleukin-10 via an antioxidant mechanism

2014 ◽  
Vol 19 (2) ◽  
pp. 290-299 ◽  
Author(s):  
Nagla A. El-Shitany ◽  
Eman A. El-Bastawissy ◽  
Karema El-desoky
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.


2020 ◽  
Vol 33 (3) ◽  
pp. 145-165 ◽  
Author(s):  
Sergio Rius-Pérez ◽  
Salvador Pérez ◽  
Pablo Martí-Andrés ◽  
María Monsalve ◽  
Juan Sastre

2002 ◽  
Vol 67 (2) ◽  
pp. 668-673 ◽  
Author(s):  
Martha Lappas ◽  
Michael Permezel ◽  
Harry M. Georgiou ◽  
Gregory E. Rice

2007 ◽  
Vol 2007 ◽  
pp. 1-7 ◽  
Author(s):  
Gang Chen ◽  
Jinxin Shi ◽  
Yasuo Ding ◽  
Hongxia Yin ◽  
Chunhua Hang

We have previously shown that traumatic brain injury (TBI) can induce an upregulation of nuclear factor kappa B (NF-κB) and proinflammatory cytokines in the gut, which play an important role in the pathogenesis of acute gut mucosal injury mediated by inflammation. In this work, we investigated whether progesterone administration modulated intestinal NF-κB activity and proinflammatory cytokines expression after TBI in male rats. As a result, we found that administration of progesterone following TBI could decrease NF-κB binding activity, NF-κB p65 protein expression, and concentrations of interleukin-1β(IL-1β), and tumor necrosis factor-α(TNF-α) in the gut. TBI-induced damages of gut structure were ameliorated after progesterone injections. The results of the present study suggest that the therapeutic benefit of post-TBI progesterone injections might be due to its inhibitory effects on intestinal NF-κB activation and proinflammatory cytokines expression.


PLoS ONE ◽  
2017 ◽  
Vol 12 (5) ◽  
pp. e0176672 ◽  
Author(s):  
Chunmei Bao ◽  
Yingqin Liu ◽  
Xin Sun ◽  
Congcong Xing ◽  
Luting Zeng ◽  
...  

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