Celiac disease (CD) is a multifactorial, inflammatory small bowel disorder characterized by nutrient malabsorption resulting from mucosal damage, the latter induced by cereal products like barley, oat, and wheat. Oxidative stress has previously been reported to play an important role in the pathogenesis of CD.
Familial Mediterranean fever (FMF) is an autosomal recessive disorder and is the most frequent of the periodic febrile inflammatory syndromes. The pathogenesis of the disease is not completely understood, even though the FMF gene has been identified. Oxidative stress and inflammation may play a role in the pathogenesis of FMF. We investigated gene polymorphisms of the antioxidative enzymes, glutathione peroxidase (GPX) and paraoxonase (PON) in FMF patients, and possible associations with FMF pathogenesis.
A mouse model of acute lung injury (ALI) was chosen in this study to explore the key genes and pathways involved in the process of ALI with microarray technology. Gene expression microarray data were downloaded from the Gene Expression Omnibus database. Mice from the experimental group were further divided into 6 subgroups, which received octadecenoate treatments for 1, 1.5, 3, 4, 18, and 24 h. Differentially co-expressed genes were screened to uncover the pathogenesis of ALI. Almost all of the differentially co-expressed genes were identified at two times: 1.5 and 3 h.
The dried roots of the plant Acanthopanax senticosus (AS) are used in traditional Oriental medicine and reportedly possess anti-inflammatory properties in vitro. However, whether AS has the same anti-inflammatory effect in vivo and the underlying mechanisms of this action remain unknown.
We aimed to evaluate the effect of genetic variants of the chemokine C-C motif receptor (CCR5) in the pathogenesis of oral squamous cell carcinoma (OSCC). A total of 127 patients diagnosed with OSCC and 104 healthy individuals were included in the study. The polymorphisms CCR5 59029 and CCR5-delta32 were assessed with the polymerase chain reaction-restricted fragment length polymorphism (PCR-RFLP) method from peripheral blood samples of both groups. There was a statistically significant difference between the control and patient groups for CCR5 59029 A/G genotypes (P 0.05).
Most studies have used in vitro systems to test inflammatory responses of nanoparticles; these may not reflect the real biological response of body organs. In fact, certain nanoparticles have provoked opposite effects under in vitro and in vivo conditions. Current understanding of the biocompatibility of gold nanoparticles is controversial. We studied the acute (1 day) and sub-chronic (5 days) effects of gold nanoparticles (10 and 50 nm in diameter) on expression of interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor alpha (TNF-α) in rat liver.
An inflammatory response induced by high glucose is a cause of endothelial dysfunction in diabetes and is an important contributing link to atherosclerosis. Diabetes is an independent risk factor of atherosclerosis and activation of retinoid X receptor (RXR) has been shown to exert anti-atherogenic effects. In the present study, we examined the effects of the RXR ligands 9-cis-retinoic acid (9-cis-RA) and SR11237 on high glucose-induced inflammation in human umbilical endothelial vein endothelial cells (HUVECs) and explored the potential mechanism.
Peroxisome proliferator-activated receptor delta (PPAR-δ) is a transcription factor implicated in metabolism and inflammation. The +294T/C polymorphism in the PPAR-δ gene is associated with risk of coronary artery disease (CAD) in dyslipidemic women and hypercholesterolemic men. Whether this polymorphism influences the risk of CAD in the absence of dyslipidemia was not known, so we investigated a possible association of this polymorphism with plasma lipid and lipoprotein levels and with risk and outcome of CAD in a normolipidemic Tunisian population.
Lungs comprise the primary organ exposed to environmental toxic chemicals, resulting in diverse respiratory ailments and other disorders, including carcinogenesis. Carcinogenesis is a multi-stage phenomenon, which involves a series of genetic alterations that begin with genomic instability provoked by certain factors such as inflammation and DNA damage and end with the development of cancer.