Measurement of Cutaneous Inflammation: Estimation of Neutrophil Content with an Enzyme Marker

Bradley, Peter P.; Priebat, Dennis A.; Christensen, Robert D.; Rothstein, Gerald

doi:10.1111/1523-1747.ep12506462

Cited by 3,217 publications

(1,888 citation statements)

References 11 publications

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“…Ceruloplasmin was analyzed using the method described by Sunderman and Nomoto (1970). Myeloperoxidase analysis was performed using the method described by Bradley et al (1982). Serum amyloid A protein was assayed using an ELISA commercial kit (SAA, by ELISA, Tridelta, Ireland) and a microplate reader (The Synergy TM 2 BioTek Instruments, Inc., Winooski, Vermont, USA).…”

Section: Blood Analysesmentioning

confidence: 99%

The nutrigenomic investigation of C57BL/6N mice fed a short-term high-fat diet highlights early changes in clock genes expression

et al. 2013

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Mice fed long-term high-fat diets (HFD) are an established model for human metabolic disorders, such as obesity and diabetes. However, also the effects of shortterm HFD feeding should be investigated to understand which are the first events that trigger the onset of a predisease condition, the so-called metabolic syndrome, that increases the risk of developing clinical diseases. In this study, C57BL/6N mice were fed a control diet (CTR) or a HFD for 1 (T1) or 2 weeks (T2). Metabolic and histological effects were examined. Cecum transcriptomes of HFD and CTR mice were compared at T2 by microarray analysis. Differentially expressed genes were validated by real-time PCR in the cecum and in the liver. After 2 weeks of diet administration, HFD mice showed an altered expression pattern in only seven genes, four of which are involved in the circadian clock regulatory pathway. Real-time PCR confirmed microarray results of the cecum and revealed the same trend of clock gene expression changes in the liver. These findings suggest that clock genes may play an important role in early controlling gut output systems in response to HFD in mice and that their expression change may also represent an early signaling of the development of an intestinal pro-inflammatory status.

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Section: Blood Analysesmentioning

confidence: 99%

The nutrigenomic investigation of C57BL/6N mice fed a short-term high-fat diet highlights early changes in clock genes expression

et al. 2013

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“…MPO was extracted and the activity was measured using a modified spectroscopic method described by Bradley et al [14] which is as follows. Tissue samples (heart) were homogenized in ice cold 50 mM potassium phosphate buffer (pH=6) containing 0.5% Hexadecyl Trimethyl Ammonium Bromide.…”

Section: Myeloperoxidase (Mpo) Assaymentioning

confidence: 99%

Tomato lycopene attenuates myocardial infarction induced by isoproterenol: Electrocardiographic, biochemical and anti–apoptotic study

Upaganlawar

Vaibhav

Balaraman

2012

Asian Pacific Journal of Tropical Biomedicine

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“…MPO was determined as a marker of tissue infiltration following the procedure of Bradley [27] and as modified by us [28]. In brief, the skin samples were homogenized in 50 mM potassium phosphate buffer, pH 6.0, containing 0.5% hexadecyltrimethyl-ammonium bromide followed by sonication of the homogenate at 4°C for three 10 s bursts with a heat system sonicator equipped with a microprobe.…”

Section: Assay For Myeloperoxidase (Mpo)mentioning

confidence: 99%

Obesity increases the risk of UV radiation-induced oxidative stress and activation of MAPK and NF-κB signaling

Katiyar

Meeran

2007

Free Radical Biology and Medicine

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Obesity has been implicated in several diseases including cancer, however, the relationship of obesity and susceptibility to ultraviolet (UV) radiation-caused skin diseases has not been investigated. As UV-induced oxidative stress has been implicated in several skin diseases, we assessed the role of obesity on UVB-induced oxidative stress in genetically obese Lep ob /Lep ob (leptin-deficient) mice. Here, we report that chronic exposure to UVB (120 mJ/cm 2 ) resulted in greater oxidative stress in the skin of obese mice in terms of higher levels of H 2 O 2 and NO production, photo-oxidative damage of lipids and proteins, and greater depletion of antioxidant defense enzymes, like, glutathione, glutathione peroxidase and catalase. As UV-induced oxidative stress mediates activation of MAPK and NF-κB signaling pathways, we determined the effect of UVB on these pathways in obese mice. Exposure of obese mice to UVB resulted in phosphorylation of ERK1/2, JNK and p38 proteins of the MAPK family. Compared to wild-type mice, the obese mice exhibited higher levels of phosphorylation of these proteins, greater activation of NF-κB/p65, and higher levels of circulating proinflammatory cytokines, including TNF-α, IL-1-β and IL-6, on UVB irradiation. Together, our study suggests for the first time that obesity in mice is associated with greater susceptibility to UVBinduced oxidative stress, and therefore may be a risk factor for skin diseases associated with UVBinduced oxidative stress.

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Measurement of Cutaneous Inflammation: Estimation of Neutrophil Content with an Enzyme Marker

Cited by 3,217 publications

References 11 publications

The nutrigenomic investigation of C57BL/6N mice fed a short-term high-fat diet highlights early changes in clock genes expression

The nutrigenomic investigation of C57BL/6N mice fed a short-term high-fat diet highlights early changes in clock genes expression

Tomato lycopene attenuates myocardial infarction induced by isoproterenol: Electrocardiographic, biochemical and anti–apoptotic study

Obesity increases the risk of UV radiation-induced oxidative stress and activation of MAPK and NF-κB signaling

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