The aetiology of inflammatory bowel diseases is unclear, but oxidative stress plays a key role in the pathogenesis. Anthocyanins--plant polyphenols--were shown to have antioxidant and anti-inflammatory properties. The aim of this study was to investigate the potential protective effects of anthocyanins on the oxidative status in mice with chemically induced colitis. Adult male mice were randomly divided into a control group drinking tap water and a colitis group drinking 1% dextran sulphate sodium solution. Animals had ad libitum access to a control wheat-based diet or food based on wheat producing anthocyanins. Bodyweight and stool consistency were monitored daily for 14 days. At the end of the experiment, colon length was measured and tissue samples were collected for the assessment of histology and oxidative status. Mice with colitis had lower body weight, higher stool score and shorter colon than control mice. Anthocyanins had neither an effect on stool consistency, nor on bodyweight loss and colon length. In the colon, liver and plasma, analysis of oxidative stress markers and antioxidant status revealed no significant differences between the groups. Food made from wheat producing anthocyanins did not protect mice from the consequences of chemically induced colitis. The measured biomarkers do not confirm the role of oxidative stress in this model of colitis. Further optimization of the anthocyanin-rich food might be needed before further experiments are conducted.
- MeSH
- anthokyaniny farmakologie terapeutické užití MeSH
- antioxidancia farmakologie terapeutické užití MeSH
- biologické markery metabolismus MeSH
- fortifikované potraviny * MeSH
- hmotnostní úbytek účinky léků MeSH
- kolitida chemicky indukované dietoterapie patologie patofyziologie MeSH
- kolon účinky léků patologie MeSH
- myši MeSH
- náhodné rozdělení MeSH
- oxidační stres účinky léků MeSH
- pšenice MeSH
- výsledek terapie MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- hodnotící studie MeSH
- práce podpořená grantem MeSH
BACKGROUND: In the present study we aimed: 1) To establish the prevalence and clinical impact of DFNB49 mutations in deaf Roma from 2 Central European countries (Slovakia and Hungary), and 2) to analyze a possible common origin of the c.1331+2T>C mutation among Roma and Pakistani mutation carriers identified in the present and previous studies. METHODS: We sequenced 6 exons of the MARVELD2 gene in a group of 143 unrelated hearing impaired Slovak Roma patients. Simultaneously, we used RFLP to detect the c.1331+2T>C mutation in 85 Hungarian deaf Roma patients, control groups of 702 normal hearing Romanies from both countries and 375 hearing impaired Slovak Caucasians. We analyzed the haplotype using 21 SNPs spanning a 5.34Mb around the mutation c.1331+2T>C. RESULTS: One pathogenic mutation (c.1331+2T>C) was identified in 12 homozygous hearing impaired Roma patients. Allele frequency of this mutation was higher in Hungarian (10%) than in Slovak (3.85%) Roma patients. The identified common haplotype in Roma patients was defined by 18 SNP markers (3.89 Mb). Fourteen common SNPs were also shared among Pakistani and Roma homozygotes. Biallelic mutation carriers suffered from prelingual bilateral moderate to profound sensorineural hearing loss. CONCLUSIONS: We demonstrate different frequencies of the c.1331+2T>C mutation in hearing impaired Romanies from 3 Central European countries. In addition, our results provide support for the hypothesis of a possible common ancestor of the Slovak, Hungarian and Czech Roma as well as Pakistani deaf patients. Testing for the c.1331+2T>C mutation may be recommended in GJB2 negative Roma cases with early-onset sensorineural hearing loss.
- MeSH
- alely MeSH
- efekt zakladatele MeSH
- exony genetika MeSH
- frekvence genu MeSH
- genotyp MeSH
- haplotypy genetika MeSH
- jednonukleotidový polymorfismus * MeSH
- kojenec MeSH
- lidé MeSH
- MARVELD2 protein genetika MeSH
- mutace * MeSH
- nedoslýchavost vrozené etnologie genetika MeSH
- prevalence MeSH
- Romové genetika MeSH
- sekvenční homologie nukleových kyselin MeSH
- věk při počátku nemoci MeSH
- Check Tag
- kojenec MeSH
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
- srovnávací studie MeSH
- Geografické názvy
- Česká republika MeSH
- Maďarsko MeSH
- Pákistán MeSH
- Slovenská republika MeSH
The aim of our study was to investigate adrenocortical function in the context of disease activity and inflammatory status in premenopausal RA females. Adrenal glucocorticoid and androgen responses to the 1 microg ACTH 1-24 test were investigated in 23 premenopausal RA and in 15 age- and BMI-matched healthy females. Twelve RA patients were on low-dose prednisone (<8.5 mg/day). Patients with DAS28>3.2 had lower (p<0.05) total plasma cortisol, 17-hydroxyprogesterone, dehydroepiandrosterone and androstenedione responses in the ACTH test compared to healthy controls. Patients with DAS28>3.2 had lower (p<0.05) dehydroepiandrosterone response in the ACTH test compared to patients with DAS28=3.2. C-reactive protein (CRP), DAS28, and interleukin (IL)-6 negatively correlated with androstenedione response to ACTH 1-24. Responses of all measured adrenal steroids were lower (p<0.05) in patients on low-dose glucocorticoids compared to healthy controls. RA patients not treated with glucocorticoids had lower total cortisol response (p=0.038) but did not differ in free plasma cortisol in the ACTH test. The results indicate an association of increased disease activity with a decrease in adrenal androgen production in RA and normal cortisol bioavailability in patients not treated with glucocorticoids.
- MeSH
- 11-beta-hydroxysteroiddehydrogenasa typ 1 metabolismus MeSH
- 17-alfa-hydroxyprogesteron krev MeSH
- adrenokortikotropní hormon diagnostické užití MeSH
- androgeny metabolismus MeSH
- dospělí MeSH
- hormony kůry nadledvin krev MeSH
- kůra nadledvin patofyziologie MeSH
- lidé MeSH
- premenopauza krev MeSH
- revmatoidní artritida krev patofyziologie MeSH
- studie případů a kontrol MeSH
- stupeň závažnosti nemoci MeSH
- tuková tkáň metabolismus MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Chronic systemic inflammation is associated with increased cardiovascular mortality in patients with rheumatoid arthritis (RA). The aim of our study was to investigate association of glucose metabolism and inflammatory markers in a group of patients with rheumatoid arthritis free of other metabolic risk factors. Twenty-two premenopausal RA females (11 patients on low-dose GC (<8.5 mg/day of prednisone or equivalent), 11 patients without glucocorticoid therapy) and 15 age- and BMI-matched healthy females underwent the oral glucose tolerance test. The insulin sensitivity indices according Matsuda (ISI(MAT)) and Cederholm (ISI(CED)) as well as HOMA2 %S were calculated. Cytokines, lipid profile, non-esterified fatty acids (NEFA) and plasminogen activator inhibitor-1 (PAI-1) were measured in baseline blood samples. Despite elevated interleukin IL-6 and TNF alpha, glucose, insulin and C-peptide responses to oral glucose load as well as ISI(MAT), ISI(CED), PAI-1 and NEFA were comparable in both RA groups and healthy controls. HOMA2 %S correlated with disease activity. In conclusions, low-dose glucocorticoid treatment does not lead to glucose metabolism impairment in RA patients without other metabolic risk factors. Increased cardiovascular mortality and morbidity is probably due to a direct effect of systemic inflammation on myocardium and/or blood vessels.
- MeSH
- analýza rozptylu MeSH
- biologické markery krev MeSH
- C-reaktivní protein metabolismus MeSH
- časové faktory MeSH
- dospělí MeSH
- glukokortikoidy aplikace a dávkování škodlivé účinky MeSH
- glukózový toleranční test MeSH
- interleukin-6 krev MeSH
- inzulin krev MeSH
- inzulinová rezistence MeSH
- krevní glukóza účinky léků metabolismus MeSH
- kyseliny mastné neesterifikované krev MeSH
- lidé MeSH
- lineární modely MeSH
- mediátory zánětu krev MeSH
- mladý dospělý MeSH
- prednison aplikace a dávkování škodlivé účinky MeSH
- premenopauza MeSH
- revmatoidní artritida krev diagnóza farmakoterapie MeSH
- studie případů a kontrol MeSH
- TNF-alfa krev MeSH
- výsledek terapie MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mladý dospělý MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH