THE ASSOCIATION BETWEEN PRO AND ANTI-INFLAMMATORY MARKERS WITH THE COMPONENTS OF METABOLIC SYNDROME.

OBJECTIVES: Metabolic syndrome (MetS) is a cluster of metabolic abnormalities that is linked with increased circulating markers of oxidative stress and low-grade inflammation. The link between inflammation and MetS is not yet fully understood. We aim to evaluate the relationship between the levels of pro and anti-inflammatory markers such as apolipoprotein A1 (Apo-A1), apolipoprotein B (Apo-B), interleukin (IL) 6, tumor necrosis factor alpha (TNF-α), fibrinogen and complement component 3 (C3) and adiponectin and MetS/MetS components. METHODS: This study was a case-control study conducted in an outpatient internal medicine clinic of the Ondokuz Mayis University Internal Medicine Department. A total of 108 subjects (59 female, 49 male) who were not under any dietary restrictions and older than 17 years were selected and divided into two groups (54 with MetS and 54 healthy controls). RESULTS: Increased levels of IL-6, C3 and Apo-B/Apo-A1 ratios and decreased levels of Apo-A1 and TNF-α (except in patients with hypertriglyceridemia) were detected in the MetS group. Apo-A1 and TNF-α exhibited decreased levels, and IL-6, fibrinogen, C3 and Apo-B levels and Apo-B/Apo-A1 ratios increased as higher numbers of MetS criteria were met in the total study group. CONCLUSIONS: We found that inflammatory marker levels were not affected by an increased number of MetS criteria met in the MetS group although these levels increased in the control group with higher numbers of MetS components. The presence of a high number of MetS components does not have an additive pro-inflammatory contribution for subjects already diagnosed with MetS.

Gingival crevicular fluid interleukin-8 and lipoxin A4 levels of smokers and nonsmokers with different periodontal status: a cross-sectional study.

BACKGROUND AND OBJECTIVE: Smoking is an important risk factor for periodontal disease and effects the pathogenesis of the disease. This study evaluated the impact of smoking on gingival crevicular fluid interleukin-8 (IL-8) and lipoxin A4 (LxA4 ) levels in patients with and without periodontal disease. MATERIAL AND METHODS: A total of 122 participants were grouped as follows: smokers with generalized aggressive periodontitis (S-GAgP, n = 15); smokers with chronic periodontitis (S-CP, n = 17); smokers with gingivitis (SG, n = 15); smokers classified as periodontally healthy (SH, n = 15); nonsmokers with generalized aggressive periodontitis (N-GAgP, n = 15); nonsmokers with chronic periodontitis (N-CP, n = 15); nonsmokers with gingivitis (NG, n = 15); and nonsmokers classified as periodontally healthy (NH, n = 15). Gingival index, plaque index, probing pocket depth and clinical attachment level were recorded. Gingival crevicular fluid IL-8 and LxA4 levels were analyzed by ELISA. RESULTS: Gingival crevicular fluid IL-8 levels varied among groups, as follows: S-GAgP>S-CP>SG>SH and N-GAgP>N-CP>NG>NH. The gingival crevicular fluid IL-8 levels were significantly higher in the S-GAgP group compared with the N-GAgP group and in the S-CP group compared with the N-CP group (p < 0.05); differences between the SG and NG and the SH and NH groups were not statistically significant (p > 0.05). Gingival crevicular fluid LxA4 levels also varied among groups, but in an inverse direction when compared with the IL-8 levels, as follows: S-GAgP 0.05). CONCLUSION: The study findings suggest that the observed increases in gingival crevicular fluid IL-8 levels and decreases in gingival crevicular fluid LxA4 levels reflect changes in immune and inflammatory responses that occur as a result of smoking.

Attenuation of bleomycin induced lung fibrosis by erdosteine and inhibition of the inducible nitric oxide synthase.

BACKGROUND AND OBJECTIVES: Despite advances in treatment modalities, the discovery of optimal medical therapies still remains a necessity in the management of pulmonary fibrosis. MATERIAL AND METHODS: The experiments were performed in 35 adult Sprague Dawley rats, randomly allotted into one of five groups (n=7). The control group was treated with 1 ml/kg, 0.9 % saline; the BLM group was given a single dose of BLM (2.5 U/kg); the BLM+ER group was treated with ER (10 mg/kg/day po) for 14 days after BLM administration; the BLM+SMT group was treated with i.p injections of SMT (20 mg/kg/ day) for 14 days after BLM administration; the BLM+ER+SMT group was treated with ER and SMT for 14 days after BLM administration. At the end of day 14, the results of histopathological, biochemical, and immunohistochemical investigations were analyzed. RESULTS: Serum TNF-α, nitrate/nitrite, and TBARS levels significantly increased in BLM group compared to control group (p < 0.001, p < 0.001 and p < 0.05 respectively). Lung tissue content of IL-6 was found to be lower in BLM+ER, BLM+SMT and BLM+ER+SMT groups compared to BLM group by immunhistochemical examinations (p < 0.01, p < 0.01 and p < 0.001, respectively). Similarly, the TNF-α reactions (p < 0.01 for each group) and NF-kB expressions were shown to be significantly different among the study groups (p < 0.05, p < 0.05 and p < 0.001, respectively). CONCLUSION: Based on our study, ER and SMT attenuate BLM-induced pulmonary fibrosis; the combination of two agents has a greater protective efficacy against fibrosis than one alone, reducing the inflammatory markers (Tab. 2, Fig. 2, Ref. 31).

Cardioprotective effect of aminoguanidine in combination with steroid therapy after blunt chest trauma.

BACKGROUND: Cardiac contusion is an important cause of mortality after blunt chest trauma (BCT). The aim of this study was to investigate the therapeutic efficacy of the usage of aminoguanidine (AG), in myocardial damage occurring after BCT, alone and in combination with methylprednisolone (MP). METHODS: Thirty-five female Wistar albino rats were randomly assigned to five groups (n = 7) including: sham controls (S); only cardiac contusion (CONT); cardiac contusion treated with methylprednisolone (CONT+MP); cardiac contusion treated with aminoguanidine (CONT+AG); and cardiac contusion treated with methylprednisolone and aminoguanidine (CONT+MP+AG). Seven days following the treatments, heart and serum specimens were evaluated histopathologically, immunohistochemically, and biochemically in all groups. RESULTS: Serum AOPP and Tn-I levels increased significantly after cardiac contusions. Haemorrhage, tissue degeneration, and necrosis development was evident following contusions. Increased iNOS expression in myocardial tissue was significantly decreased in the CONT+AG+MP group compared to CONT+AG and CONT+MP groups (p = 0.001 and p = 0.011, respectively). The combined treatment of AG and MP increased Bcl-2 expression significantly after contusions compared to the other treatment groups. CONCLUSIONS: Combined usage of AG, a selective iNOS inhibitor, with MP, in cardiac contusions, showed a more powerful cardioprotective effect by increasing Bcl-2 expression and reducing iNOS expression (Tab. 3, Fig. 4, Ref. 33).

The relationship between anticancer effect of metformin and the transcriptional regulation of certain genes (CHOP, CAV-1, HO-1, SGK-1 and Par-4) on MCF-7 cell line.

BACKGROUND: 1,1-dimethylbiguanide hydrochloride (biguanide metformin) is a hypoglycemic agent that is widely used in the treatment of Type 2 diabetes. Use of metformin was found to be associated with the lower risk of cancer. It is suggested that metformin has an anticancer and antiproliferative effect and affects the apoptosis by activating the AMPK and inhibiting the mammalian target of rapamycin (mTOR). Although the effects of metformin treatment of various types of cancers are defined with many mechanisms, the literature provides only sufficient information about how it affects the SGK-1, Par-4 and Cav-1 mRNA expressions and the impact of this effect on cytotoxicity. The breast cancer is globally one of the most important causes of cancer-related mortality for women. We, therefore investigated the possible effects of metmorfin on proliferation, cytotoxicity and some unfolded protein response (UPR) genes in the breast cancer cells (MCF-7). MATERIALS AND METHODS: We administrated 0.31 mM, 2.5 mM and 10 mM of metformin alone and in combination with 2-DG to the MCF-7 cells and monitored the cell viability and proliferation with real-time cell analyzer system for 48 hours. We also measured CHOP, Cav-1, HO-1, SGK-1 and Par-4 genes mRNA expression levels using Real Time-Polymerase Chain Reaction (RT-PCR). We considered the GAPDH gene as reference gene and the control groups as calibrator. We performed an analysis for relative gene expressions of the study groups. RESULTS: Metformin caused transcriptional regulation of UPR and tumor-related genes in MCF-7 cells and inhibited the proliferation depending on the dose, resulting in cytotoxic effect. CONCLUSIONS: We consider that administration of metformin with chemotherapeutic agents could be an effective method in treatment of breast cancer through mechanisms such as reduced resistance to chemotherapy and increased cytotoxic activity.

Urinary leukotriene E4 and prostaglandin F2a concentrations in children with migraine: a randomized study.

OBJECTIVES: Pro-inflammatory mediators are thought to play both peripheral and central roles in migraine pathophysiology. Prostaglandins and leukotrienes, known as the eicosanoids, are degradation products of arachidonic acid and constitute signalization components of inflammatory pathways. This study was designed to assess concentrations of leukotriene E4 (LT-E4) and prostaglandin F2a (PG-F2a) in children with migraine. MATERIALS AND METHODS: This study involved patients aged ≤18 years who presented to the Ondokuz Mayis University Children's Hospital with migrainous headache between January and October 2011. Urinary LT-E4 and PG-F2a concentrations were measured in patients during a headache episode and at a headache-free time and in a control group. RESULTS: The patient group consisted of 38 girls and 26 boys aged 5-18 years diagnosed with migraine and having at least 6 months of headache, whereas the control group consisted of 21 girls and 29 boys. Mean ± standard deviation (SD) urinary LT-E4 concentrations were significantly higher in patients during a migraine episode than in controls (1466.8±1052.5 pg/ml vs 811.6±460.0 pg/ml, P<0.001). In patients with migraine, both urinary LT-E4 (P<0.001) and PG-F2a (P=0.021) levels were significantly higher during headache than during non-headache periods. CONCLUSION: Urinary LT-E4 and PG-F2a were both significantly higher in children with migraine during headache than during non-headache periods. The elevation in the levels of these inflammatory mediators was compatible with the hypothesis relating neuroinflammation in trigeminal vascular blood vessels with migraine pathophysiology. Leukotriene antagonists may be effective in the prophylaxis of migraine attacks.

The role of S100B protein, neuron-specific enolase, and glial fibrillary acidic protein in the evaluation of hypoxic brain injury in acute carbon monoxide poisoning.

The main purpose of this study was to assess the role of S100B protein, neuron-specific enolase (NSE), and glial fibrillary acidic protein (GFAP) in the evaluation of hypoxic brain injury in acute carbon monoxide (CO)-poisoned patients. This cross-sectional study was conducted among the patients with acute CO poisoning who referred to the emergency department in a 1-year period. Serum levels of S100B protein, NSE, and GFAP were determined on admission. A total of 55 CO-poisoned patients (mean age ± standard deviation, 45 ± 20.3 years; 60% women) were included in the study. The control group consisted of 25 healthy adults. The patients were divided into two groups according to whether they were conscious or unconscious. The serum levels of S100B, NSE, and GFAP were higher in patients than that in the control group. There was no significant difference between unconscious and conscious patients with respect to these markers. There was a statistically significant difference between the conscious and unconscious patients and the control group in terms of S100B and NSE levels. There was also a statistically significant difference between the unconscious patients and the control group in terms of GFAP levels. Increased serum S100B, NSE, and GFAP levels are associated with acute CO poisoning. These biomarkers can be useful in assessing the clinical status of patients with CO poisoning.

The effects of α-tocopherol on oxidative damage and serum levels of Clara cell protein 16 in aspiration pneumonitis induced by bile acids.

Our aim in this study is to examine the effects of α-tocopherol (AT) on rats with aspiration pneumonitis induced with bile acids (BAs). The animals were divided in to four groups, namely saline group (n = 7), saline + AT group (n = 7), BA group (n = 7), and BA + AT group (n = 7). Saline and BA groups aspirated intratracheally with 1 ml/kg saline and 1 ml/kg bile acids, respectively. AT was given at 20 mg/kg/day dosage for 7 days to the groups. AT group was given 20 mg/kg/day AT for 7 days. Malondialdehyde (MDA), Clara cell protein 16 (CC-16), catalase (CAT), superoxide dismutase (SOD), as well as peribronchial inflammatory cell infiltration, alveolar septal infiltration, alveolar edema, alveolar exudate, alveolar histiocytes, and necrosis were evaluated. The CAT activity of the BA group was significantly lower than the saline group. In the BA + AT group, there was a significant increase in SOD and CAT activities when compared with that of the BA group. The CC-16 and MDA contents in the BA group were significantly higher than in the saline group. The CC-16 and MDA levels of the BA + AT group were significantly lower than BA group. Histopathologic changes were seen in BA group, and there was a significant decrease in the BA + AT group. In conclusion, AT might be beneficial in the treatment of aspiration pneumonitis induced by BAs because AT decreased oxidative damage and resulted in a decrease in CC-16 levels.