Decreased serum allopregnanolone and progesterone levels in male patients with bipolar disorder and their effects on cognitive functions.

The progression of bipolar disorder (BD) is characterized by recurrent episodes of depression, mania, and hypomania, thus affecting the daily functionality of individuals. Previous studies have shown that a large proportion of patients diagnosed with BD who are in clinical remission experience significant functional disorders. The present study aimed to investigate the relationships between cognitive impairment and serum progesterone, allopregnanolone and BDNF levels in male bipolar disorder patients who are in the euthymic period. Our study included 41 euthymic male patients with bipolar disorder and 40 age, sex, body mass index (BMI) and smoking-matched male healthy control subjects. Neuropsychiatric tests such as the Stroop Test TBAG Form, Auditory Verbal Digit Span Test- Form B (VADS-B) and Cancellation Test were administered to all participants, and 5-7 ml of peripheral venous blood sample was taken from all participants. Serum allopregnanolone, progesterone and BDNF levels were also measured in all participants. Serum allopregnanolone and progesterone levels were found to be lower in bipolar patients, and it was observed that the serum level of allopregnanolone decreased as the disease duration increased. The serum BDNF levels were similar between groups. The cognitive functions assessed using the Stroop, VADS-B and cancellation tests were found to be better in healthy subjects. The neurocognitive test performances of all participants were strongly positively correlated with allopregnanolone levels. The present study supports the hypothesis that allopregnanolone acts as an endogenous mood stabilizer.

Prenatal immobility stress: Relationship with oxidative stress, inflammation, apoptosis, and intrauterine growth restriction in rats.

BACKGROUND: Prenatal stress is a significant risk factor affecting pregnant women and fetal health. In the present study, we aimed to investigate the effect of immobility stress at different periods of pregnancy on oxidative stress, inflammation, placental apoptosis and intrauterine growth retardation in rats. METHODS: Fifty adult virgin female Wistar albino rats were used. Pregnant rats were exposed to 6 h/day immobilization stress in a wire cage at different stages of pregnancy. Groups I and II (Day 1-10 stress group) were sacrificed on the 10th day of pregnancy, and Group III, Group IV (10-19th-day stress group), and Group V (1-19th-day stress group) were sacrificed on the 19th day of pregnancy. Inflammatory cytokines, including interleukin-6 (IL-6) and interleukin-10 (IL-10), serum corticotropin-releasing hormone (CRH), and corticosterone levels were measured by enzyme-linked immunosorbent assay. Malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) levels in the placenta were spectrophotometrically measured. Histopathological analyses of the placenta were evaluated by hematoxylin and eosin staining. Tumor necrosis factor-alpha (TNF-α) and caspase-3 immunoreactivity in placenta tissues were determined by the indirect immunohistochemical method. Placental apoptosis was determined by the TUNEL staining method. RESULTS: We found that the immobility stress during pregnancy significantly increased serum corticosterone levels. Our results showed that the immobility stress diminished the number and weight of fetuses in rats compared to the non-stress group. The immobility stress caused significant histopathological changes in the connection zone and labyrinth zone and increased placental TNF-α and caspase-3 immunoreactivity and placental apoptosis. In addition, immobility stress significantly increased the levels of pro-inflammatory IL-6 and MDA and caused a significant decrease in the levels of antioxidant enzymes such as SOD, CAT, and anti-inflammatory IL-10. CONCLUSIONS: Our data suggest that immobility stress causes intrauterine growth retardation by activating the hypothalamic-pituitary-adrenal axis and deteriorating placental histomorphology and deregulating inflammatory and oxidative processes.

Serum chromogranin A levels are associated with the SYNTAX score in coronary artery disease.

OBJECTIVE: In this article, we investigated the association of chromogranin A with coronary artery disease. METHODS: Biochemical parameters and chromogranin A levels obtained from peripheral blood samples during coronary angiography were analyzed in 90 patients. Patients were classified into two groups, namely, SYNergy between PCI with TAXUS and Cardiac Surgery score ≥1 (n=45) and SYNergy between PCI with TAXUS and Cardiac Surgery score=0 (n=45). This is a cross-sectional, prospective study. RESULTS: Serum chromogranin A levels were significantly higher in the group with SYNergy between PCI with TAXUS and Cardiac Surgery score ≥1 compared to the group with SYNergy between PCI with TAXUS and Cardiac Surgery score=0 (1381.5±418.9 ng/mL and 1121.2±290.7 ng/mL, respectively; p=0.002). Serum chromogranin A levels were correlated with SYNergy between PCI with TAXUS and Cardiac Surgery score (r=0.556, p<0.04). ROC analysis showed that the area under the curve for serum chromogranin A levels was 0.687 (p=0.007), and the best cutoff value of 1,131 ng/mL had a sensitivity of 67% and a specificity of 65% for the prediction of coronary artery disease. CONCLUSION: Serum chromogranin A levels were increased in coronary artery disease patients with SYNergy between PCI with TAXUS and Cardiac Surgery score ≥1. Increasing serum chromogranin A levels are proportional to the SYNergy between PCI with TAXUS and Cardiac Surgery score.

Is meteorin-like (Metrnl) a novel biomarker to distinguish patients with obstructive sleep apnea (OSA) and patients with OSA at vascular risk.

PURPOSE: Metrnl, a newly discovered adipokine with significant expression in white adipose tissue, promotes energy expenditure and contributes to the development of cardiovascular disorders. Endocan is a surrogate marker for endothelial dysfunction and is linked to cardiovascular risk factors. Higher cardiovascular morbidity and mortality have been linked to obstructive sleep apnea (OSA). In this study, we investigated the potential of serum Metrnl and endocan as biomarkers to identify patients with OSA who are at increased cardiovascular risk and differentiate them from healthy controls. METHODS: The study included the evaluation of serum levels of endocan and Metrnl in individuals with OSA and healthy controls. All participants underwent full polysomnography to evaluate their sleep, and carotid intima-media thickness (CIMT) was measured in each of them. RESULTS: Patients with OSA (n = 117) had considerably lower levels of Metrnl and significantly higher levels of endocan than controls (n = 59). Once confounding factors were taken into account, both Metrnl and endocan were effective predictors of OSA. Additionally, the severity of OSA, as determined by the apnea-hypopnea index (AHI), was linked to Metrnl and endocan levels. The study also found a significant and independent inverse association between CIMT and Metrnl, along with a positive association with endocan after making multiple adjustments. Furthermore, there was a significant and independent connection between CIMT and AHI. CONCLUSION: Based on these findings, Metrnl and endocan have the potential to be valuable markers for identifying patients with OSA who are at increased risk of early vascular damage.

Cardiovascular disease risk prediction in scleroderma.

OBJECTIVE: Cardiovascular disease risk prediction in scleroderma is important. In this study of scleroderma patients, the aim was to investigate the relationship between cardiac myosin-binding protein-C, sensitive troponin T, and trimethylamine N-oxide and cardiovascular disease risk with the Systematic COronary Risk Evaluation 2 model of the European Society of Cardiology. METHODS: Systematic COronary Risk Evaluation 2 risk groups of 38 healthy controls and 52 women with scleroderma were evaluated. Cardiac myosin-binding protein-C, sensitive troponin T, and trimethylamine N-oxide levels were analyzed with commercial ELISA kits. RESULTS: In scleroderma patients, cardiac myosin-binding protein-C and trimethylamine N-oxide levels were higher than healthy controls but sensitive troponin T was not (p<0.001, p<0.001, and p=0.274, respectively). Out of 52 patients, 36 (69.2%) were at low risk, and the other 16 (30.8%) patients were at high-moderate risk with the Systematic COronary Risk Evaluation 2 model. At the optimal cutoff values, trimethylamine N-oxide could discriminate high-moderate risk with sensitivity 76%, specificity 86% and cardiac myosin-binding protein-C with sensitivity 75%, specificity 83%. Patients with high trimethylamine N-oxide levels (≥10.28 ng/mL) could predict high-moderate- Systematic COronary Risk Evaluation 2 risk 15 times higher than those with low trimethylamine N-oxide (<10.28 ng/mL) levels (odds ratio [OR]: 15.00, 95%CI 3.585-62.765, p<0.001). Similarly, high cardiac myosin-binding protein-C (≥8.29 ng/mL) levels could predict significantly higher Systematic COronary Risk Evaluation 2 risk than low cardiac myosin-binding protein-C (<8.29 ng/mL) levels (OR: 11.00, 95%CI 2.786-43.430). CONCLUSION: Noninvasive cardiovascular disease risk prediction indicators in scleroderma, cardiac myosin-binding protein-C, and trimethylamine N-oxide could be recommended to distinguish between high-moderate risk and low risk with the Systematic COronary Risk Evaluation 2 model.

Investigation of serum E-Cadherin, VEGF121, Survivin, Tenascin C and Tetraspanin 8 levels in patients with glioblastoma.

OBJECTIVE: The aim of this study is to determine biomarkers, which may be used in order to understand the pathophysiology, the diagnosis, progression surveillance/monitoring, and treatment efficacy of high graded glial tumors. BACKGROUND: Radiological imaging in the diagnosis and relapse surveillance of glial tumors is sometimes insufficient. There is need for additional methods of diagnosis and surveillance in order to rule out contradictory circumstances. METHOD: Using enzyme like immune sorbent assay method, E-Cadherin, Tenascin C, Tetraspanin 8, Survivin and VEGF121 levels were investigated in serum and tumor tissues of 28 patients diagnosed with pathological glioblastoma, and in the serum of 26 healthy individuals. Correlation between tumor tissue values and Ki67 percentage, and P53 mutation, and difference between unhealthy and healthy serum levels were sought. RESULTS: It was found out that E-Cadherin and VEGF 121 levels in the unhealthy serum were high in comparison to the control group (p 0.05). CONCLUSION: EC and VEGF121 are biomarkers, which have the potential to be used in the diagnosis, recurrence and treatment follow-up in high graded glial tumors (Tab. 2, Fig. 1, Ref. 37). Text in PDF www.elis.sk Keywords: E-Cadherin, VEGF, Survivin, Tenascin-C, Tetraspanin, glioblastoma.

Low Antioxidant Enzyme Levels and Oxidative Stress in Laryngopharyngeal Reflux (LPR) Patients.

OBJECTIVE: Laryngopharyngeal reflux disease (LPR) is a characterized by symptoms different from gastroesophageal reflux disease (GERD). LPR can causes chronic mucosal inflammation which may lead to an increase in cytokine production, and a systemic decrease in antioxidant enzyme levels. Our aim in this study is to evaluate antioxidant enzyme levels in patients with LPR. METHODS: Reflux Symptom Index (RSI) questionnaire, extraesophageal symptom questionnaire which is included in RSI and Reflux Finding Score (RFS) evaluation with 70° rigid laryngoscope were performed to patients who applied to the otolaryngology clinic with a typical LPR complaint, and 60 patients who had an RSI score above 13 and an RFS score above 7 were included in the study. Thirty people consisting of healthy volunteers were included in the control group. Antioxidant enzyme SOD, GSH-Px and CAT levels were measured in the blood serum of the patients and compared with the control group. Results obtained from biochemical tests were expressed as mean ± SE. Descriptive statistical methods (mean ± standard error) were used for the independent t test for the control and study group. P < 0.05 was considered statistically significant. RESULTS: In the LPR group, 28 (46%) were women, 32 (53%) were men, and age range was 21-60, average age was 36.45 ± 1.147.There was no significant difference between LPR and control group in terms of age, gender and Body Mass Index (BMI). In the LPR group, the lowest score for RSI was 14 and the highest score was 39. The average RSI was 23.67. RFS ranges from 8-22. The mean RFS was 13.50. A highly significant statistical correlation was observed between RSI and total RFS (P < 0.001). There was a significant difference between the antioxidant enzyme levels of the control group and the LPR group. Antioxidant enzyme levels of the control group were SOD 274.10 ± 26.836 U / L, GSH-Px 174.20 ± 20.699 µU / mL and CAT 42.2898 ± 20.699 KU / L. Antioxidant enzyme level results of the LPR group were SOD 147 ± 14.022 U / L (P < 0.01), GSH-Px 88.28 ± 9.113 µU / mL (P < 0.01) and CAT 12.67 ± 0.799 KU / L (P < 0.001). The RSI results ranges from 4 to 39 and the RFS from 8 to 22. Antioxidant enzyme levels demonstrated fairly consistent reliability with individual variables from both RFS and RFS. There was also a highly significant statistical correlation between RSI and RFS. CONCLUSION: We found that the antioxidant enzymes SOD, GPX and catalase enzyme levels were significantly lower in LPR patients. Treatment modalities to reduce oxidative stress (OS) in LPR should be investigated.

Procollagen C-proteinase enhancer-1 and renal failure in multiple myeloma.

BACKGROUND: Renal involvement is present in approximately 50% of multiple myeloma (MM) cases and is associated with a poor prognosis. Procollagen C-Proteinase Enhancer 1 (PCPE-1) is an extracellular matrix glycoprotein that has been shown to increase collagen production by enhancing the activity of Procollagen C-Proteinase (PCP) involved in collagen fibrillogenesis and contribute to the fibrotic process. This study investigates the relationship between PCPE-1 and renal function in myeloma patients. METHODS: Eighty-one adults, consisting of 61 patients diagnosed with MM and 20 healthy controls, were included in this cross-sectional study. The MM patients with renal injury (RI) were classified as "MM-RI( +)" and those with no RI as "MM-RI(-)". RESULTS: The median serum PCPE-1 level was 10.7 (5.0-39.4) ng/mL for the entire study population, 9.9 (5.0-13.6) ng/mL for the control group, 10.0 (6.4-22.5) ng/mL for the MM-RI(-) group, and 11.4 (8.1-39.4) ng/mL for the MM-RI( +) group. The difference between the control group and MM-RI( +) group was statistically significant (p < 0.013). PCPE-1 levels negatively correlated with estimated glomerular filtration rate (eGFR), serum albumin, and hemoglobin levels but positively correlated with serum creatinine and CRP levels in the entire study population. Among MM patients, only serum phosphorus and beta-2-microglobulin (ß2M) were positively correlated with PCPE-1. PCPE-1 levels was not affected by other parameters in the entire study population and in the MM group. CONCLUSIONS: Although serum PCPE-1 was higher in the MM-RI( +) group, it was thought to be associated with low GFR reflecting non-specific kidney injury rather than myeloma-related kidney injury.

C-Reactive Protein-to-Albumin Ratio as a Prognostic Inflammatory Marker in COVID-19.

Objectives As a result of developed generalized inflammation, the main prognostic factor determining morbidity and mortality in coronavirus disease 2019 (COVID-19) patients is acute respiratory distress syndrome. The purpose of our study was to define (1) the laboratory tests that will contribute to the diagnosis and follow-up of COVID-19 patients, (2) the differences between the laboratory-confirmed (LC), unconfirmed (LUC), and control (C) groups, and (3) the variation between groups of acute-phase reactants and biomarkers that can be used as an indicator of disease severity and inflammation. Materials and Methods A total of 102 patients undergoing treatment with COVID-19 interim guidelines were evaluated. Reverse transcriptase-polymerase chain reaction (RT-PCR) test was positive in 56 (LC), classified as mild or severe, and negative in 46 (LUC) patients. In addition, 30 healthy subjects (C) with negative RT-PCR tests were also evaluated. All statistical analyses were performed with the SPSS 22.0 program and the p -values for significant findings were less than 0.05. Parametric/nonparametric distribution was determined by performing the Kolmogorov-Smirnov test for all groups. Student's t -test was used for variables with parametric distribution and the Mann-Whitney U-test for variables with the nonparametric distribution. A cut-off level for biomarkers was determined using the ROC (receiver operator characteristic) curve. Results In the LC group, platelet, platecrit, mean platelet volume, platelet diameter width, white blood cell, lymphocyte, eosinophil, neutrophil, immature granulocyte, immature lymphocyte, immature monocyte, large immune cell, and atypical lymphocyte counts among the complete blood count parameters of mature and immature cell counts showed a significant difference according to the C and LUC groups. C-reactive protein, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and C-reactive protein-to-albumin ratio (CAR) indices were significantly elevated in LC patients and were significantly higher in patients classified as severe compared to mild. When CAR optimal cutoff was determined as 0.475, area under the curve was 0.934, sensitivity was 90.91%, specificity was 86.21%, positive predictive value was 92.59%, and negative predictive value was 83.33%. The diagnostic accuracy for CAR was 89.29%. Conclusion The CAR index with the highest diagnostic value and the highest predictability could be the most useful biomarker in the diagnosis and evaluation of disease severity in COVID-19 patients.

Serum Calprotectin Level as an Inflammatory Marker in Newly Diagnosed Hypertensive Patients.

BACKGROUND: Hypertension is one of the leading causes of cardiovascular mortality. Although the pathogenetic process involved is not yet fully understood, the disease involves endothelial damage and inflammation. Calprotectin is an inflammatory marker that rises in parallel with disease activity in conditions such as systemic inflammatory diseases, infection, and atherosclerosis. The purpose of this study was to evaluate inflammation through serum calprotectin levels in newly diagnosed primary hypertension patients. METHODS: Forty-nine newly diagnosed hypertensive patients and 38 healthy adults were included in the study. Patients' office blood pressure values, biochemical findings, and demographic characteristics were recorded. Serum calprotectin levels were measured using ELISA. Parameters affecting serum calprotectin levels and determinants of hypertension were evaluated. RESULTS: Serum calprotectin levels were 242.8 (72.4-524) ng/mL in the control group and 112.6 (67.4-389.8) ng/mL in the hypertensive patient group, the difference being statistically significant (p=0.001). There was no correlation between serum calprotectin levels and other parameters (blood pressure values, age, gender, serum creatinine, uric acid, and calcium levels) in the hypertensive group. A lower serum calprotectin level was found to be independently related to hypertension (ß = -0.009, p=0.005). Serum calprotectin at a cutoff level of 128.6 ng/mL differentiated hypertensives from healthy controls with a sensitivity of 69.4% and specificity of 68.4% (AUC = 0.767). CONCLUSIONS: The results of this study were the opposite of our hypothesis that a higher calprotectin level may reflect subclinical endothelial damage in newly diagnosed hypertensive patients. Further comparative studies involving patients at different stages of hypertension may contribute to clarifying the relationship between calprotectin and hypertension. We conclude that molecular studies seem essential for understanding the place of calprotectin in hypertension-associated inflammation, a complex process.

Toxicological assessment of low-dose bisphenol A, lead and endosulfan combination: chronic toxicity study in male rats.

In the present study, toxic effects, both alone and combined, of bisphenol A (BPA), lead (Pb) and endosulfan (ES) in the low doses were investigated in rat liver and kidney functions. In the study, bisphenol A (BPA), lead (Pb) and endosulfan (ES) were chosen because although they are the chemicals people are most frequently exposed to, no combined toxic effect studies were conducted with these chemicals. Sixty-four male Wistar albino rats were used in the study, and they were randomly divided into eight groups (n = 8 per group); control, BPA (5 mg/kg), Pb (100 ppm), ES (0.61 mg/kg), BPA+Pb, BPA+ES, Pb+ES and BPA+P+ES. The rats were sacrificed after 65 days of treatment. Severe histopathological changes in the liver and kidney tissues were observed in the rats exposed to BPA+Pb+ES combination. Elevated malondialdehyde (MDA) in the liver and decreased superoxide dismutase activity (SOD) in the kidney tissue were detected in the BPA+Pb+ES group compared to those of the control group. It was found that serum alanine aminotransferase (ALT) and blood urea nitrogen (BUN) and creatinine (CREA) levels were higher in the BPA+Pb+ES combination group than the control group. Also, combined exposure of BPA, Pb and ES caused apoptotic cell numbers and inducible nitric oxide (iNOS) to increase in the liver and kidney tissues. The results of the present study suggested that the BPA, Pb and ES caused more dramatic changes to both histological architecture and cell apoptosis in the liver and kidney tissues when there was a combined exposure.

MicroRNA 21 and microRNA 155 levels in resistant hypertension, and their relationships with aldosterone.

AIM: MicroRNAs (miRNAs) are non-coding RNA molecules that serve as regulators following gene expression transcription. While studies have investigated the role of miRNAs in the pathogenesis of essential hypertension (HT), very few have considered their place in the pathogenesis of resistant hypertension (RH). The purpose of this study was to investigate levels of miRNA 21 and miRNA 155 in RH and their relationships with aldosterone. METHOD: Thirty-two normotensive patients, 30 newly diagnosed HT patients, and 20 RH patients were included in the study. Patients' demographic data were recorded, and office blood pressure measurement and 24-h ambulatory blood pressure monitoring (24-h ABPM) were performed. Blood specimens were collected for miRNA 21, miRNA 155 and aldosterone measurement. MiRNA 21 and miRNA 155 levels in the control and patient groups and their relations with other demographic and biochemical parameters were then subjected to analysis. RESULTS: No difference was determined in miRNA 155 levels between the groups, but miRNA 21 and aldosterone levels were significantly higher in the RH group (p < 0.001 and <0.05, respectively). At correlation analysis, miRNA 21 exhibited positive correlation with aldosterone, age, office SBP, 24-h ABPM all-day SBP. A 9.6 copy/uL level for miRNA 21 predicted presence or absence of RH with 95% sensitivity and 71% specificity (AUC:0.823, 95% CI (0.72-0.92). CONCLUSION: The study results revealed significantly higher miRNA 21 and aldosterone in RH patients than in healthy individuals and newly diagnosed hypertensives.

Royal jelly attenuates gastric mucosal injury in a rat ethanol-induced gastric injury model.

The aim of the study was to investigate traditionally used Royal Jelly (RJ) for treating an ethanol-induced gastric ulcer model in rats. A total of 32 Wistar albino male rats were divided into 4 groups of 8: group I = Control, group II = Ethanol, group III = RJ + Ethanol, and group IV = Lansoprazole + Ethanol. In groups II, III, and IV, animals were administered 1 ml of absolute ethanol orally after a 24-h fast to induce ulcer formation. The histopathological changes in the gastric mucosa were determined using hematoxylin-eosin (H&E) staining. Immunohistochemically, inducible nitric oxide (iNOS) and nuclear factor kappa beta (Nf-κß) markings were evaluated in gastric tissue. Cell death in the gastric mucosa was determined by the TUNEL method. Oxidative status markers, superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), and myeloperoxidase (MPO) levels were determined spectrophotometrically. Expression of the interleukin - 1 beta (IL-1ß) and tumor necrosis factor-α (TNF-α) genes in gastric tissues was determined by real-time PCR; and TNF-α, IL-10, and IL-1ß levels were determined. RJ was found to inhibit iNOS and Nf-κß activity in the gastric mucosa and prevent epithelial cell apoptosis. In particular, pro-inflammatory cytokines TNF-α and IL-1ß levels were significantly decreased in the RJ + Ethanol group compared to the Ethanol group. In addition, a decrease in the MPO level indicated that RJ prevented tissue damage, especially by preventing inflammatory cell infiltration. The study demonstrated a possible gastroprotective effect of RJ in a rat ethanol-induced gastric ulcer model.

Relationship between Microfibrillar-Associated Protein 4 Levels and Subclinical Myocardial Damage in Chronic Kidney Disease.

INTRODUCTION: Chronic kidney disease (CKD) is a widespread health problem, in which mortality is most frequently due to cardiovascular diseases. Microfibrillar-associated protein 4 (MFAP4) is an extracellular matrix protein. MFAP4 is involved in several biological processes, particularly the maintenance of vascular integrity and extracellular matrix remodeling. Our review of the literature revealed no data concerning MFAP4 levels in CKD and its relationship with myocardial functions. OBJECTIVE: The purpose of this study was therefore to investigate MFAP4 levels in CKD, parameters affecting these, and the relationship with myocardial functions. MATERIALS AND METHODS: Seventy-nine CKD patients and 30 healthy controls were included in the study. Routine biochemical tests and echocardiography were performed once demographic data had been recorded. Blood specimens were collected for MFAP4 analysis, and the results were subjected to statistical analysis. RESULTS: MFAP4 levels were significantly higher in the patient group than in the control group (p< 0.001). Doppler parameters revealed more frequent LV diastolic impairment in the patient group. Tissue Doppler systolic velocity and global longitudinal strain were significantly impaired, revealing the subclinical LV systolic dysfunction in CKD patients. MFAP4 elevation in the patient group was positively correlated with aortic root (AR), global circumferential strain (GCS), and GCS rate. CONCLUSION: Our results showed MFAP4 elevation in CKD for the first time in the literature, and that this elevation may be related to GCS and AR dilation. We think that, once supported by further studies, MFAP4 may constitute a marker in the evaluation of myocardial functions in CKD.

Effect of hesperetin on inflammatory and oxidative status in trinitrobenzene sulfonic acid-induced experimental colitis model.

In our study, the effect of hesperetin on inflammatory and oxidative status in trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis model was investigated through different methods. Eighteen Wistar albino male rats were divided in to three groups: Group I (Control, n = 8; 1 ml physiological saline), Group II (Colitis, n = 8; 1 ml TNBS), Group III (Hesperetin, n = 8; 1 ml TNBS and 100 mg/kg hesperetin). Macroscopic and microscopic scores were calculated to determine the damage to the colon at the end of the experiment. Serum tumor necrosis factor-α (TNF-α) and tissue interleukin-6 (IL-6) levels were determined using the ELISA method. Myeloperoxidase (MPO), superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) levels were investigated spectrophotometrically. The TUNEL method was used for the detection of apoptotic cells in the colon tissue. Inducible nitric oxide synthase (iNOS) and nuclear factor-kappa-B (NF-ĸß) expression in the colon were determined immunohistochemically. Hesperetin administration has shown to significantly reduce levels of MPO, MDA, and proinflammatory agents (TNF-α, IL-6, and NF-ĸß). It has also been proven to inhibit mucosal apoptosis. This study indicates that hesperetin is protective against TNBS-induced colitis model via antiinflammatory, antioxidant and antiapoptotic effects.

The Effects of Ferulic Acid Against Oxidative Stress and Inflammation in Formaldehyde-Induced Hepatotoxicity.

This study was designed to elucidate the protective effects of ferulic acid (FA) on formaldehyde-induced hepatotoxicity by measuring some routine biochemical parameters, cytokine levels, and oxidative stress-related parameters in addition to YKL-40 in male Wistar albino rats. Tissue superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) activities, and tissue malondialdehyde (MDA) levels were measured. Also, serum YKL-40, TNF-α, IL-6, IL-1ß, IL-8, total protein, albumin, total bilirubin concentrations, and AST, ALT, ALP, and LDH activities were measured. Histological specimens were examined in light microscopy. Formaldehyde significantly increased tissue MDA, and serum cytokine levels and also decreased activities of antioxidant enzymes. FA treatment decreased MDA and cytokine levels and increased activities of antioxidant enzymes. FA also alleviated degeneration due to formaldehyde toxicity. We suggested that FA can be used as a promising hepatoprotective agent against formaldehyde toxicity because of the obvious beneficial effects on oxidative stress parameters.

The effects of melatonin on liver functions in arsenic-induced liver damage.

OBJECTIVE: Arsenic exposure is increasing in communities due to environmental pollution and industrial development. Arsenic is toxic to organ systems because it causes oxidative stress, enzymatic inhibition, and damage to protein structures. The liver, for example, is an organ that may be damaged by arsenic, and this damage may cause various clinical conditions like hepatic failure or cancer. Melatonin is a hormone that acts like an antioxidant, an anti-inflammatory agent, and a cytoprotective agent. In this study, we aimed to evaluate melatonin's protective effects on livers damaged by arsenic toxicity. MATERIALS AND METHODS: Twenty-four Sprague-Dawley male rats were classified into three groups: a control group, an arsenic applied group, and an arsenic plus 10 mg/kg melatonin applied group. At the end of the fifteen-day experiment, the rats were sacrificed. Albumin, interleukin-6 (IL-6), total protein, alanine transaminase, aspartate transaminase, macrophage migration inhibitory factor, and monocyte chemotactic protein-1 measurements were obtained. RESULTS: In rats with liver damage due to arsenic exposure, melatonin administration significantly decreased the levels of IL-6, macrophage migration inhibitory factor, and monocyte chemotactic protein-1 (p<0.001, p=0.02 and p=0.04, respectively). CONCLUSION: After evaluating liver enzymes and inflammatory markers, this study determined that melatonin exposure improves liver tissue damage caused by arsenic exposure, with the degree of improvement varying based on the levels of arsenic exposure.

The Effects of Quercetin on Acute Lung Injury and Biomarkers of Inflammation and Oxidative Stress in the Rat Model of Sepsis.

Experimental studies indicate that sepsis causes remote organ injury although the molecular mechanism has not been clearly defined. In this report, the role of oxidative damage, and inflammation on lung injury, following sepsis model by cecal ligation and puncture, and the effects of quercetin, antioxidant, and anti-inflammatory flavonoid, in the lung tissue were investigated. In the present study, we found that administration of single-dose quercetin before cecal ligation and puncture procedure, while markedly diminishing the levels of YKL-40 and oxidant molecules (xanthine oxidase (XO), nitric oxide (NO), and malondialdehyde (MDA)), increases the antioxidant enzymes levels. Quercetin is beneficial to acute lung injury by decreasing the levels of oxidative stress markers and increasing the antioxidant enzyme activities. Quercetin also causes a decrease in the serum levels of YKL-40 and periostin in the oxidative lung injury induced by the experimental sepsis model.

Effect of CPAP on New Endothelial Dysfunction Marker, Endocan, in People With Obstructive Sleep Apnea.

Obstructive sleep apnea (OSA) is associated with increased cardiovascular (CV) morbidity and mortality. Endocan is a surrogate endothelial dysfunction marker that may be associated with CV risk factors. In this study, we tested whether serum endocan is a biomarker for OSA. Serum endocan levels were measured at baseline in 40 patients with OSA and 40 healthy controls and after 3 months of continuous positive airway pressure (CPAP) treatment in the patients with OSA. All participants were evaluated by full polysomnography. Flow-mediated dilatation (FMD) and carotid intima media thickness (cIMT) were measured in all participants. Endocan levels were significantly higher in patients with OSA than in healthy controls. After adjusting confounders, endocan was a good predictor of OSA. Endocan levels correlated with OSA severity (measured by the apnea-hypopnea index [AHI]). After 3 months of CPAP treatment, endocan levels significantly decreased. Endocan levels were significantly and independently correlated with cIMT and FMD after multiple adjustments. The cIMT and FMD also had significant and independent correlation with AHI. Endocan might be a useful marker for the predisposition of patients with OSA to premature vascular disease.