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Background Endothelin-1 (ET-1) is an agent closely associated with inflammation and has recently been recognized as a significant factor in degenerative processes. This study aimed to investigate the correlation between serum ET-1 level and radiological and clinical manifestations of lumbar disc herniation (LDH) and intervertebral disc degeneration (IDD) pathologies. Methodology The study was conducted with 50 healthy controls and 50 LDH patients. The pain level of the patients was analyzed with the Visual Analog Scale (VAS), and their functionality was analyzed with the Oswestry Disability Index (ODI). The disc degeneration and disc herniation grades were determined using magnetic resonance imaging. Serum ET-1 levels of the participants were measured using the enzyme-linked immunosorbent assay method. Results ET-1 level was significantly higher in the patient group compared to the controls (p < 0.01). A positive correlation was determined between serum ET-1 level and Pfirrmann grade in the patient group (p < 0.01). No correlation was determined between the MacNab grade, VAS, and ODI scores and ET-1 (p = 0.397, p = 0.137, and p = 0.208, respectively). There was no significant difference between the serum ET-1 levels of the patients with or without neurological deficits (p = 0.312). Conclusions The correlation between the serum ET-1 levels and IDD grade suggested that the former could serve as a biomarker to determine the degree of degeneration in the future. However, further research is required to determine the underlying mechanisms.
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The aim of this study was to investigate the effects of melatonin on the serum asymmetric dimethylarginine (ADMA) levels and the expressions of vaspin, visfatin, dimethylarginine dimethylaminohydrolase (DDAH), and signal transducer and activator of transcription-3 (STAT-3) for evaluation of endothelial function and inflammation in the hypercholesterolemic rats. Rats were divided into 5 groups: (1) control, (2) hypercholesterolaemia, (3) melatonin administrated concurrently with cholesterol diet, (4) melatonin administrated only last 2 weeks and fed with cholesterol diet, (5) atorvastatin administered only last 2 weeks fed with cholesterol diet. Although an increase was observed in the expressions of visfatin and STAT-3 and the serum ADMA levels, the vaspin and DDAH protein expressions were found to decrease with hypercholesterolemic diets. Melatonin was determined to restore all the parameters to the normal levels. In conclusion, melatonin may have protective and therapeutic effects on hypercholesterolaemia by regulating vaspin, STAT-3, DDAH, and ADMA signalling pathways and create similar effects with atorvastatin.
Subject(s)
Atherosclerosis , Hypercholesterolemia , Hyperlipidemias , Melatonin , Rats , Animals , Melatonin/pharmacology , Melatonin/therapeutic use , Nicotinamide Phosphoribosyltransferase , Hypercholesterolemia/complications , Hypercholesterolemia/drug therapy , Atorvastatin/pharmacology , Atorvastatin/therapeutic use , Inflammation/drug therapy , Atherosclerosis/drug therapy , Atherosclerosis/etiology , Nitric Oxide/metabolismABSTRACT
Objectives: This study aims to define serum levels of netrin-1 and netrin receptors in patients with fibromyalgia (FM) and osteoarthritis (OA). Patients and methods: This cross-sectional study was conducted with a total of 150 female participants (mean age: 47.2±16.1 years; range, 18 to 89 years) at Firat University between June 2016 and December 2016. The participants were evaluated in three groups: the FM group with 50 patients, the OA group with 50 patients, and the control group, which included 50 healthy volunteers. Netrin-1, netrin receptors (DCC, UNC5B, and UNC5D), interleukin (IL)-6, IL-10, and IL-17 levels were analyzed by the enzyme-linked immunosorbent assay from the serum samples of the participants. Results: The level of serum netrin-1 was significantly lower in the FM group than in the control and OA groups (p<0.01 and p<0.001, respectively). However, the difference between patients with OA and healthy controls in terms of netrin-1 was not statistically significant (p>0.05). In addition, serum levels of netrin receptors and cytokines in the FM group were similar to the control group (p>0.05). However, serum DCC, UNC5D, IL-6, and IL-10 levels were higher in the OA group compared to the control group (p<0.001, p<0.05, p<0.01, and p<0.001, respectively). Conclusion: Serum netrin-1 level is suppressed in FM, which suggests that netrin-1 is influential in FM pathogenesis.
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The aim of this study was to investigate the protective effects of pomegranate extract and tangeretin alone or in combination in DMBA-induced rat breast cancer model. A total of 68 female rats were randomly divided into 8 groups. The first 4 groups were designed as controls for cancer and treatment groups, and the control groups were composed of only control (C), Pomegranate (P), Tangeretin (T), and Pomegranate+Tangeretin (P+T) groups. The other four groups were designed as cancer and treatment groups and were composed of DMBA (D) and DMBA+Pomegranate (D+P), DMBA+Tangeretin (D+T), DMBA+Pomegranate+Tangeretin (D+P+T) groups. Tumor markers and angiogenesis parameters were studied from plasma samples obtained from rats. Histopathological, immunohistochemical, and TUNEL analyses and expressions of proteins affecting apoptosis and cell cycle were determined in breast tissue samples. In the DMBA group, plasma CA15-3, CEA, VEGF, MMP-9, and NF-κB levels were significantly increased compared to the controls, but significant decreases were observed in these parameters except MMP-9 in the treatment groups. It was observed that p53 and Bax expressions significantly increased in both D+P and D+P+T groups compared to the DMBA group, and these findings were supported by Tunel and immunohistochemical findings. Cyclin D1 expressions were found to be significantly decreased only in the D+T group and supported by TUNEL and immunohistochemical findings. Immunohistochemical ER-α and Ki-67 immune reactivities were significantly decreased in all treatment groups compared to the DMBA group. Our results showed that combined application of pomegranate extract and tangeretin may be more beneficial in preventing breast cancer development.
Subject(s)
Flavones/pharmacology , Mammary Neoplasms, Experimental/prevention & control , Plant Extracts/pharmacology , Pomegranate/chemistry , 9,10-Dimethyl-1,2-benzanthracene/adverse effects , Animals , Apoptosis/drug effects , Carcinogens , Chemoprevention , Drug Combinations , Estrogen Receptor alpha/metabolism , Female , Flavones/chemistry , Ki-67 Antigen/metabolism , Mammary Neoplasms, Experimental/pathology , NF-kappa B/metabolism , Plant Extracts/chemistry , Rats , Rats, Sprague-Dawley , Tumor Suppressor Protein p53/metabolism , bcl-2-Associated X Protein/metabolismABSTRACT
Breast cancer is the most common cancer among women in the world and the incidence is increasing alarmingly. It was aimed to determine the effect of raloxifene (RAL) and fluoxetine (FLX) on selected parameters in 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary carcinoma. Thirty-two female Wistar albino rats were assorted into four groups: DMBA (group I), DMBA+RAL (group II), DMBA+FLX (group III), and DMBA+RAL+FLX (group IV). Mammary tissue vascular endothelial growth factor (VEGF), macrophage colony-stimulating factor (M-CSF), matrix metalloproteinase-9 (MMP-9), and tissue inhibitors of matrix metalloproteinase-1 (TIMP-1) levels were determined by the enzyme-linked immunosorbent assay method. The tissue VEGF levels were lower in group IV compared with DMBA group. Decreased M-CSF levels were observed in all therapeutic groups rather than the DMBA group, but the most effective decrease was found in group IV. Compared with the DMBA group, MMP-9 levels were statistically significantly decreased in group II and group IV. However, TIMP-1 levels were higher in the whole therapeutic groups rather than the DMBA group and the most effective increase was observed in group IV. Results of the present study suggest that combined therapy of RAL with FLX might lead to a better outcome targeting breast tumor.
Subject(s)
9,10-Dimethyl-1,2-benzanthracene/toxicity , Antineoplastic Agents/therapeutic use , Carcinogens/toxicity , Fluoxetine/therapeutic use , Mammary Neoplasms, Experimental/drug therapy , Raloxifene Hydrochloride/therapeutic use , Animals , Body Weight/drug effects , Enzyme-Linked Immunosorbent Assay , Female , Mammary Neoplasms, Experimental/chemically induced , Rats , Rats, Wistar , Weight Gain/drug effectsABSTRACT
BACKGROUND: The aim of this study was to evaluate the therapeutic effects of thalidomide and etanercept on lipopolysaccharide (LPS)-induced sepsis in a rat model. METHODS: Thirty male Wistar Albino rats were divided into 5 groups: Control, LPS, LPS+Thalidomide, LPS+Etanercept, and LPS+Thalidomide+Etanercept. The control group was given a 1 mL intraperitoneal (i.p.) injection of 0.9% saline solution. For endotoxic treatment, the rats were injected with a single i.p. dose of LPS (Escherichia coli 0111: B4 (5 mg/kg). Thalidomide (0.5 mg/kg) and etanercept (1 mg/kg) were administered i.p. to the therapeutic groups. Hepatic tissue tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1) and platelet-derived growth factor (PDGF) levels were determined by enzyme-linked immunosorbent assay and malondialdehyde (MDA) levels and total oxidant status (TOS) were measured using appropriate methods. RESULTS: In vivo results exhibited elevated liver tissue TNF-α, IL-6, ICAM-1, PDGF, MDA, and TOS levels in the LPS-treated animals compared with the controls. The analysis of liver tissue supported the findings of biochemical alterations and indicated a therapeutic role for thalidomide and etanercept. Treatment of septic animals with these agents resulted in a remarkable decrease in the selected proinflammatory cytokines, angiogenic factors, and reactive oxygen parameters. CONCLUSION: Restoration of cytokine balance and oxidant status to normal levels following treatment with selected therapeutic agents suggests that thalidomide and etanercept can help to avoid the potentially devastating effects of sepsis.
Subject(s)
Etanercept/pharmacology , Lipopolysaccharides/adverse effects , Sepsis/metabolism , Thalidomide/pharmacology , Animals , Cytokines/analysis , Cytokines/metabolism , Disease Models, Animal , Liver/drug effects , Liver/metabolism , Male , Rats , Rats, WistarABSTRACT
OBJECTIVE: Secondary hyperparathyroidism (SHPT) and anemia are the primary and most common complications in patients receiving hemodialysis (HD). Neutrophil gelatinase-associated lipocalin (NGAL) is a new marker to assess iron deficiency and manage iron therapy for HD patients. The aim of this study was to determine any association between serum NGAL level and anemia without iron deficiency in patients with SHPT on chronic HD. METHODS: Total of 61 SHPT patients on chronic HD were enrolled in the study and divided into 3 groups: mild SHPT group (n=17), moderate SHPT group (n=21), and severe SHPT group (n=23). Hemogram, biochemical assays, and level of ferritin, high sensitivity C-reactive protein (hs-CRP), and NGAL were evaluated in all groups. RESULTS: Serum NGAL level was significantly higher and hemoglobin (Hb) level was significantly lower in severe SHPT patients compared with both mild and moderate SHPT patients. Furthermore, in severe SHPT group, serum NGAL level was significantly positively correlated with serum parathyroid hormone (r=0.79; p=0.00) and hs-CRP (r=0.52; p=0.01) level and negatively correlated with serum Hb (r=-0.56; p=0.00) level. CONCLUSION: SHPT was important factor affecting anemia in HD patients. Even when iron deficiency anemia is excluded in patients with SHPT, there was significant negative correlation between serum NGAL and Hb.
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BACKGROUND: Chronic kidney diseases are known to influence nitric oxide metabolites (NOx) and asymmetric dimethylarginine (ADMA), though the exact mechanism is still poorly understood. AIMS: The purpose of the present study was to examine eNOS Glu298Asp gene polymorphism, plasma NOx and ADMA concentration in subjects with and without End-stage Renal Disease. STUDY DESIGN: Case-control study. METHODS: In this study, genotype distributions of Glu-298Asp in exon 7 of the eNOS gene polymorphisms in 130 hemodialysis and 64 peritoneal dialysis patients were compared with 92 controls. NOx was measured by using the Griess reaction while arginine, ADMA and SDMA measurements were performed by HPLC. Genotyping for eNOS Glu298Asp polymorphism was detected with the polymerase chain reaction and/or polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. RESULTS: When the genotype frequencies of TT and GT genes were compared between both groups, there was no detected statistically important difference, even-though a TT genotype frequency was 27 (20.8%) versus 17 (26.6%), GT heterozygote genotype frequency was 52 (40%) versus 22 (34.4%), and GG homozygote genotype frequency was 51 (39.2%) versus 25 (39.1%), respectively (p>0.05). NOx, SDMA and ADMA concentrations were significantly elevated in subjects with hemodialysis patients as compared to their corresponding controls. Whereas nitrite was found to be significantly decreased in the patient with peritoneal dialysis. CONCLUSION: Not observed any connection between the Glu298Asp polymorphism in the eNOS gene and end-stage Renal Diseases in our study population under different dialysis treatments. However, higher ADMA and SDMA concentrations in subjects with ESRD support the existing hypothesis that NOx overproduction affects endothelial dysfunction. Thus, the reduction of ADMA and SDMA concentrations might play a protective role in ESRD patients.
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PURPOSE: To evaluate the effects of platelet rich plasma (PRP) on the healing of fascia wherein peritonitis has been created. METHODS: Twenty eight Wistar Albino rats were divided into four groups. Only a primary fascial repair following laparotomy was performed on Group 1, a primary fascial repair performed and PRP treatment applied following laparotomy on Group 2, and a fecal peritonitis created following laparotomy and a primary fascial repair carried out on Group 3. A fecal peritonitis was created following laparotomy and primary fascial repair and PRP treatment on the fascia was carried out on Group 4. RESULTS: TNF-α was found to be significantly lower in the control group (Group 1). It was detected at the highest level in the group in which fecal peritonitis was created and PRP applied (Group 4). TGF-ß was determined as being significantly higher only in Group 4. Histopathologically, the differences between the groups in terms of cell infiltration and collagen deposition were not found to be significant. CONCLUSION: When platelet rich plasma was given histologically and biochemicaly as wound healing parameters cellular infiltration, collagen accumulation, and tissue hydroxyiproline levels were not increased but neovascularization, fibroblast activation and TNF Alfa levels were increased and PRP accelerated wound healing.
Subject(s)
Fascia/physiology , Peritonitis/complications , Platelet-Rich Plasma , Wound Healing , Animals , Collagen/drug effects , Collagen/metabolism , Endopeptidases , Fascia/blood supply , Gelatinases/metabolism , Hydroxyproline/analysis , Hydroxyproline/metabolism , Membrane Proteins/metabolism , Models, Animal , Neovascularization, Physiologic , Peritonitis/metabolism , Random Allocation , Rats, Wistar , Serine Endopeptidases/metabolism , Transforming Growth Factor beta/analysis , Transforming Growth Factor beta/metabolism , Tumor Necrosis Factor-alpha/analysis , Tumor Necrosis Factor-alpha/metabolismABSTRACT
ABSTRACT PURPOSE : To evaluate the effects of platelet rich plasma (PRP) on the healing of fascia wherein peritonitis has been created. METHODS: Twenty eight Wistar Albino rats were divided into four groups. Only a primary fascial repair following laparotomy was performed on Group 1, a primary fascial repair performed and PRP treatment applied following laparotomy on Group 2, and a fecal peritonitis created following laparotomy and a primary fascial repair carried out on Group 3. A fecal peritonitis was created following laparotomy and primary fascial repair and PRP treatment on the fascia was carried out on Group 4. RESULTS: TNF-α was found to be significantly lower in the control group (Group 1). It was detected at the highest level in the group in which fecal peritonitis was created and PRP applied (Group 4). TGF-β was determined as being significantly higher only in Group 4. Histopathologically, the differences between the groups in terms of cell infiltration and collagen deposition were not found to be significant. CONCLUSION: When platelet rich plasma was given histologically and biochemicaly as wound healing parameters cellular infiltration, collagen accumulation, and tissue hydroxyiproline levels were not increased but neovascularization, fibroblast activation and TNF Alfa levels were increased and PRP accelerated wound healing.
Subject(s)
Animals , Peritonitis/complications , Wound Healing , Platelet-Rich Plasma , Fascia/physiology , Peritonitis/metabolism , Serine Endopeptidases/metabolism , Random Allocation , Transforming Growth Factor beta/analysis , Transforming Growth Factor beta/metabolism , Collagen/drug effects , Collagen/metabolism , Tumor Necrosis Factor-alpha/analysis , Tumor Necrosis Factor-alpha/metabolism , Rats, Wistar , Gelatinases/metabolism , Neovascularization, Physiologic , Models, Animal , Fascia/blood supply , Hydroxyproline/analysis , Hydroxyproline/metabolism , Membrane Proteins/metabolismABSTRACT
BACKGROUND AND AIMS: Pulmonary thromboembolism (PTE) is a frequent disease with difficult diagnosis and high mortality. Misdiagnosis occurs in 2/3 patients and mortality rates reach up to 30%. The aim of our study was to investigate the role of adiponectin used in emergency service in diagnosis of PTE. MATERIALS AND METHODS: 95 patients with suspected PTE included in the study. Plasma adiponectin and D-dimer levels were measured and chest X-ray and multidetector row computed tomography scan obtained. Diagnosis was supported by vascular filling defect on tomography. Control group consisted of patients with suspected PTE and normal chest computed tomography findings. RESULTS: Mean D-dimer level was 4241.66 ± 1082.98 ng/mL in patients and 2211.21 ± 1765.53 ng/mL in the control group (p ≤ 0.05). Mean adiponectin level was 5.46 ± 4.39 µg/mL in patients and 7.68 ± 4.67 µg/mL in the control group (p ≤ 0.05). Wells and Geneva scores were higher in patients compared to the control group. CONCLUSIONS: As a result, we conclude that lower adiponectin levels have an important role in the diagnosis of PTE.
Subject(s)
Adiponectin/blood , Pulmonary Embolism/blood , Pulmonary Embolism/diagnostic imaging , Tomography, X-Ray Computed , Aged , Female , Fibrin Fibrinogen Degradation Products/metabolism , Heart Rate , Humans , Male , Middle Aged , Pulmonary Embolism/pathology , Radiography, ThoracicABSTRACT
INTRODUCTION: In this study, we aimed to investigate the histological and clinical effect of angiotensin-converting enzyme (ACE) and ACE gene polymorphism in nonalcoholic fatty liver disease (NAFLD) and their roles in the progression of the disease. MATERIALS AND METHODS: Liver function tests, body mass index, waist circumference, lipid parameters, fasting blood glucose (FBG), hemoglobin A1c (HbA1c), homeostasis model assessment-IR (HOMA-IR), ACE, and ACE gene polymorphism were evaluated in the NAFLD group and control group. The study group was evaluated by dividing the group into four subgroups by ACE gene polymorphism (D/D homozygous, I/I homozygous, D/I heterozygous, I/D heterozygous). Liver biopsies were evaluated according to Brunt Classification. RESULTS: A total of 31 patients who were diagnosed with NAFLD and 40 healthy individuals were included in the study. The ACE level was found to be 11.69 ± 1.99 in the NAFLD group and 11.52 ± 1.72 in the control group (p = 0.70). There was a negative correlation between ACE levels and HOMA-IR levels (p = 0.008, r= -0.512). Biochemical parameters were not different among ACE gene polimorphism subgroups, except FBG (between D/D, I/D and D/I, I/D; p = 0.02). When the ACE levels were compared in terms of grade and stage, no significant difference was found (for stage and grade p = 0.68). The ACE gene polymorphism subgroups did not differ by histopathologic findings; grade and stage (for grade p = 0.42, for stage p = 0.92). CONCLUSION: In this study, we could not find a correlation of ACE and ACE gene polymorphism with metabolic risk factors and the disease severity in NAFLD. HOW TO CITE THIS ARTICLE: Tekatas DD, Bahcecioglu IH, Ispiroglu M, Sahin A, Ilhan N, Yalniz M, Demirel U. Role of Renin-Angiotensin-converting Enzyme Level and ACE Gene Polymorphism in Patients with Nonalcoholic Fatty Liver Disease. Euroasian J Hepato-Gastroenterol 2016;6(2):137-142.
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OBJECTIVE: Recent studies indicate a relationship between early membrane rupture (EMR) and proinflammatory cytokines like tumor necrosis factor (TNF) and interleukin (IL) and angiogenic factors like vascular endothelial growth factor (VEGF). In this study, we aimed to investigate the relationship between EMR and maternal and cord blood plasma levels of TNF-alpha, IL-1 beta and VEGF. METHODS: This prospective, cross-sectional study was conducted with 85 pregnant women. The patients were divided into four groups as Group I (term EMR group, n = 21), Group II (preterm EMR group, n = 23), Group III (preterm non-EMR group, n = 19) and Group IV (term non-EMR group, n = 22). Plasma levels were assayed with ELISA method. RESULTS: IL-1 beta levels were significantly lower, but TNF-alpha levels were significantly higher in maternal and cord plasma of EMR participants compared to non-EMR participants. There was no significant difference for VEGF levels. Cord plasma TNF-alpha levels were significantly higher than maternal plasma levels in EMR participants and cord plasma. VEGF levels were significantly higher than maternal levels in all participants. CONCLUSIONS: Higher TNF-alpha levels in our EMR participants indicate an inflammatory process during EMR. Higher cord plasma VEGF levels may point out placental or fetal production. Further studies conducted with expanded populations are needed to discuss our results.
Subject(s)
Fetal Blood/metabolism , Fetal Membranes, Premature Rupture/blood , Interleukin-1beta/blood , Tumor Necrosis Factor-alpha/blood , Vascular Endothelial Growth Factor A/blood , Adult , Cross-Sectional Studies , Female , Humans , Infant, Newborn , Interleukin-1beta/analysis , Mothers , Pregnancy/blood , Tumor Necrosis Factor-alpha/analysis , Vascular Endothelial Growth Factor A/analysis , Young AdultABSTRACT
AIM/BACKGROUND: Pistacia terebinthus is used as a coffee substitute in the East and Southern Anatolia regions of Turkey. It contains unsaturated fatty acids, tocopherols, polyphenols and carotenoids. P. terebinthus has anti-inflammatory and potential antioxidant activity. In this study we evaluated the protective effects of P. terebinthus coffee (PTC) on thioacetamide (TAA)-induced liver injury in rats. MATERIALS AND METHODS: Twenty-eight male Sprague-Dawley rats were equally randomized into four groups. Chronic liver injury was induced with TAA (100 mg/kg i.p. three times weekly). The first group of rats served as control and received only tap water (G1), and the remaining groups of rats received PTC, p.o (G2); TAA (G3); TAA plus PTC, p.o (G4), respectively. RESULTS: After 8 weeks, PTC intake significantly reduced fibrosis/inflammation scores (p PTC intake reduced transforming growth factor beta (TGF-ß) concentrations in the liver (p PTC intake. DISCUSSION AND CONCLUSION: PTC intake provided beneficial effects against TAA-induced liver injury in rats. PTC probably suppresses the proinflammatory cytokines through NF-κB signaling pathway.
Subject(s)
Inflammation/drug therapy , Liver Cirrhosis, Experimental , Liver , Oxidative Stress/drug effects , Pistacia , Teas, Herbal , Triterpenes/pharmacology , Animals , Antioxidants/pharmacology , Disease Models, Animal , Liver/drug effects , Liver/metabolism , Liver/pathology , Liver Cirrhosis, Experimental/chemically induced , Liver Cirrhosis, Experimental/metabolism , Liver Cirrhosis, Experimental/physiopathology , Liver Cirrhosis, Experimental/prevention & control , Male , Noxae/toxicity , Rats , Rats, Sprague-Dawley , Thioacetamide/toxicity , Transforming Growth Factor beta/metabolism , Treatment OutcomeABSTRACT
PURPOSE: Vascular access (VA) devices may contribute to chronic inflammation in hemodialysis (HD). Pentraxin 3 (PTX3) is a recently discovered acute phase protein that responds more rapidly than other inflammatory markers. This study compared PTX3 and other markers between HD patients and healthy controls. METHODS: The study population included 30 patients with tunneled permanent catheter (TPC), 30 patients with arteriovenous fistula (AVF) and 30 healthy controls. Hemogram, biochemical assays, ferritin, high sensitive C-reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α) and PTX3 were evaluated in all groups. RESULTS: PTX levels were highest in HD patients with TPC, intermediated in HD patients with AVF and lowest in healthy controls (5.2 + 2.4 vs. 3.1 + 1.3 vs. 1.8 + 0.7, p<0.001 for all comparisons). PTX3 levels correlated strongly to hs-CRP (r = 0.857) and moderately to TNF-α, NLR, ferritin and total neutrophil count. PTX3 and albumin levels had a negative correlation. PTX3 levels were higher in patients with 8 months of TPC than those with 7 months or less. CONCLUSIONS: PTX3 levels are significantly elevated in all patients on HD, but presence and extended duration of TPC are associated with incrementally higher levels of PTX3 and other inflammatory markers. PTX3 and NLR may be useful in assessing chronic inflammatory states in HD.
Subject(s)
C-Reactive Protein/metabolism , Catheterization/instrumentation , Catheters, Indwelling , Inflammation Mediators/blood , Inflammation/blood , Renal Dialysis , Serum Amyloid P-Component/metabolism , Vascular Access Devices , Adult , Aged , Arteriovenous Shunt, Surgical , Biomarkers/blood , Case-Control Studies , Catheterization/adverse effects , Equipment Design , Female , Humans , Inflammation/diagnosis , Inflammation/etiology , Male , Middle Aged , Risk Factors , Time Factors , Treatment Outcome , Up-Regulation , Young AdultABSTRACT
The cholesteryl ester transfer protein (CETP) plays a crucial role in high-density lipoprotein (HDL) metabolism. Genetic variants that alter CETP concentration may cause significant alterations in HDL-cholesterol (HDL-C) concentration. In this case-control study, we analyzed the genotype frequencies of CETP Taq1B polymorphisms in coronary artery disease patients (CAD; n=210) and controls (n=100). We analyzed the role of the CETP Taq1B variant in severity of CAD, and its association with plasma lipids and CETP concentration. DNA was extracted from 310 patients undergoing coronary angiography. The Taq1B polymorphism was genotyped using polymerase chain reaction-restriction fragment length polymorphism (RFLP) analysis. Lipid concentrations were measured by an auto analyzer and CETP level by a commercial enzyme-linked immunosorbent assay (ELISA) kit. In our study population, the B2 allele frequency was higher in control subjects than patients with single, double or triple vessel disease. B2B2 genotype carriers had a significantly higher high-density lipoprotein cholesterol (HDL-C) concentration than those with the B1B1 genotype in controls (51.93±9.47versus 45.34±9.93; p<0.05) and in CAD patients (45.52±10.81 versus 40.38±9.12; p<0.05). B2B2 genotype carriers had a significantly lower CETP concentration than those with the B1B1 genotype in controls (1.39±0.58 versus 1.88±0.83; p< 0.05) and in CAD patients (2.04±1.39versus 2.81±1.68; p< 0.05). Our data suggest that the B2 allele is associated with higher concentrations of HDL-C and lower concentrations of CETP, which confer a protective effect on coronary artery disease.
Subject(s)
Cholesterol Ester Transfer Proteins/genetics , Coronary Artery Disease/genetics , DNA Restriction Enzymes/genetics , Deoxyribonucleases, Type II Site-Specific/genetics , Polymorphism, Genetic/genetics , Severity of Illness Index , Aged , Case-Control Studies , Cholesterol Ester Transfer Proteins/physiology , Cholesterol, HDL/metabolism , Coronary Angiography , Coronary Artery Disease/epidemiology , Coronary Artery Disease/physiopathology , DNA Restriction Enzymes/physiology , Deoxyribonucleases, Type II Site-Specific/physiology , Female , Gene Frequency/genetics , Genotype , Humans , Lipid Metabolism/physiology , Lipoproteins, HDL/metabolism , Male , Middle Aged , Pilot Projects , Turkey/epidemiologyABSTRACT
The polyphenol curcumin has several pharmacological effects, including antioxidant, anti-inflammatory and anti-cancer features. In this study, we evaluated the effects of curcumin in cisplatin-induced nephrotoxicity in rats. Male Wistar rats were divided into four groups: (1) control; (2) cisplatin (7 mg/kg body weight, intraperitoneal as a single dose); (3) curcumin (100 mg/kg via gavage, for 10 days); and (4) cisplatin and curcumin. The cisplatin-treated rats exhibited kidney injury manifested by increased serum urea and creatinine (p<0.05). The kidney tissue from the cisplatin treated rats also exhibited a significant increase in the malondialdehyde (MDA) levels (p<0.05). The treatment with curcumin prevented a rise in the serum urea, creatinine and MDA levels when compared to the control group kidneys (p<0.05). The analysis the nicotinamide phosphoribosyltransferase (NAMPT) and sirtuin (SIRT) proteins (SIRT1, SIRT3 and SIRT4), which play important roles in the resistance to stress and the modulation of the threshold of cell death, showed similar trends (p<0.05). In the cisplatin-only treated rats, the induced renal injury decreased the levels of the NAMPT and SIRT proteins. Conversely, the curcumin increased the levels of the NAMPT and SIRT proteins in the cisplatin-treated rats (p<0.05). These data suggest that curcumin can potentially be used to reduce chemotherapy-induced nephrotoxicity, thereby enhancing the therapeutic window of cisplatin.
Subject(s)
Curcumin/pharmacology , Kidney Diseases , Kidney/pathology , Animals , Anti-Inflammatory Agents/pharmacology , Antineoplastic Agents/toxicity , Antioxidants/pharmacology , Blood Urea Nitrogen , Cisplatin/toxicity , Creatinine/blood , Glutathione/metabolism , Kidney Diseases/chemically induced , Kidney Diseases/drug therapy , Kidney Diseases/metabolism , Kidney Diseases/pathology , Male , Nicotinamide Phosphoribosyltransferase/metabolism , Rats , Rats, Wistar , Sirtuins/metabolism , Treatment OutcomeABSTRACT
BACKGROUND AND AIM: An association between circulating adipocyte fatty acid-binding protein (A-FABP) levels and coronary artery disease (CAD) has been reported. In this case-control study, we investigated the relationship between plasma levels of A-FABP and the severity of CAD in Turkish subjects. We also assessed its relationship to alternative biomarkers. METHODS: Two hundred and eighty patients undergoing coronary angiography were enrolled in the study. By means of coronary angiography, the study population was divided into subjects without any angiographically detectable CAD (no vessel disease; n = 88) and individuals with single-vessel disease (n = 65), or double- or triple-vessel disease (n = 127). Lipid concentrations were measured by an autoanalyser and A-FABP, lipoprotein associated phospholipase A2 (Lp-PLA2), oxidised-low density lipoprotein (ox-LDL) and high-sensitivity C-reactive protein (hsCRP) levels by a commercial enzyme-linked immunosorbent assay (ELISA) kit. RESULTS: In our study population, total cholesterol and LDL cholesterol levels did not differ significantly between the groups. Levels of high density lipoprotein cholesterol, A-FABP, Lp-PLA2, ox-LDL and hsCRP were significantly different among groups. The higher levels of A-FABP, Lp-PLA2, ox-LDL and hsCRP levels were shown in patients with double/triple-vessel disease. There was not a significant correlation between A-FABP and other biomarkers in CAD patients. CONCLUSIONS: Initially, plasma levels of A-FABP were significantly elevated in CAD patients with double/triple-vessel disease. Our results demonstrated alterations in A-FABP levels with severity of CAD and, therefore, indirectly support the hypothesis of an active role for A-FABP in the pathogenesis of CAD.
ABSTRACT
BACKGROUND: Neutrophil gelatinase-associated lipocalin (NGAL) is a member of lipocalin family and released from many tissues and cells. We aimed to investigate the relationship among serum NGAL levels, the inflammation markers (IL-6, hs-CRP, TNF-α) and different vascular access types used in dialysis patients. METHODS: The study population included 90 patients and 30 healthy age-matched controls. The patients were divided into three groups (I, II, III) and group IV included the controls. In group I and II, the patients were with central venous permanent catheter and arterio-venous fistula, respectively. Group III included 30 patients with chronic renal failure. Hemogram, biochemical assays, ferritin, IL-6, hs-CRP, TNF-α, and NGAL were evaluated in all groups. RESULTS: Serum NGAL levels were markedly higher in group I than in group II (7645.80 ± 924.61 vs. 4131.20 ± 609.87 pg/mL; p < 0.05). Positive correlation was detected between NGAL levels and duration of catheter (r: 0.903, p: 0.000), hs-CRP (r: 0.796, p: 0.000), IL-6 (r: 0.687, p: 0.000), TNF-α (r: 0.568, p: 0.000) levels and ferritin (r: 0.318, p: 0.001), whereas NGAL levels were negatively correlated with serum albumin levels (r: -0.494, p: 0.000). In multiple regression analysis, duration of catheter hs-CRP and TNF-α were predictors of NGAL in hemodialysis patients. CONCLUSION: Inflammation was observed in hemodialysis patients and increases with catheter. Our findings show that a strong relationship among serum NGAL levels, duration of catheter, hs-CRP and TNF-α. NGAL may be used as a new inflammation marker in hemodialysis patients.
Subject(s)
Arteriovenous Shunt, Surgical/adverse effects , Central Venous Catheters/adverse effects , Inflammation , Kidney Failure, Chronic/therapy , Lipocalins/blood , Proto-Oncogene Proteins/blood , Renal Dialysis , Acute-Phase Proteins , Adult , Biomarkers/blood , C-Reactive Protein/analysis , Female , Humans , Inflammation/blood , Inflammation/etiology , Interleukin-6/blood , Kidney Failure, Chronic/blood , Lipocalin-2 , Male , Middle Aged , Renal Dialysis/adverse effects , Renal Dialysis/methods , Statistics as Topic , Tumor Necrosis Factor-alpha/bloodABSTRACT
Solid organ injuries following blunt trauma are frequently encountered. The use of non-operative approach is gradually increasing. Thus, research on the methods that could enhance healing in solid organ injuries is in progress. Agents known to have antioxidant property were used after an experimentally induced blunt hepatic trauma. Thirty-two Wistar albino rats weighing 200 g were dropped from a height of 40 cm on to the right upper abdominal quadrant to produce a grade II-III hepatic injury. Rats were divided into control, Zn-administered, Cu-administered, and vitamin complex-administered groups, with eight rats in each. Aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) levels were measured in the blood samples. The percentage of cells displaying Ki-67 nuclear staining was estimated. The sections were stained with hematoxylin and eosin and the degree of inflammation in the samples was semi-quantitatively assessed. Treatment with zinc, copper, and Cernevit® caused varying levels of decrease in AST, ALT, and LDH levels compared to the control group. Ki-67 positivity was significantly lower in group I compared with groups II and III (p = 0.002). Ki-67 positivity was significantly higher in group II compared to the other groups (p < 0.05). A marked improvement was observed in inflammation in group II. Copper and zinc treatment decreased inflammation as well as blood levels of AST and ALT, and enhanced the healing of traumatized hepatic tissue. However, Cernevit® reduced only the degree of inflammation.