The role of CRP and inflammation in the pathogenesis of age-related macular degeneration

Age-related macular degeneration (AMD) is a complex, degenerative and progressive disease invol-ving the multiple genetic and environmental factors that can result in severe visual loss. The etiology of AMD is not well understood. Many theories exist and feature mechanisms of oxidative stress, athe-rosclerotic-like changes, genetic predisposition and inflammation. The most recent clinical studies appointed to a great role of inflammation and C-reactive protein (CRP) in the pathogenesis of AMD. There is a large body of evidence indicating the association of CRP with endothelial dysfunction, oxidative stress and production of reactive oxygen species (ROS), as well as with lipid status disorder in AMD patients. According to recent studies, CRP is definitely not only the inflammatory marker but also a mediator of development of the vascular disorders in the retinal circulation. The results obtai-ned from the present studies may help our understanding the pathogenesis of the retinal vascular disease associated with high levels of CRP

The association of enzymatic and non-enzymatic antioxidant defense parameters with inflammatory markers in patients with exudative form of age-related macular degeneration

There are evidence that oxidative stress and inflammation are involved in the pathogenesis of the age-related macular degeneration (AMD). The aim of this study was to analyze the antioxidant defense parameters and inflammatory markers in patients with exudative form of AMD (eAMD), their mutual correlations and association with the specific forms of AMD. The cross-sectional study, included 75 patients with the eAMD, 31 patients with the early form, and 87 aged-matched control subjects. Significantly lower SOD, TAS and albumin values and higher GR, CRP and IL-6 were found in the eAMD compared to the early form (p lt 0.05). Significant negative correlations were found between GPx and fibrinogen (r = -0.254), TAS and IL-6 (r = -0.999) and positive correlations between uric acid and CRP (r = 0.292), IL-6 and uric acid (r = 0.398) in the eAMD. A significant association of CRP (OR: 1.16, 95% CI: 1.03-1.32, p = 0.018), fibrinogen (OR: 2.21, 95% CI: 1.14-4.85, p = 0.021), TAS (OR: 7.45, 95% CI: 3.97-14.35, p = 0.0001), albumin (OR: 1.25, 95% CI: 1.11-1.41, p = 0.0001) and uric acid (OR: 1.006, 95% CI: 1.00-1.02, p = 0.003) was found with the eAMD. In conclusion it may be suggested, there is a significant impairment of antioxidant and inflammatory parameter levels in eAMD patients. In addition, significant association exists between the tested inflammatory markers and antioxidant parameters with late-eAMD

Antioxidative status of saliva before and after non-surgical periodontal treatment

Introduction. Oxidative stress and antioxidants play an important role in the pathogenesis of inflammatory disease, including chronic periodontitis (CP). Saliva contains enzymatic (glutathione peroxidase - GPx, superoxide dismutase - SOD, etc.) and non-enzymatic (albumin - ALB, uric acid - UA, glutathione, etc.) antioxidants. Objective. The aims of this study were to investigate: a) level of SOD, GPx, UA, ALB and total antioxidative status (TAS) of saliva in CP patients before and after non-surgical treatment, and b) correlations between clinical periodontal parameters and levels of salivary antioxidants. Methods. Saliva was collected from 21 CP patients before and after non-surgical treatment. The condition of periodontium was assessed by plaque index, gingival index, bleeding on probing, probing depth and clinical attachment loss. Level of investigated antioxidants (except GPx) and TAS was determined using colorimetric method and commercial kits. GPx activity was determined using UV method and commercial kits. Results. After the treatment significant increase of UA, ALB, Gpx, TAS was detected (p lt 0.01) and decrease of SOD activity (p>0.05). A significant correlation was observed between GPx and PI (r=0.575, p=0.008), SOD and GI (r=0.525, p=0.017) before therapy, and SOD and bleeding on probing (BP) (r=0.59, p=0.006), TAS and BP (r=0.453, p=0.045) after therapy. Conclusion. These data suggest that levels of salivary antioxidants generally increase after non-surgical periodontal treatment. Correlation between some clinical periodontal parameters and level of salivary antioxidants was found.Uvod. Oksidativni stres i antioksidansi igraju važnu ulogu u patogenezi zapaljenjskih oboljenja, uključujući i hroničnu parodontopatiju. Pljuvačka sadrži enzimske antioksidanse, kao što su glutation-peroksidaza (GPx) i superoksid-dismutaza (SOD), i neenzimske antioksidanse, poput albumina (ALB), mokraćne kiseline (UA), glutationa itd. Cilj rada. Cilj istraživanja bio je da se ispitaju nivoi SOD, GPx, UA i ALB i utvrdi ukupan antioksidantni status pljuvačke (TAS) kod osoba s hroničnom parodontopatijom pre i posle kauzalne terapije, te ustanove korelacije između kliničkih pokazatelja stanja parodoncijuma i nivoa antioksidansa u pljuvački. Metode rada. Pljuvačka je sakupljena od 21 pacijenta s hroničnom parodontopatijom pre i posle kauzalne terapije. Stanje parodoncijuma je procenjivano pomoću: plak-indeksa (PI), gingivalnog indeksa (GI), indeksa krvarenja gingive (BP), dubine parodontalnog džepa i nivoa pripojnog epitela. Nivo ispitivanih antioksidansa (osim GPx) i TAS određivan je pomoću kolorimetrijske metode i komercijalnih reagensa. GPx je određivan primenom UV metode i komercijalnih reagensa. Rezultati. Nakon terapije ustanovljeni su značajno povećanje koncentracije UA, GPx i TAS (p lt 0,01) i smanjenje aktivnosti SOD (p>0,05). Primećena je i značajna korelacija između GPx i PI (r=0,575; p=0,008), te SOD i GI (r=0,525; p=0,017) pre terapije, odnosno SOD i BP (r=0,59; p=0,006), kao i TAS i BP (r=0,453; p=0,045) posle nje. Zaključak. Dobijeni nalazi pokazuju da se nivoi antioksidansa u pljuvački povećavaju nakon kauzalne terapije parodontopatije. Uočene su pozitivne korelacije između kliničkih pokazatelja stanja parodoncijuma i ispitivanih koncentracija antioksidansa u pljuvački

Structural myocardial alterations in diabetes and hypertension: the role of galectin-3.

Background: Galectin-3 is a protein widely distributed in the heart, brain and blood vessels, and has a regulatory role in inflammation, immunology and cancer. Many studies demonstrated that the increased level of galectin-3 is associated with progressive fibrosis and stiffening of the myocardium. The aim of this study was to investigate the role of galectin-3 in patients with type 2 diabetes (T2D) and/or arterial hypertension (HT). Methods: Study population included 189 patients, with no coronary artery disease, divided into three groups: group 1 (T2D), group 2 (T2D+HT), and group 3 (HT). All subjects underwent routine laboratory tests, as well as specific biomarkers assessment [galectin-3, glycosylated hemoglobin (HbA1c), N- terminal fragment B-type natriuretic peptide (NT-proBNP)]. Cardiological evaluation included physical examination, transthoracic tissue Doppler echocardiography and stress echocardiography. Results: The results of this study demonstrated significantly increased levels of galectin-3, blood glucose, and HbA1c in group 2. Also, echocardiographicaly, left ventricular (LV) diameters and IVS thickness were increased in this group of patients. Furthermore, in the same cohort a positive correlation between galectin-3 and NT-pro BNP, and galectin-3 and LV mass were demonstrated. In addition, a negative correlation between galectin-3 and LV end-diastolic diameter was revealed. Conclusions: This study revealed that levels of galectin-3 were higher in patients with both T2D and HT, and correlated with LV mass, indicating the potential role of this biomarker for early detection of myocardial structural and functional alteration

Type 2 Diabetic Patients with Ischemic Stroke: Decreased Insulin Sensitivity and Decreases in Antioxidant Enzyme Activity Are Related to Different Stroke Subtypes

We analyzed (a) insulin sensitivity (IS) and (b) glutathione peroxidase (GSH-Px), glutathione reductase (GR), and superoxide dismutase (SOD) antioxidant enzyme activity in type 2 diabetic (T2D) patients with atherothrombotic infarction (ATI) (group A), lacunar infarction (LI) (B), or without stroke (C) and in nondiabetics with ATI (D), LI (E), or without stroke (F). ATI and LI were confirmed by brain imaging IS levels were determined by minimal model (Si index), and the enzyme activity by spectrophotometry. In T2D patients, Si was lower in A and B versus C (1.14 ± 0.58, 1.00 ± 0.26 versus 3.14 ± 0.62 min −1 /mU/l × 10 4 , < 0.001) and in nondiabetics in D and E versus F (3.38 ± 0.77, 3.03 ± 0.72 versus 6.03 ± 1.69 min −1 /mU/l × 10 4 , < 0.001). Also, GSH-Px and GR activities were lower in A and B versus C (GSH-Px: 21.96 ± 3.56, 22.51 ± 1.23 versus 25.12 ± 1.67; GR: 44.37 ± 3.58, 43.50 ± 2.39 versus 48.58 ± 3.67 U/gHb; < 0.001) and in D and E versus F (GSH-Px: 24.75 ± 3.02, 25.57 ± 1.92 versus 28.56 ± 3.91; GR: 48.27 ± 6.81, 49.17 ± 6.24 versus 53.67 ± 3.96 U/gHb; < 0.001). Decreases in Si and GR were significantly related to both ATI and LI in T2D. Our results showed that decreased IS and impaired antioxidant enzymes activity influence ischemic stroke subtypes in T2D. The influence of insulin resistance might be exerted on the level of glutathione-dependent antioxidant enzymes

Type 2 Diabetic Patients with Ischemic Stroke: Decreased Insulin Sensitivity and Decreases in Antioxidant Enzyme Activity Are Related to Different Stroke Subtypes

We analyzed (a) insulin sensitivity (IS) and (b) glutathione peroxidase (GSH-Px), glutathione reductase (GR), and superoxide dismutase (SOD) antioxidant enzyme activity in type 2 diabetic (T2D) patients with atherothrombotic infarction (ATI) (group A), lacunar infarction (LI) (B), or without stroke (C) and in nondiabetics with ATI (D), LI (E), or without stroke (F). ATI and LI were confirmed by brain imaging IS levels were determined by minimal model (Si index), and the enzyme activity by spectrophotometry. In T2D patients, Si was lower in A and B versus C (1.14±0.58, 1.00±0.26 versus 3.14±0.62 min−1/mU/l × 104, P<0.001) and in nondiabetics in D and E versus F (3.38±0.77, 3.03±0.72 versus 6.03±1.69 min−1/mU/l × 104, P<0.001). Also, GSH-Px and GR activities were lower in A and B versus C (GSH-Px: 21.96±3.56,  22.51±1.23 versus 25.12±1.67; GR: 44.37±3.58,  43.50±2.39 versus 48.58±3.67 U/gHb; P<0.001) and in D and E versus F (GSH-Px: 24.75±3.02,  25.57±1.92 versus 28.56±3.91; GR: 48.27±6.81,  49.17±6.24 versus 53.67±3.96 U/gHb; P<0.001). Decreases in Si and GR were significantly related to both ATI and LI in T2D. Our results showed that decreased IS and impaired antioxidant enzymes activity influence ischemic stroke subtypes in T2D. The influence of insulin resistance might be exerted on the level of glutathione-dependent antioxidant enzymes