Oxidative stress parameters and inflammatory and immune mediators as markers of the severity of sepsis

Introduction: Sepsis is a complex inflammatory syndrome with diverse etiology and wide spectrum of severity. The aim of this study was to investigate whether inflammatory mediators, in comparison with oxidative parameters, are associated with severity of sepsis. Methodology: Plasma neopterin, adenosine deaminase (ADA), vascular cell adhesion molecule (VCAM), intracellular adhesion molecule (ICAM), interleukin (IL)-1, IL-6, and tumor necrosis factor alpha (TNF-alpha), as inflammatory mediators, and serum nitric oxide (NOx), nitrotyrosine (NT), oxidized LDL (oxLDL) levels, serum paraoxonase 1 (PON1) activity, and erythrocyte glutathione (GSH) levels as oxidative stress parameters of 12 patients with mild sepsis, 25 patients with severe sepsis, and 20 healthy control subjects were evaluated. NOx, GSH levels and PON1 activity were determined by colorimetric methods, whereas neopterin, VCAM, ICAM, IL-1, IL-6, TNF-alpha, NT, and oxLDL levels were measured by enzyme-linked immunosorbent assay (ELISA)

Oxidative stress parameters and inflammatory and immune mediators as markers of the severity of sepsis

Introduction: Sepsis is a complex inflammatory syndrome with diverse etiology and wide spectrum of severity. The aim of this study was to investigate whether inflammatory mediators, in comparison with oxidative parameters, are associated with severity of sepsis. Methodology: Plasma neopterin, adenosine deaminase (ADA), vascular cell adhesion molecule (VCAM), intracellular adhesion molecule (ICAM), interleukin (IL)-1, IL-6, and tumor necrosis factor alpha (TNF-alpha), as inflammatory mediators, and serum nitric oxide (NOx), nitrotyrosine (NT), oxidized LDL (oxLDL) levels, serum paraoxonase 1 (PON1) activity, and erythrocyte glutathione (GSH) levels as oxidative stress parameters of 12 patients with mild sepsis, 25 patients with severe sepsis, and 20 healthy control subjects were evaluated. NOx, GSH levels and PON1 activity were determined by colorimetric methods, whereas neopterin, VCAM, ICAM, IL-1, IL-6, TNF-alpha, NT, and oxLDL levels were measured by enzyme-linked immunosorbent assay (ELISA)

Effects of curcumin on proinflammatory cytokines and tissue injury in the early and late phases of experimental acute pancreatitis

Background & aims: Acute pancreatitis (AP) varies from mild to severe necrotizing changes with high mortality. The objective of the current study was to investigate the effects of curcumin on tissue injury and proinflammatory cytokines in the early and late phases of AP

The effects of resveratrol on tissue injury, oxidative damage, and pro-inflammatory cytokines in an experimental model of acute pancreatitis

Acute pancreatitis (AP) is an acute inflammatory condition that results from the digestion of pancreatic tissue by its own enzymes released from the acinar cells. The objective of this study was to investigate the effects of resveratrol on oxidative damage, pro-inflammatory cytokines, and tissue injury involved with AP induced in a rat model using sodium taurocholate (n=60). There were three treatment groups with 20 rats per group. Groups I and II received 3 % sodium taurocholate solution, while group III underwent the same surgical procedure yet did not receive sodium taurocholate. In addition, group II received 30 mg/kg resveratrol solution. Rats were sacrificed at 2, 6, 12, and 24 h time points following the induction of AP. Blood and pancreatic tissue samples were collected and subjected to biochemical assays, Western blot assays, and histopathologic evaluations. Resveratrol did not reduce trypsin levels and prevent tissue damage. Resveratrol prevented I kappa B degradation (except for 6 h) and decreased nuclear factor-kappa B (NF-kappa B), activator protein-1 (AP-1) (except for 24 h), and levels of TNF-alpha, IL-6 (except for 24 h), and iNOS in the pancreatic tissue at all time points (P<0.05). Serum nitric oxide (NO) levels were reduced as well (P<0.05). Thus, we concluded that resveratrol did not reduce trypsin levels and did not prevent tissue injury despite the reduction in oxidative damage and pro-inflammatory cytokine levels detected in this model of AP

Effects of curcumin on proinflammatory cytokines and tissue injury in the early and late phases of experimental acute pancreatitis

Background & aims: Acute pancreatitis (AP) varies from mild to severe necrotizing changes with high mortality. The objective of the current study was to investigate the effects of curcumin on tissue injury and proinflammatory cytokines in the early and late phases of AP