Background: Among different mechanisms, oxidative stress has a possible role in neural injury in cerebrovascular events. Objectives: Assessment the oxidants-antioxidants imbalance in ischemic and hemorrhagic strokes. Materials and Methods: Serum level of malondialdehyde, the main marker of lipid peroxidation, and total antioxidant capacity were measured in a group of 48 stroke patients consis...

BACKGROUND Reactive oxygen species (ROS) play a major role in causing injury in ischemia-reperfusion (I/R). Mitochondrial DNA (mtDNA) is particularly vulnerable to oxidative damage. We propose that increased mitochondrial ROS production is likely to damage mtDNA, causing further injury to mitochondria, and postconditioning (POC) may ameliorate kidney I/R injury by mitigating mitochondrial damag...

Objective(s): Carbon tetrachloride (CCl4) causes pulmonary toxicity. Infliximab (Ib) is a potent inhibitor of tumor necrosis factor-alpha (TNF-α). We aimed to investigate whether Ib has a protective effect on CCl4 induced lung injury. Materials and Methods:Rats were divided into control, CCl4, and CCl4+Ib groups. A single dose of 2 ml/kg CCI4 was administered to CCI4 group and a single dose of...

The glucagon-like peptide 1 (GLP-1) analogue Exendin-4 (Ex-4) could perform anti-oxidative effects against oxidative damage both in vitro and in vivo. However, little was known about the direct protection of Exendin-4 on RPE cells against oxidative stress and its underlying mechanism. The present study examined the protective effects of Exendin-4 on RPE cells against H2O2 treatment in vitro and...

BACKGROUND Chronic nicotine (Ch-NIC) exposure exacerbates ischemia/reperfusion (I/R)-induced oxidative stress and acute kidney injury (AKI), and mitochondrial production of reactive oxygen species (ROS) in cultured renal proximal tubule cells (RPTCs). Because Ser36-phosphorylated p66shc modulates mitochondrial ROS production and injury of RPTCs, we hypothesized that Ch-NIC exacerbates AKI by in...

This study aimed to investigate the protective effects of dexmedetomidine on lipopolysaccharide (LPS)-induced lung injury in Wistar rats. 24 female Wistar rats were randomly assigned into 3 groups (n = 8): a control group, a LPS-challenged group, and a LPS plus dexmedetomidine group. Inflammation, oxidative stress, Nrf2/Keap1, and Akt signal were determined. The results showed that LPS caused i...