Publications by authors named "Sanem Ascı"
Article Synopsis
- * A study on female rats examined the effects of cannabidiol (CBD) on neuroinflammation by dividing them into four groups, including those receiving lipopolysaccharide (LPS) and CBD treatments.
- * Results showed that CBD treatment improved neuron survival and reduced oxidative stress by regulating various proteins and synthesis pathways, reversing the damaging effects caused by LPS exposure.
Background: Doxorubicin (DOX) may cause various neurological side effects in the brain. Lercanidipine (LRD) has antioxidant, anti-inflammatory, and anti-apoptotic properties. The aim of this study was to investigate the potential benefits of.
View Article and Find Full Text PDFSide effects of doxorubicin (DOX) are mainly due to oxidative stress, with the involvement of inflammatory and apoptotic mechanisms. Agomelatine (AGO) is a melatonin receptor agonist with antioxidant, anti-inflammatory, and anti-apoptotic features. This study aimed to evaluate the effects of AGO with different doses on DOX-induced neurotoxicity.
View Article and Find Full Text PDFArticle Synopsis
- - The study investigated the effects of lipopolysaccharide (LPS) on oxidative damage and inflammation in the brains of rats, focusing on the hippocampus and cerebellum, and examined the potential protective role of pregabalin (PG).
- - Researchers divided 24 female rats into three groups: a control group, a group treated with LPS to induce inflammation, and a group treated with both LPS and pregabalin. Key measurements included DNA damage and various blood and brain tissue markers related to oxidative stress and inflammation.
- - Results showed increased damage and inflammatory markers in the LPS-treated rats, but the group treated with LPS and pregabalin had lower oxidative stress levels, suggesting that pregabalin
Background: Stroke is one of the most common causes of death and the leading cause of disability in adults. Cerebral ischemia/reperfusion injury causes cerebral edema, hemorrhage, and neuronal death.
Aims: In post-ischemic reperfusion, free radical production causes brain tissue damage by oxidative stress.