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Vincetoxicum arnottianum ameliorate inflammation by suppressing oxidative stress and pro-inflammatory mediators in rat.

07:00 EST 11th January 2020 | BioPortfolio

Summary of "Vincetoxicum arnottianum ameliorate inflammation by suppressing oxidative stress and pro-inflammatory mediators in rat."

Aerial parts of Vincetoxicum arnottianum (Wight) Wight (Family Apocynaceae) are used by local communities for inflammation, healing of wound and injuries and also for urticaria.

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Journal Details

This article was published in the following journal.

Name: Journal of ethnopharmacology
ISSN: 1872-7573
Pages: 112565

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A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).

The appearance of carbonyl groups (such as aldehyde or ketone groups) in PROTEINS as the result of several oxidative modification reactions. It is a standard marker for OXIDATIVE STRESS. Carbonylated proteins tend to be more hydrophobic and resistant to proteolysis.

A protein deglycase that repairs methylglyoxal- and glyoxal-glycated amino acids and proteins, releasing repaired proteins and lactate or glycolate. It deglycates CYSTEINE, ARGININE and LYSINE residues to reactivate proteins by reversing glycation and prevent the formation of ADVANCED GLYCATION END PRODUCTS. It protects cells against OXIDATIVE STRESS and CELL DEATH by functioning as an oxidative stress sensor and redox-sensitive MOLECULAR CHAPERONE and PROTEASE. Mutations in the PARK7 gene are associated with autosomal-recessive, early-onset PARKINSON DISEASE.

A direct-acting oxidative stress-inducing agent used to examine the effects of oxidant stress on Ca(2+)-dependent signal transduction in vascular endothelial cells. It is also used as a catalyst in polymerization reactions and to introduce peroxy groups into organic molecules.

An activating transcription factor that plays a key role in cellular responses to GENOTOXIC STRESS and OXIDATIVE STRESS.

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