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Acta Biomedica Scientia

Volume 11, Issue 2, 2024
Mcmed International
Acta Biomedica Scientia
Issn
2348 - 215X (Print), 2348 - 2168 (Online)
Frequency
bi-annual
Email
editorabs@mcmed.us
Journal Home page
http://mcmed.us/journal/abs
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Abstract
Title
THE PATHOLOGICAL EFFECTS OF RESVERATROL ON NEUTROPHIL ACTIVATION AND INFLAMMATION: IN VITRO FINDINGS
Author
Dr. Praveen CS1*, Dr. Elakkya K
Email
keyword
Resveratrol, Neutrophil Activation, Oxidative Burst, Inflammation
Abstract
Resveratrol (RES), a polyphenolic compound found in various plants, has demonstrated significant antioxidant and antiinflammatory properties. This study investigates the pathological effects of RES on neutrophil activation and inflammation in vitro. Neutrophils, as key players in immune responses, produce reactive oxygen species (ROS) during inflammatory processes, contributing to tissue damage in various diseases. RES was tested on human neutrophils in both intracellular and extracellular settings to evaluate its ability to modulate oxidative burst and neutrophil activity. In this study, RES was found to dose-dependently inhibit neutrophil chemiluminescence (CL) induced by phorbol 12-myristate 13-acetate (PMA) and the calcium ionophore A23187. RES treatment reduced the oxidative burst, as well as the production of free radicals, in both whole blood and isolated neutrophils. Furthermore, RES inhibited the phosphorylation of protein kinase C (PKC) isoenzymes ? and ?II, which are involved in the activation of neutrophils and subsequent ROS production. Although RES did not induce significant apoptosis in neutrophils, it effectively reduced nitrite accumulation in macrophages, suggesting a suppression of inducible nitric oxide synthase (iNOS) activity. These findings indicate that RES interferes with key signaling pathways in neutrophils, reducing oxidative stress and inflammatory responses. RES may provide therapeutic potential for treating inflammatory disorders such as ischemic reperfusion injury and other conditions involving excessive neutrophil activation.
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