4.5 Article

Influence of myrcene on inflammation, matrix accumulation in the kidney tissues of streptozotocin-induced diabetic rat

Journal

SAUDI JOURNAL OF BIOLOGICAL SCIENCES
Volume 28, Issue 10, Pages 5555-5560

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ELSEVIER
DOI: 10.1016/j.sjbs.2020.11.090

Keywords

Anti-inflammation; Myrcene; Matrix accumulation; Oxidative stress; Diabetic rats

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This study investigated the protective effects of Myrcene on oxidative stress, inflammation, and matrix accumulation in the renal tissues of diabetic rats induced by Streptozotocin. Myrcene was found to reduce glucose oxidative stress and exhibit an anti-inflammatory effect by inhibiting NF-kB signaling pathway, suggesting its potential therapeutic value in regulating inflammatory activities and matrix accumulation.
There is only limited literature studies on the activities of inflammation and matrix accumulation in the renal tissues of rats induced with diabetes through Streptozotocin. The present the investigation involves the examination of the protective actions of Myrcene (MYN), a monoterpene on the oxidative stress, inflammation, and matrix accumulation. For this purpose an experimental setup was created which involves injecting MYN 50 mg/kg for about 45 days in the STZ diabetic rats. Modifications in the enzymes, collagens, growth factor B1 and Kappa factor P65 were identified and tracked. The levels of the inflammatory markers like TF-a1, ICAM-1, VCAM-1, MCP-1 were tracked and noted. The current experimental results showed an alteration in the glucose metabolism and enhanced condition. Also an increased level of TGF-b-1 and Nuclear factor-kB expression was seen in the renal tissues. MYN was found to reduce glucose oxidative stress and exhibit an anti-inflammatory effect via inhibiting NF-kB signalling. The conclusion of the current study reveals that MYN regulates the inflammatory activities and matrix accumulation by inhibiting the activities of inflammatory cytokine, pro-inflammatory signalling. (c) 2020 The Author(s). Published by Elsevier B.V. on behalf of King Saud University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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