J Biomed Transl Res.
2019 Mar;20(1):1-7. 10.12729/jbtr.2019.20.1.001.
Anti-inflammatory activities of sinensetin on LPS-stimulated L6 skeletal muscle cells
- Affiliations
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- 1Department of Physical Therapy, International University of Korea, Jinju 52833, Korea.
- 2Research Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea. gonskim@gnu.ac.kr
- 3Department of Nursing Science, International University of Korea, Jinju 52833, Korea. iuknurse@nate.com
- KMID: 2448283
- DOI: http://doi.org/10.12729/jbtr.2019.20.1.001
Abstract
- Inflammation is an important protective response mechanism that occurs against microbial invasion or injury. However, excessive inflammation may lead to cause of morbidity and mortality in diseases. The activated macrophages plays a vital role in inflammatory response by stimulation of lipopolysaccharide (LPS) and tumor necrosis factor-α (TNF-α). This activation further damages the host by inducing certain pro-inflammatory mediators such as nitric oxide (NO), interleukin-1β (IL-1β), interleukin-6 (IL-6), TNF-α, inducible nitrous oxide (iNOS) and cyclooxygenase (COX-2). Flavonoids are bioactive compounds with potential effects as anti-cancer, anti-inflammation, anti-viral and anti-bacterial activities. Polymethoxyflavones (PMFs) are unique to citrus plants which are of specific interest owing to their biological effects that includes lipoprotein metabolism and anti-inflammatory activity. Sinensetin is one of the PMFs having five methoxy groups on the basic benzo-γ-pyrone skeleton with a carbonyl group at the C4 position. Sinensetin have been known for exerting various pharmacological activities including anti-angiogenesis, anti-diabetic and anti-inflammatory activities. However, there are no studies focused on the anti-inflammatory effects of sinensetin on skeletal muscle cells. In the present study, we investigated the anti-inflammatory effect of flavonoids isolated from Sinensetin on the production of pro-inflammatory mediators mediated by nuclear factor-kappa B (NF-κB) by inhibition of signal transduction in LPS - induced L6 skeletal muscle cells.
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