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- Title
Irisin Ameliorates Hypoxia/Reoxygenation-Induced Inflammation and Apoptosis in PC12 Cells by Inhibiting TLR4/MYD88 Signaling Pathway.
- Authors
Jinli Wang; Fenfen Xu; Yuan Zheng; Xu Cheng; Piaopiao Zhang; Hongyang Zhao
- Abstract
Cardiovascular disease including cerebral ischemic stroke is the major complication that increases the morbidity and mortality in patients with diabetes mellitus as much as four times. It has been well established that irisin, with its ability to regulate glucose and lipid homeostasis as well as anti-inflammatory and anti-apoptotic properties, has been widely examined for its therapeutic potentials in managing metabolic disorders. However, the mechanism of irisin in the regulation of cerebral ischemic stroke remains unclear. Using PC12 cells as a model, we have shown that hypoxia/reoxygenation inhibits cell viability and increases lactic dehydrogenase. Irisin, in a dose-dependent manner, reversed these changes. The increase in inflammatory mediators (IL-1β, IL-6, and TNF-α) by hypoxia/reoxygenation was reversed by irisin. Furthermore, the cell apoptosis promoted by hypoxia/reoxygenation was also inhibited by irisin. Irisin suppressed TLR4/MyD88 signaling pathway leading to amelioration of inflammation and apoptosis in PC12 cells. Thus, inhibition of TLR4/MyD88 signaling pathway via irisin could be an important mechanism in the regulation of hypoxia/reoxygenation-induced inflammation and apoptosis in PC12 cells.
- Subjects
ANIMAL experimentation; HYPOXEMIA; APOPTOSIS; CELL lines; CELLULAR signal transduction; DOSE-response relationship in biochemistry; FIBRONECTINS; INFLAMMATION; LACTATE dehydrogenase; SECRETION; CELL survival
- Publication
Current Topics in Nutraceutical Research, 2019, Vol 17, Issue 3, p329
- ISSN
1540-7535
- Publication type
Article
- DOI
10.37290/ctnr2641-452x.17:329-336