A Protective Role of Glibenclamide in Inflammation-Associated Injury.
Gensheng ZhangXiuhui LinShufang ZhangHuiqing XiuChuli PanWei CuiPublished in: Mediators of inflammation (2017)
Glibenclamide is the most widely used sulfonylurea drug for the treatment of type 2 diabetes mellitus (DM). Recent studies have suggested that glibenclamide reduced adverse neuroinflammation and improved behavioral outcomes following central nervous system (CNS) injury. We reviewed glibenclamide's anti-inflammatory effects: abundant evidences have shown that glibenclamide exerted an anti-inflammatory effect in respiratory, digestive, urological, cardiological, and CNS diseases, as well as in ischemia-reperfusion injury. Glibenclamide might block KATP channel, Sur1-Trpm4 channel, and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome activation, decrease the production of proinflammatory mediators (TNF-α, IL-1β, and reactive oxygen species), and suppress the accumulation of inflammatory cells. Glibenclamide's anti-inflammation warrants further investigation.
Keyphrases
- oxidative stress
- nlrp inflammasome
- ischemia reperfusion injury
- reactive oxygen species
- induced apoptosis
- blood brain barrier
- rheumatoid arthritis
- traumatic brain injury
- emergency department
- lipopolysaccharide induced
- metabolic syndrome
- inflammatory response
- cell proliferation
- brain injury
- weight loss
- signaling pathway
- endoplasmic reticulum stress
- smoking cessation