A Protective Role of Glibenclamide in Inflammation-Associated Injury

被引：72

作者：

Zhang, Gensheng ^{[1
]}

Lin, Xiuhui ^{[1
]}

Zhang, Shufang ^{[2
]}

Xiu, Huiqing ^{[1
]}

Pan, Chuli ^{[1
]}

Cui, Wei ^{[1
]}

机构：

[1] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Crit Care Med, Hangzhou 310009, Zhejiang, Peoples R China

[2] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Cardiol, Hangzhou 310009, Zhejiang, Peoples R China

来源：

MEDIATORS OF INFLAMMATION | 2017年 / 2017卷

基金：

中国国家自然科学基金;

关键词：

SENSITIVE POTASSIUM CHANNELS; K-ATP CHANNELS; CYTOKINE GENE-EXPRESSION; NLRP3; INFLAMMASOME; NALP3; OXIDATIVE STRESS; NITRIC-OXIDE; ACUTE-PANCREATITIS; SEPTIC SHOCK; ACTIVATION;

D O I：

10.1155/2017/3578702

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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-alpha, IL-1 beta, and reactive oxygen species), and suppress the accumulation of inflammatory cells. Glibenclamide's anti-inflammation warrants further investigation.

引用

页数：11

共 111 条

[1] Glibenclamide ameliorates ischemia-reperfusion injury via modulating oxidative stress and inflammatory mediators in the rat hippocampus [J].

Abdallah, Dalaal M. ;

Nassar, Noha N. ;

Abd-El-Salam, Rania M. .

BRAIN RESEARCH, 2011, 1385 :257-262

[2] Long term testicular ischemia-reperfusion injury-induced apoptosis: Involvement of survivin down-regulation [J].

Al-Maghrebi, May ;

Kehinde, Elijah O. ;

Anim, Jehoram T. .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2010, 395 (03) :342-347

[3] KATP channels and insulin secretion:: a key role in health and disease [J].

Ashcroft, FM .

BIOCHEMICAL SOCIETY TRANSACTIONS, 2006, 34 :243-246

[4] A view of SUR/KIR6.X, KATP channels [J].

Babenko, AP ;

Aguilar-Bryan, L ;

Bryan, J .

ANNUAL REVIEW OF PHYSIOLOGY, 1998, 60 :667-687

[5] Importance of ABC Transporters in Drug Development [J].

Benadiba, Marcel ;

Maor, Yehoshua .

CURRENT PHARMACEUTICAL DESIGN, 2016, 22 (38) :5817-5829

[6] The microbial and danger signals that activate Nod-like receptors [J].

Benko, Szilvia ;

Philpott, Dana J. ;

Girardin, Stephen E. .

CYTOKINE, 2008, 43 (03) :368-373

[7] THE ACCP-SCCM CONSENSUS CONFERENCE ON SEPSIS AND ORGAN FAILURE [J].

BONE, RC ;

SIBBALD, WJ ;

SPRUNG, CL .

CHEST, 1992, 101 (06) :1481-1482

[8] Calcium and ROS-mediated activation of transcription factors and TNF-α cytokine gene expression in macrophages exposed to ultrafine particles [J].

Brown, DM ;

Donaldson, K ;

Borm, PJ ;

Schins, RP ;

Dehnhardt, M ;

Gilmour, P ;

Jimenez, LA ;

Stone, V .

AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2004, 286 (02) :L344-L353

[9] Role of KATP channels in sepsis [J].

Buckley, James F. ;

Singer, Mervyn ;

Clapp, Lucie H. .

CARDIOVASCULAR RESEARCH, 2006, 72 (02) :220-230

[10] Glibenclamide for the Treatment of Ischemic and Hemorrhagic Stroke [J].

Caffes, Nicholas ;

Kurland, David B. ;

Gerzanich, Volodymyr ;

Simard, J. Marc .

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2015, 16 (03) :4973-4984

← 1 2 3 4 5 6 7 8 9 10 →