Effects of antidiabetic drugs on NLRP3 inflammasome activity, with a focus on diabetic kidneys

被引:110
作者
Yaribeygi, Habib [1 ]
Katsiki, Niki [2 ]
Butler, Alexandra E. [3 ]
Sahebkar, Amirhossein [4 ,5 ,6 ]
机构
[1] Shahid Beheshti Univ Med Sci, Chron Kidney Dis Res Ctr, Tehran, Iran
[2] Aristotle Univ Thessaloniki, Hippokrat Hosp, Med Sch, Propedeut Dept Internal Med 2, Thessaloniki, Greece
[3] Antidoping Lab Qatar, Life Sci Res Div, Sports City Rd, Doha, Qatar
[4] Mashhad Univ Med Sci, Neurogen Inflammat Res Ctr, Mashhad, Iran
[5] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Biotechnol Res Ctr, Mashhad, Iran
[6] Mashhad Univ Med Sci, Sch Pharm, Mashhad, Iran
关键词
TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; INSULIN-RESISTANCE; OXIDATIVE STRESS; FACTOR-ALPHA; ACTIVATION; INHIBITOR; EMPAGLIFLOZIN; INTERLEUKIN-1; MACROPHAGES;
D O I
10.1016/j.drudis.2018.08.005
中图分类号
R9 [药学];
学科分类号
100702 [药剂学];
摘要
Inflammatory responses have a pivotal role in the development of diabetic nephropathy (DN). The nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome is a newly recognized and potent inflammatory mediator that induces inflammatory responses in several disorders, including DN. The suppression of procytokine release and inflammatory response is integral to the prevention of complications arising from the inflammatory process. In this review, we discuss the role of the NLRP3 inflammasome in the pathogenesis of DN, focusing on its effects on interleukin (IL)-1 beta and IL-18. Furthermore, we review the potential anti-inflammatory effects of antidiabetic drugs used in routine clinical practice, such as insulin, biguanides, Sodium-glucose co-transporter-2 (SGLT2) inhibitors, sulfonylureas, thiazolidinediones, and dipeptidyl peptidase-4 (DPP-4) inhibitors. In addition, we discuss whether these drugs can also modulate NLRP3 inflammasome activity in renal tissues.
引用
收藏
页码:256 / 262
页数:7
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