Glimepiride is a second-generation sulfonylurea that stimulates pancreatic β cells to release insulin. Glimepiride is used for the treatment of type 2 diabetes mellitu as monotherapy as well as in combination with metformin or insulin[1].
In vitro, Glimepiride (0, 0.3, 0.6, 1.2, 2.5 and 5μM; 1h) stimulated the release of CD14 from RAW 264 cells[2]. Glimepiride (10μM; 1, 4 and 7 days) induced the proliferation and differentiation of rat osteoblasts in a high glucose microenvironment[3]. Glimepiride (10µM; 30min) induces NO production by HCAECs[4].
In vivo, Glimepiride (1, 2 or 4mg/kg; 4 days; p.o.) prevents 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine induced dopamine neurons degeneration through attenuation of glia activation and oxidative stress in mice[5]. Glimepiride (4mg/kg; 3 weeks; i.p.) ameliorates renal toxicity induced by cadmium in mice[6].
References:
[1] Basit A, Riaz M, Fawwad A. Glimepiride: evidence-based facts, trends, and observations (GIFTS). [corrected]. Vasc Health Risk Manag. 2012;8:463-72.
[2] Ingham V, Williams A, Bate C. Glimepiride reduces CD14 expression and cytokine secretion from macrophages. J Neuroinflammation. 2014 Jun 21;11:115.
[3] Ma P, Gu B, Xiong W, Tan B, Geng W, Li J, Liu H. Glimepiride promotes osteogenic differentiation in rat osteoblasts via the PI3K/Akt/eNOS pathway in a high glucose microenvironment. PLoS One. 2014 Nov 12;9(11):e112243.
[4] Ueba H, Kuroki M, Hashimoto S, Umemoto T, Yasu T, Ishikawa SE, Saito M, Kawakami M. Glimepiride induces nitric oxide production in human coronary artery endothelial cells via a PI3-kinase-Akt dependent pathway. Atherosclerosis. 2005 Nov;183(1):35-9.
[5] Oduola-Akande MD, Ishola IO, Olubodun-Obadun TG, Akande AJ, Adeyemi OO. Glimepiride Prevents 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Induced Dopamine Neurons Degeneration Through Attenuation of Glia Activation and Oxidative Stress in Mice. Neurotox Res. 2023 Jun;41(3):212-223.
[6] ElMahdy MK, Zaki MO, Al-Karmalawy AA, Abdo W, Alnasser SM, Antar SA. Glimepiride ameliorates renal toxicity induced by cadmium in mice: Modulation of Jun N terminal kinase (JNK)/nuclear factor kappa B (NF-κB) and phosphatidylinositol 3-kinases (PI3K)/protein kinase (AKT) pathways. Life Sci. 2022 Dec 15;311(Pt B):121184.
Glimepiride为第二代磺酰脲类药物，可刺激胰岛β细胞释放胰岛素，作为单药或与二甲双胍、胰岛素联合用于治疗2型糖尿病[1]。
体外实验显示，Glimepiride (0, 0.3, 0.6, 1.2, 2.5和5μM; 1h)可促进RAW264细胞CD14脱落[2]。在高糖微环境中，Glimepiride (10μM; 1, 4和7天)诱导大鼠成骨细胞增殖与分化[3]。Glimepiride (10μM; 30min)亦能诱导人冠状动脉内皮细胞(HCAECs)产生一氧化氮[4]。
体内研究证实，Glimepiride (1, 2或4mg/kg; 4天; 口服)可通过减弱胶质细胞活化及氧化应激预防1-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的小鼠多巴胺神经元变性[5]。此外，Glimepiride (4mg/kg; 3周; 腹腔注射)可减轻镉诱导的小鼠肾毒性[6]。