LR-90 (50 mg/L, p.o. for 27 weeks) significantly reduces plasma lipids, modestly affects hyperglycaemia in ZDF rats[2]. LR-90 (50 mg/L) decreases renal AGE, AGER and lipid peroxidation[2]. Animal Model: Male ZDF rats (13 to 40 weeks)[2] Dosage: 50 mg/L Administration: P.O. for 27 weeks Result: Significantly reduced plasma triacylglycerol and cholesterol by ∼55% and ∼30%, respectively. Modestly affected hyperglycaemia and blood pressure. Lowered the body weight.
In Vitro
LR-90 (0, 25, 50, 100, and 200 μM) inhibits RAGE, MCP-1, COX-2, IP-10 and NOX2 mRNA expression in THP-1 cells in a dose-dependent manner, after pretreatment 1 h befor S100b stimulatation for 4 hours[1]. LR-90 (0, 25, 50, 100, and 200 μM) dose-dependently and significantly blocks THP-1 cells adherence to endothelial cells after pretreatment 1 h befor S100b stimulatation for 24 hours[1]. LR-90 (0, 25, 50, 100, and 200 μM, for 24 hours) shows no effect on the cell viability of THP-1 cells[1]. Cell Viability Assay[1] Cell Line: THP-1 cells Concentration: 0, 25, 50, 100, and 200 μM Incubation Time: 24 hours Result: Showed no cytotoxicity to THP-1 cells. RT-PCR[1] Cell Line: THP-1 cells Concentration: 0, 25, 50, 100, and 200 μM Incubation Time: One hour before S100b addition for 4 hours Result: Dose-dependently inhibited mRNA expression of RAGE, MCP-1, COX-2, IP-10, and NOX2 stimulated with S100b.
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Figarola JL, et al. Anti-inflammatory effects of the advanced glycation end product inhibitor LR-90 in human monocytes. Diabetes. 2007 Mar;56(3):647-55.
[2]. Figarola JL, et al. LR-90 prevents dyslipidaemia and diabetic nephropathy in the Zucker diabetic fatty rat. Diabetologia. 2008 May;51(5):882-91.
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