Naringin attenuates the vascular calcification in a model of experimental Diabetes mellitus

Abstract

Vascular calcification (VC) is one important complication of type 1 Diabetes mellitus (DM). Several studies suggest that the antioxidant naringin (NAR) supplementation is beneficial for the treatment of DM, but its effect on the VC has not been investigated. The aim of this work was to know whether NAR could attenuate the VC in Wistar male rats with DM.

Three groups of animals were used: 1) controls, 2) diabetic rats (treated with 60 mg streptozotocin /kg b.w.: STZ), 3) diabetic rats treated with NAR (40 mg/kg b.w.). After 30 days of treatment, plasma was withdrawn and rats were sacrificed to obtain the aortas. Endothelial cells (EC) from aortas were cultured and NO•, indicator of vascular health, was measured by the Griess´s method.

NO• production was significantly reduced in STZ rats, which was highly blocked by NAR (213,40 ± 33.3; 143,69±19.88*; 184,66±11.99; C; STZ; STZ + NAR 40; *p<0.01). In control aortas, estrona (E1) and genistein (Gen) stimulate NO• synthesis via estrogen receptor, but in aortas from STZ rats there is lack of NO• stimulation by those hormones. However, NAR restores the capability to stimulate NO• production under E1 and Gen. Isolated aortas from the different groups of animals were exposed to a pro-calcific medium with glicerophosphate for 7 days; the aortas were decalcified and the released calcium was measured by a commercial kit. Calcium content from aortas of STZ rats was 74% higher (p< 0.01) than that from the control rats. NAR treatment reduced calcium incorporation to values closed to the control ones.  These data were confirmed by AgNO3 staining.

Aortas from STZ rats showed multiple sites of calcification, effect that was abolished by NAR treatment. All data suggest that NAR could prevent damage of the vascular architecture and functionality in diabetic rats.