Beneficial In Vitro Effects of a Low Myo -Inositol Dose in the Regulation of Vascular Resistance and Protein Peroxidation under Inflammatory Conditions.

Oxidative stress induces functional changes in arteries. Therefore, the effect of myo -inositol, a possible anti-inflammatory/antioxidant agent was studied on human plasma and rat thoracic arteries. Aortic rings from male Wistar rats (3 months of age) were incubated with myo -inositol (1, 10 and 100 μM, 120 min) and analyzed using the gas chromatography (GC) method. In another experiment, aortic rings were protected first with myo -inositol (1 µM, 60 min) and then subjected to a thromboxane receptor agonist (U-46619, 0.1 nM, 60 min). Therefore, these four groups under the following conditions were studied: (i) the control in the vehicle; (ii) myo -inositol; (iii) the vehicle plus U-46619; (iv) myo -inositol plus U-46619. The hemostatic parameters of human plasma and an H 2 O 2 /Fe 2+ challenge for lipid and protein peroxidation were also performed. Myo -inositol was not absorbed into the pre-incubated aortic rings as measured by the GC method (0.040 µg/mg, p ≥ 0.8688). The effect of myo -inositol was more significant in the impaired arteries due to U-46619 incubation, which resulted in an improved response to acetylcholine (% Emax: 58.47 vs. 86.69), sodium nitroprusside (logEC 50 : -7.478 vs. -8.076), CORM-2 (% Emax: 44.08 vs. 83.29), pinacidil (logEC 50 : -6.489 vs. -6.988) and noradrenaline (logEC 50 : -7.264 vs. -6.525). This was most likely a possible response to increased nitric oxide release (×2.6-fold, p < 0001), and decreased hydrogen peroxide production (×0.7-fold, p = 0.0012). KCl-induced membrane depolarization was not modified ( p ≥ 0.4768). Both the plasma protein carbonylation (×0.7-fold, p = 0.0006), and the level of thiol groups (×3.2-fold, p = 0.0462) were also improved, which was not significant for TBARS (×0.8-fold, p = 0.0872). The hemostatic parameters were also not modified ( p ≥ 0.8171). A protective effect of myo -inositol was demonstrated against prooxidant damage to human plasma and rat thoracic arteries, suggesting a strong role of this nutraceutical agent on vasculature which may be of benefit against harmful environmental effects.