Background The drink obtained by fermentation of milk with kefir grains,
Background The drink obtained by fermentation of milk with kefir grains, a complex matrix containing acid bacteria and yeasts, has been shown to have beneficial effects in various diseases. the SHR (37??4?%, compared to the Wistar rats: 74??5?%), was significantly attenuated in the SHR group chronically treated with kefir (52??4?%). The difference in the area under the curve between before and after the NADPH oxidase blockade or NO synthase blockade of aortic rings from SHR were of approximately +90 and ?60?%, respectively, when compared with Wistar rats. In the aortic rings from your SHR-kefir group, these BI-847325 manufacture ideals were reduced to +50 and ?40?%, respectively. Circulation cytometric analysis of aortic endothelial cells exposed improved ROS production and decreased NO bioavailability in the SHR, which were significantly attenuated by the treatment BI-847325 manufacture with kefir. Scanning electronic microscopy showed vascular endothelial surface injury in SHR, which was partially safeguarded following administration of kefir for 60?days. In addition, the recruitment of endothelial progenitor cells was decreased in the non-treated SHR and partially restored by kefir treatment. Conclusions Kefir treatment for 60?days was able to improve the endothelial function in SHR by partially restoring the ROS/NO imbalance and the endothelial architecture due to endothelial progenitor cells recruitment. sp.spp.), as well as and yeasts (graphsshow production of superoxide anion (a), hydrogen peroxide (b), peroxynitrite/hydroxyl radical (c), nitric … The circulation cytometry approach was also used to evaluate the number of endothelial cells (through CD31-APC) and the production of NO (through DAF) in the aortic arch from your three groups of animals (Fig.?5). The number of aortic endothelial cells was related in the SHR and Wistar rats in the Rabbit Polyclonal to ARMCX2 time-point of 7?days, but the ideals declined in the SHR and at the time-point of 60?days the number of cells was significantly diminished with this group (33?%, p?0.05) compared with the Wistar rats (12.9??1.3 CD31-positive cell count). The chronic administration of kefir for 60?days to SHR group abolished this difference in the number of CD31-positive cells in the aorta (Fig.?5e). As expected, similar results were observed in the analysis of NO production in the aortas of the three groups of animals. The NO production from the endothelial cells isolated from your aortic arch of the SHR was significantly diminished (16?%) compared with the Wistar rats (1712??86 MFI). Kefir administration for 60?days to SHR abolished the difference in the NO production in the aortas from these animals (Fig.?5d). Mechanisms of endothelial dysfunction in the SHR: the role of NOS To address the mechanisms by which kefir produces the beneficial effects on endothelial function, first we investigated the participation of the molecular NO/cGMP pathway in this process by examining the endothelium-dependent vasodilator response of aortic rings to ACh when NOS was inhibited with L-NAME. Figure?6a shows the concentrationCresponse curves to ACh in the presence and absence of inhibition of the NOS pathway by L-NAME in the three groups of animals at the 60-day time-point. Pre-blockade of the aortic rings with L-NAME caused a marked reduction in the vasodilator response to ACh in the Wistar group, reaching an Rmax of 11??1?% (Fig.?6b). The remaining relaxation under the blockade of NOS with L-NAME is attributed to the relaxing factors of the prostanoids pathway, such as the prostacyclin PGI2. As expected, the untreated SHR exhibited a contractile effect in response to ACh (Rmax of approximately 7??4?%). The administration of kefir to SHR for 60?days reversed the contraction to a relaxation response (Rmax 3??0.1?%) (Fig.?6b). Consequently, the AUC (difference between before and after L-NAME blockade) was greater in the Wistar rats (257??12 a.u.) than in the SHR (132??9 a.u., p?0.05) and kefir administration for 60?days caused a significant improvement in the BI-847325 manufacture AUC (174??8 a.u, p?0.05) (Fig.?6c). Fig.?6 Contribution of the nitric oxide bioavailability to the endothelial BI-847325 manufacture dysfunction in SHR administered kefir for 60?days. Theline graph(a) shows the changes in the doseCresponse to acetylcholine following the endothelial NO synthase blockade ... The above results.