Effect of mesenchymal stromal cell transplantation on nitric oxide metabolism in rat cortex during ischemia-reperfusion

One of the causes of stroke is acute impairment of cerebral blood flow, which initiates with the formation of acute neuronal energy deficiency, activation of the “ischaemic cascade”, and nitrosative stress. Reactive nitrogen species, namely nitric oxide and peroxynitrite, play a central role in tissue damage. The search for new therapeutic strategies to address these processes remains relevant. The objective of this study was to evaluate the effect of transplantation of mesenchymal stromal cells of various origins, their lysates, and citicoline on nitric oxide metabolism in the somatosensory cortex of the eyes using an ischaemia-reperfusion model. An experimental model was established using 126 rats, with bilateral 20-minute occlusion of the internal carotid arteries followed by reperfusion. The animals were divided into groups according to the substances administered: mesenchymal stromal cells extracted from Wharton’s jelly of the human umbilical cord, human and rat adipose tissue, rat fetal fibroblasts, lysates of mesenchymal stromal cells from Wharton’s jelly, and citicoline. On days 7 and 14 after treatment, indicators of nitric oxide metabolism in the somatosensory cortex following ischaemia-reperfusion were analysed. The results demonstrated that transplantation of mesenchymal stromal cells from Wharton’s jelly of the human umbilical cord and rat fetal fibroblasts, as well as administration of citicoline, significantly altered total nitric oxide synthase activity during the observed periods. It was found that mesenchymal stromal cells derived from human Wharton’s jelly, particularly when combined with citicoline, reduced nitrosative stress. Thus, the ischaemia-reperfusion model induced an imbalance in the functioning of the nitric oxide system. The greatest protective effect was observed with transplantation of mesenchymal stromal cells from Wharton’s jelly of the human umbilical cord, which effectively safeguarded neurons from nitrosative stress, in a manner comparable to citicoline