| Autor: |
Filippov AG; Institute of General Pathology and Pathophysiology, Baltiyskaya St., 8, 125315 Moscow, Russia., Alexandrin VV; Institute of General Pathology and Pathophysiology, Baltiyskaya St., 8, 125315 Moscow, Russia., Ivanov AV; Institute of General Pathology and Pathophysiology, Baltiyskaya St., 8, 125315 Moscow, Russia., Paltsyn AA; Institute of General Pathology and Pathophysiology, Baltiyskaya St., 8, 125315 Moscow, Russia.; Russian Medical Academy for Continuing Professional Education, Barricadnaya St., 2/1 b. 1, 125993 Moscow, Russia., Sviridkina NB; Institute of General Pathology and Pathophysiology, Baltiyskaya St., 8, 125315 Moscow, Russia., Virus ED; Institute of General Pathology and Pathophysiology, Baltiyskaya St., 8, 125315 Moscow, Russia., Bulgakova PO; Institute of General Pathology and Pathophysiology, Baltiyskaya St., 8, 125315 Moscow, Russia., Burmiy JP; Institute of Microelectronic Technology and Ultra-High-Purity Materials, Akademika Osip'yana Str., 6, 142432 Chernogolovka, Russia., Kubatiev AA; Institute of General Pathology and Pathophysiology, Baltiyskaya St., 8, 125315 Moscow, Russia.; Russian Medical Academy for Continuing Professional Education, Barricadnaya St., 2/1 b. 1, 125993 Moscow, Russia. |
| Abstrakt: |
Platinum nanoparticles (nPts) have neuroprotective/antioxidant properties, but the mechanisms of their action in cerebrovascular disease remain unclear. We investigated the brain bioavailability of nPts and their effects on brain damage, cerebral blood flow (CBF), and development of brain and systemic oxidative stress (OS) in a model of cerebral ischemia (hemorrhage + temporary bilateral common carotid artery occlusion, tBCAO) in rats. The nPts (0.04 g/L, 3 ± 1 nm diameter) were administered to rats ( N = 19) intraperitoneally at the start of blood reperfusion. Measurement of CBF via laser Doppler flowmetry revealed that the nPts caused a rapid attenuation of postischemic hypoperfusion. The nPts attenuated the apoptosis of hippocampal neurons, the decrease in reduced aminothiols level in plasma, and the glutathione redox status in the brain, which were induced by tBCAO. The content of Pt in the brain was extremely low (≤1 ng/g). Thus, nPts, despite the extremely low brain bioavailability, can attenuate the development of brain OS, CBF dysregulation, and neuronal apoptosis. This may indicate that the neuroprotective effects of nPts are due to indirect mechanisms rather than direct activity in the brain tissue. Research on such mechanisms may offer a promising trend in the treatment of acute disorders of CBF. |
