Khodanovich M Yu, Kisel' A A, Chernysheva G A, Smol'yakova V I, Kudabaeva M S, Krutenkova E P, Tyumentseva Ya А, Plotnikov M B
Laboratory of Neurobiology, Research Institute of Biology and Biophysics, Tomsk State University, Tomsk, Russia.
Laboratory of Pharmacology of Blood Circulation, E. D. Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
Bull Exp Biol Med. 2019 Dec;168(2):224-228. doi: 10.1007/s10517-019-04679-7. Epub 2019 Nov 28.
This study aimed at assessing the regenerative effect of p-tyrosol in transient global cerebral ischemia modeled in adult male Wistar rats by reversible occlusion of the three major vessels originating from the aortic arch and supplying the blood to the brain. p-Tyrosol was administered intraperitoneally in a dose of 20 mg/kg over 10 days after surgery. The death of NeuN mature neurons and the number of newly formed DCX neurons were assessed in the CA1 field of the hippocampus that is highly susceptible to damage in this model. We found that ischemia induced death of more than 50% mature neurons in the hippocampal CA1 field (p<0.001). p-Tyrosol stimulated the formation and growth of new neurons in the normally non-proliferative CA1 region of the hippocampus (p<0.05) and produced a neuroprotective effect on mature neurons (p<0.01).
本研究旨在通过可逆性阻断发自主动脉弓并为大脑供血的三大主要血管，评估对成年雄性Wistar大鼠建立的短暂性全脑缺血模型中，对羟基苯乙酮的再生作用。术后10天内，以20mg/kg的剂量腹腔注射对羟基苯乙酮。在该模型中极易受损的海马CA1区，评估NeuN成熟神经元的死亡情况以及新形成的双皮质素（DCX）神经元的数量。我们发现，缺血导致海马CA1区超过50%的成熟神经元死亡（p<0.001）。对羟基苯乙酮刺激了海马正常情况下不增殖的CA1区新神经元的形成和生长（p<0.05），并对成熟神经元产生了神经保护作用（p<0.01）。
