Lili Zhang1#, ZhenYang2#, Yijia Guo1, Yapeng Lin1, Biao Wang1, Yin Tang3*
1Department of Neurology, The First Affiliated Hospital of Chengdu Medical College, Chengdu, 610500, China - 2Department of Cardiology, The First Affiliated Hospital of Chengdu Medical College, Chengdu, 610500, China - 3Department of Pathology, The First Affiliated Hospital of Chengdu Medical College, Chengdu, 610500, China
In recent years, more and more patients with cerebral hemorrhage have lost their lives due to cerebral small vessel disease. In this article, we study the neuroprotective effects of G-CSF on matrix metalloproteinase-9 (MMP-9) and glial fibrous acidic protein (GFAP) in rats with cerebrovascular disease. In this paper, the neuroprotective effect of G-CSF is evaluated and its mechanism is based on the neuroprotective effect of G-CSF on the neurological function, focal area, and surrounding tissues of cerebral small vessel disease. In this study, 41 rats were used, 3 of which were discarded without reperfusion, and 38 were divided into the treatment group and the sham operation group. The results of the study show that the combined treatment of G-CSF and rHuEPO in rats with cerebral small vessel disease can significantly improve the recovery effect of rats, increase the levels of RBC, Hct, and HGB, and improve the nutritional status of rats. In a mouse model of cerebral small vessel disease, G-CSF significantly reduces the level of nerve cells in the endosteum, and nerve cells do not express G-CSF receptors. G-CSF treatment increases the formation and activity of neuroclasts in mice and humans. The inhibitory effect of G-CSF-induced nerve cells is through the inhibition of nerve cell differentiation. Nerve cells account for the highest proportion of brain tissue, accounting for about 95% of all nerve cells.
Granulocyte Colony Stimulating Factor, Neuroprotective Mechanism, Cerebral Small Vessel Disease Rats, Treatment of Cerebral Hemorrhage Disease.