FANGCHINOLINE AMELIORATES THE EXPRESSIONS OF ANGIOGENIC MOLECULE IN CEREBRAL ISCHEMIA INDUCED NEURONAL DEGENERATION IN NEONATAL RATS

被引:7
作者
Han Daicheng [1 ]
Xia Shiwen [1 ]
Zhu Huaping [1 ]
Liu Yong [1 ]
Zhou Qianqian [1 ]
Hu Changxia [1 ]
机构
[1] Hubei Maternal & Child Hlth Hosp, Dept Neonatol, Wuhan 430070, Hubei, Peoples R China
关键词
Fangchinoline; cerebral ischemia; Neurodegeneration; Angiogenesis; MECHANISMS;
D O I
10.1515/tnsci-2018-0018
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Background: Present investigation evaluates the beneficial effect of fangchinoline on cerebral ischemia induced neuronal degeneration in neonatal rats and also postulates the possible mechanism of its action. Methodology: Cerebral ischemia was produced by the ligation of right common carotid artery in neonatal rats on postnatal day 5 (P5) and further pups were treated with fangchinoline 3, 10 and 30 mg/kg, i.p. for the period of 3 days. Effect of fangchinoline was estimated by determining the brain injury and enzyme linked immunosorbent assay (ELISA) method was used for the estimation of pro-inflammatory mediators and markers of oxidative stress in the cerebral tissues of neonatal rats. Moreover western blot assay and histopathology study was also performed on the brain tissue. Results: Result of this investigation reveals that the percentage of brain injury significantly reduces and enhancement of myelin basic protein in the cerebral tissues of fangchinoline than ischemic group. Treatment with fangchinoline attenuates the altered level of proinflammatory mediators and markers of oxidative stress in the cerebral tissue of cerebral ischemia induced neuronal injury neonatal rats. Moreover expressions of inducible nitric oxide synthtase (iNOS), vascular endothelial growth factor (VEGF), p53 and nuclear receptor factor-2 (Nrf2) in the brain tissue attenuated by fangchinoline treated group. Conclusion: In conclusion, fangchinoline ameliorates the cerebral ischemia induced neuronal injury in neonatal rats by enhancing angiogenesis molecules.
引用
收藏
页码:117 / 122
页数:6
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