Protective effect of troxerutin and cerebroprotein hydrolysate injection on cerebral ischemia through inhibition of oxidative stress and promotion of angiogenesis in rats
Autor: | Weiyi Feng, Xueqian Li, Xue Zhao, Yingchen Zhuo, Shixiang Wang, Wenbing Ma, Xuanlin Liu, Qiaowei Zheng, Peipei Zhao, Fengru Tang, Kai Cheng |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Male troxerutin Cancer Research Troxerutin Ischemia Pharmacology Biochemistry Neuroprotection cerebral ischemia Brain Ischemia Brain ischemia 03 medical and health sciences angiogenesis 0302 clinical medicine Cell Movement Genetics medicine Cell Adhesion Human Umbilical Vein Endothelial Cells Animals Humans Molecular Biology Cerebrovascular Ischemia Tube formation Neovascularization Pathologic business.industry Cerebral infarction Cerebral hypoxia Anticoagulants Articles medicine.disease Rats Disease Models Animal Hydroxyethylrutoside Oxidative Stress 030104 developmental biology Neuroprotective Agents Oncology 030220 oncology & carcinogenesis Molecular Medicine cerebroprotein hydrolysate business Reactive Oxygen Species Biomarkers medicine.drug |
Zdroj: | Molecular Medicine Reports |
ISSN: | 1791-3004 |
Popis: | Brain ischemia, including cerebral ischemia and cerebrovascular ischemia, leads to poor oxygen supply or cerebral hypoxia, and causes brain tissue death or cerebral infarction/ischemic stroke. The troxerutin and cerebroprotein hydrolysate injection (TCHI), is widely applied in China to improve blood supply in ischemic brain tissues and to enhance neuroprotective effects in clinical practice. However, the benefits and detailed underlying mechanism elaborating the effectiveness of TCHI in cerebrovascular diseases require further investigation. Therefore, in the present study, experimental in vivo and in vitro models were employed to investigate the potential mechanisms of TCHI on cerebral ischemic injury. The results demonstrated that TCHI increased the lactate dehydrogenase levels in the brain homogenate and conversely decreased lactic acid levels. TCHI was further observed to significantly increase superoxide dismutase activity and decrease malondialdehyde levels in ischemic brain tissues. In addition, TCHI significantly induced vascular maturation processes, including proliferation, adhesion, migration and tube formation in cultured human umbilical vein endothelial cells. Additionally, TCHI significantly stimulated microvessel formation in the rat aortic ring and chick chorioallantoic membrane assays. Taken together, these results provided strong evidence that TCHI stimulated angiogenesis at multiple steps, and indicated that TCHI attenuated cerebral ischemic damage through the amelioration of oxidative stress and promotion of angiogenesis. |
Databáze: | OpenAIRE |
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