Protective effect of troxerutin and cerebroprotein hydrolysate injection on cerebral ischemia through inhibition of oxidative stress and promotion of angiogenesis in rats

Mol Med Rep. 2019 Apr;19(4):3148-3158. doi: 10.3892/mmr.2019.9960. Epub 2019 Feb 15.


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.

MeSH terms

  • Animals
  • Anticoagulants / pharmacology*
  • Biomarkers
  • Brain Ischemia / drug therapy
  • Brain Ischemia / etiology
  • Brain Ischemia / metabolism*
  • Brain Ischemia / pathology*
  • Cell Adhesion
  • Cell Movement
  • Disease Models, Animal
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Hydroxyethylrutoside / analogs & derivatives*
  • Hydroxyethylrutoside / pharmacology
  • Male
  • Neovascularization, Pathologic / metabolism*
  • Neuroprotective Agents / pharmacology*
  • Oxidative Stress / drug effects*
  • Rats
  • Reactive Oxygen Species / metabolism


  • Anticoagulants
  • Biomarkers
  • Hydroxyethylrutoside
  • Neuroprotective Agents
  • Reactive Oxygen Species
  • troxerutin