Effects and mechanism of Weinaokang (维脑康) on reperfusioninduced vascular injury to cerebral microvessels after global cerebral ischemia

Yong-qiu Zheng; Jian-xun Liu; Xin-zhi Li; Li Xu

doi:10.1007/s11655-010-0145-5

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Effects and mechanism of Weinaokang (维脑康) on reperfusioninduced vascular injury to cerebral microvessels after global cerebral ischemia

OriginalPaper | Updated：2021-08-27

- Effects and mechanism of Weinaokang (维脑康) on reperfusioninduced vascular injury to cerebral microvessels after global cerebral ischemia
- Effects and mechanism of Weinaokang (维脑康) on reperfusioninduced vascular injury to cerebral microvessels after global cerebral ischemia
- 中国结合医学杂志（英文版） 2010年16卷第2期页码：145-150
- Affiliations：
  
  Research Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences,Beijing,China
- Author bio：
- Funds：
  
  Supported by the Project of National Natural Science Foundation of China (No. 30830118), the National Key New Drug Project (No. 2009ZX09102-137, 2009ZX09502-014)
- DOI：10.1007/s11655-010-0145-5
  中图分类号：
- 纸质出版日期：2010，
  
  网络出版日期：2010-5-16，
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Zheng, Yq., Liu, Jx., Li, Xz. et al. Effects and mechanism of Weinaokang (维脑康) on reperfusioninduced vascular injury to cerebral microvessels after global cerebral ischemia., Chin. J. Integr. Med. 16, 145–150 (2010). https://doi.org/10.1007/s11655-010-0145-5

Yong-qiu Zheng, Jian-xun Liu, Xin-zhi Li, et al. Effects and mechanism of Weinaokang (维脑康) on reperfusioninduced vascular injury to cerebral microvessels after global cerebral ischemia[J]. Chinese Journal of Integrative Medicine, 2010,16(2):145-150.
Zheng, Yq., Liu, Jx., Li, Xz. et al. Effects and mechanism of Weinaokang (维脑康) on reperfusioninduced vascular injury to cerebral microvessels after global cerebral ischemia., Chin. J. Integr. Med. 16, 145–150 (2010). https://doi.org/10.1007/s11655-010-0145-5 DOI：

Yong-qiu Zheng, Jian-xun Liu, Xin-zhi Li, et al. Effects and mechanism of Weinaokang (维脑康) on reperfusioninduced vascular injury to cerebral microvessels after global cerebral ischemia[J]. Chinese Journal of Integrative Medicine, 2010,16(2):145-150. DOI： 10.1007/s11655-010-0145-5.

摘要

To study the effects of the Weinaokang (维脑康

WNK)

the active compounds extracted from Ginkgo

Ginseng

and saffron

on ischemia/reperfusion (I/R)-induced vascular injury to cerebral microvessels after global cerebral ischemia. Male C57BL/6J mice were randomly divided into 5 groups (10 animals/group): the sham group (0.5% CMC-Na

20 mL/kg)

the I/R model group (0.5% CMCNa

20 mL/kg)

the I/R+Crocin control group (20 mg/kg)

the I/R+high dose WNK group (20 mg/kg)

and the I/R+low dose WNK group (10 mg/kg). Bilateral common carotid artery occlusion (BCCAO

20 min) in mice

followed by 24 h reperfusion

was built. The generation of nitric oxide (NO)

the activity of nitric oxide synthase (NOS)

the phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2)

and the expression of matrix metalloproteinases-9 (MMP-9) and G protein-coupled receptor kinase 2 (GRK2) in cortical microvascular homogenates were evaluated. The ultrastructural morphology of cortical microvascular endothelial cells (CMEC) was observed. The transient global cerebral ischemia (20 min)

followed by 24 h of reperfusion

significantly promoted the generation of NO and the activity of NOS. The reperfusion led to serious edema with mitochondrial injuries in the cortical CMEC

as well as enhanced membrane GRK2 expression and reduced cytosol GRK2 expression. Furthermore

enhanced phosphorylation of ERK1/2 and decreased expression of MMP-9 were detected in cortical micovessels after I/R (20 min/24 h). As well as the positive control Crocin (20 mg/kg

21days)

pre-treatment with WNK (20

10 mg/kg

21 days) markedly inhibited nitrative injury and modulated the ultrastructure of CMEC. Furthermore

WNK inhibited GRK2 translocation from cytosol to the membrane (at 20 mg/kg) and reduced ERK1/2 phosphorylation and MMP-9 expression in cortical microvessels. WNK and its active compounds (Crocin) are effective to suppress I/R-induced vascular injury to cerebral microvessels after global cerebral ischemia with the target on GRK2 pathways.

Abstract

To study the effects of the Weinaokang (维脑康

WNK)

the active compounds extracted from Ginkgo

Ginseng

and saffron

20 mL/kg)

the I/R model group (0.5% CMCNa

20 mL/kg)

the I/R+Crocin control group (20 mg/kg)

the I/R+high dose WNK group (20 mg/kg)

and the I/R+low dose WNK group (10 mg/kg). Bilateral common carotid artery occlusion (BCCAO

20 min) in mice

followed by 24 h reperfusion

was built. The generation of nitric oxide (NO)

the activity of nitric oxide synthase (NOS)

the phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2)

followed by 24 h of reperfusion

significantly promoted the generation of NO and the activity of NOS. The reperfusion led to serious edema with mitochondrial injuries in the cortical CMEC

as well as enhanced membrane GRK2 expression and reduced cytosol GRK2 expression. Furthermore

enhanced phosphorylation of ERK1/2 and decreased expression of MMP-9 were detected in cortical micovessels after I/R (20 min/24 h). As well as the positive control Crocin (20 mg/kg

21days)

pre-treatment with WNK (20

10 mg/kg

21 days) markedly inhibited nitrative injury and modulated the ultrastructure of CMEC. Furthermore

关键词

cerebral ischemia/reperfusionG protein-coupled receptor kinasenitric oxide synthaseextracellular signal-regulated kinase1/2microvascular endothelial cell

Keywords

cerebral ischemia/reperfusionG protein-coupled receptor kinasenitric oxide synthaseextracellular signal-regulated kinase1/2microvascular endothelial cell

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