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Rutaecarpine Inhibits Intimal Hyperplasia in A Balloon-Injured Rat Artery Model
Rutaecarpine Inhibits Intimal Hyperplasia in A Balloon-Injured Rat Artery Model
- 中国结合医学杂志（英文版） 2018年24卷第6期 页码：429-435
- Affiliations：
1. Key Laboratory of Basic Pharmacology of Guizhou and Department of Pharmacology, Zunyi Medical College,Zunyi,China
2. Molecular Oncology Laboratory, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University,Shanghai,China
3. Institute of Chinese Medical Sciences, University of Macau, Macau SAR,China
- Author bio：
- Funds：
DOI：10.1007/s11655-017-2900-3
中图分类号：纸质出版日期：2018，
网络出版日期：2017-9-1，
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Xu, Y., Chen, Xp., Zhang, F. et al. Rutaecarpine Inhibits Intimal Hyperplasia in A Balloon-Injured Rat Artery Model., Chin. J. Integr. Med. 24, 429–435 (2018). https://doi.org/10.1007/s11655-017-2900-3
Yang Xu, Xiu-ping Chen, Feng Zhang, et al. Rutaecarpine Inhibits Intimal Hyperplasia in A Balloon-Injured Rat Artery Model[J]. Chinese Journal of Integrative Medicine, 2018,24(6):429-435.
Xu, Y., Chen, Xp., Zhang, F. et al. Rutaecarpine Inhibits Intimal Hyperplasia in A Balloon-Injured Rat Artery Model., Chin. J. Integr. Med. 24, 429–435 (2018). https://doi.org/10.1007/s11655-017-2900-3 DOI：
Yang Xu, Xiu-ping Chen, Feng Zhang, et al. Rutaecarpine Inhibits Intimal Hyperplasia in A Balloon-Injured Rat Artery Model[J]. Chinese Journal of Integrative Medicine, 2018,24(6):429-435. DOI： 10.1007/s11655-017-2900-3.
摘要
To investigate the effect and potential mechanisms of rutaecarpine (Rut) in a rat artery balloon-injury model. The intimal hyperplasia model was established by rubbing the endothelia with a balloon catheter in the common carotid artery (CCA) of rats. Fifty rats were randomly divided into five groups
ie. sham
model
Rut (25
50 and 75 mg/kg) with 10 rats of each group. The rats were treated with or without Rut (25
50
75 mg/kg) by intragastric administration for 14 consecutive days following injury. The morphological changes of the intima were evaluated by hematoxylin-eosin staining. The expressions of proliferating cell nuclear antigen (PCNA) and smooth muscle (SM) α-actin in the ateries were assayed by immunohistochemical staining. The mRNA expressions of c-myc
extracellular signal-regulated kinase 2 (ERK2)
MAPK phosphatase-1 (MKP-1) and endothelial nitric oxide synthase (eNOS) were determined by real-time reverse transcription-polymerase chain reaction. The protein expressions of MKP-1 and phosphorylated ERK2 (p-ERK2) were examined by Western blotting. The plasma contents of nitric oxide (NO) and cyclic guanosine 3'
5'-monophosphate (cGMP) were also determined. Compared with the model group
Rut treatment significantly decreased intimal thickening and ameliorated endothelial injury (P<0.05 or P<0.01). The positive expression rate of PCNA was decreased
while the expression rate of SM α-actin obviously increased in the vascular wall after Rut (50 and 75 mg/kg) administration (P<0.05 or P<0.01). Furthermore
the mRNA expressions of c-myc
ERK2 and PCNA were downregulated while the expressions of eNOS and MKP-1 were upregulated (P<0.05 or P<0.01). The protein expressions of MKP-1 and the phosphorylation of ERK2 were upregulated and downregulated after Rut (50 and 75 mg/kg) administration (P<0.05 or P<0.01)
respectively. In addition
Rut dramatically reversed balloon injury-induced decrease of NO and cGMP in the plasma (P<0.05 or P<0.01). Rut could inhibit the balloon injury-induced carotid intimal hyperplasia in rats
possibly mediated by promotion of NO production and inhibiting ERK2 signal transduction pathways.
Abstract
To investigate the effect and potential mechanisms of rutaecarpine (Rut) in a rat artery balloon-injury model. The intimal hyperplasia model was established by rubbing the endothelia with a balloon catheter in the common carotid artery (CCA) of rats. Fifty rats were randomly divided into five groups
ie. sham
model
Rut (25
50 and 75 mg/kg) with 10 rats of each group. The rats were treated with or without Rut (25
50
75 mg/kg) by intragastric administration for 14 consecutive days following injury. The morphological changes of the intima were evaluated by hematoxylin-eosin staining. The expressions of proliferating cell nuclear antigen (PCNA) and smooth muscle (SM) α-actin in the ateries were assayed by immunohistochemical staining. The mRNA expressions of c-myc
extracellular signal-regulated kinase 2 (ERK2)
MAPK phosphatase-1 (MKP-1) and endothelial nitric oxide synthase (eNOS) were determined by real-time reverse transcription-polymerase chain reaction. The protein expressions of MKP-1 and phosphorylated ERK2 (p-ERK2) were examined by Western blotting. The plasma contents of nitric oxide (NO) and cyclic guanosine 3'
5'-monophosphate (cGMP) were also determined. Compared with the model group
Rut treatment significantly decreased intimal thickening and ameliorated endothelial injury (P<0.05 or P<0.01). The positive expression rate of PCNA was decreased
while the expression rate of SM α-actin obviously increased in the vascular wall after Rut (50 and 75 mg/kg) administration (P<0.05 or P<0.01). Furthermore
the mRNA expressions of c-myc
ERK2 and PCNA were downregulated while the expressions of eNOS and MKP-1 were upregulated (P<0.05 or P<0.01). The protein expressions of MKP-1 and the phosphorylation of ERK2 were upregulated and downregulated after Rut (50 and 75 mg/kg) administration (P<0.05 or P<0.01)
respectively. In addition
Rut dramatically reversed balloon injury-induced decrease of NO and cGMP in the plasma (P<0.05 or P<0.01). Rut could inhibit the balloon injury-induced carotid intimal hyperplasia in rats
possibly mediated by promotion of NO production and inhibiting ERK2 signal transduction pathways.
关键词
rutaecarpineballoon-injuryIntimal Hyperplasiaextracellular signal-regulated kinase 2Nitric Oxide
Keywords
rutaecarpineballoon-injuryIntimal Hyperplasiaextracellular signal-regulated kinase 2Nitric Oxide
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