2001Chinese Journal of Hospital PharmacyRequires access

The effect of ahylysantinfarctase on the expression of C-myc oncogene by rabbit vascular smooth muscle cells after denudation

Ai Shu

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Abstract

OBJECTIVE:To elucidate the mechanisms of ahylysantinfarctase to inhibit the vascular restinosis for its clinical application.METHODS:A restinotic model was constructed by injury of rabbit iliac arteries with balloon catheters and a probe designed for rabbit C-myc mRNA was used to detect the expression of it by intimal vSMCs on the vascular cross sections using an in situ hybridization technique at the indicated times. Ahylysantinfarctase was given muscularly (0.01 u·kg-1·d-1) and the relation of this gene expression to the proliferation of vSMCs and vascular intimal formation were estimated.RESULTS:C-myc expression reached its peak level and its positive cells were even distributed in vascular intimas one week after denudation (29.23 positive cells/mm2) and ahylysantinfarctase could significantly inhibit the expression of C-myc oncogene (10.73 positive cellsper mm2) as we ca lculated the average number of C-myc mRNA positive cells per millimetre intimal area at×400 magnification.CONCLUSIONS:The inhibition of the expression of C-myc oncogene could reduce or stop the formation of vascular intimal lesions and the use of this drug could benefit to managment of restionosis after a successful percutaneo us transluminal coronary angioplasty.

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OBJECTIVE:To elucidate the mechanisms of ahylysantinfarctase to inhibit the vascular restinosis for its clinical application.METHODS:A restinotic model was constructed by injury of rabbit iliac arteries with balloon catheters and a probe designed for rabbit C-myc mRNA was used to detect the expression of it by intimal vSMCs on the vascular cross sections using an in situ hybridization technique at the indicated times. Ahylysantinfarctase was given muscularly (0.01 u·kg-1·d-1) and the relation of this gene expression to the proliferation of vSMCs and vascular intimal formation were estimated.RESULTS:C-myc expression reached its peak level and its positive cells were even distributed in vascular intimas one week after denudation (29.23 positive cells/mm2) and ahylysantinfarctase could significantly inhibit the expression of C-myc oncogene (10.73 positive cellsper mm2) as we ca lculated the average number of C-myc mRNA positive cells per millimetre intimal area at×400 magnification.CONCLUSIONS:The inhibition of the expression of C-myc oncogene could reduce or stop the formation of vascular intimal lesions and the use of this drug could benefit to managment of restionosis after a successful percutaneo us transluminal coronary angioplasty.

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Available abstract

OBJECTIVE:To elucidate the mechanisms of ahylysantinfarctase to inhibit the vascular restinosis for its clinical application.METHODS:A restinotic model was constructed by injury of rabbit iliac arteries with balloon catheters and a probe designed for rabbit C-myc mRNA was used to detect the expression of it by intimal vSMCs on the vascular cross sections using an in situ hybridization technique at the indicated times. Ahylysantinfarctase was given muscularly (0.01 u·kg-1·d-1) and the relation of this gene expression to the proliferation of vSMCs and vascular intimal formation were estimated.RESULTS:C-myc expression reached its peak level and its positive cells were even distributed in vascular intimas one week after denudation (29.23 positive cells/mm2) and ahylysantinfarctase could significantly inhibit the expression of C-myc oncogene (10.73 positive cellsper mm2) as we ca lculated the average number of C-myc mRNA positive cells per millimetre intimal area at×400 magnification.CONCLUSIONS:The inhibition of the expression of C-myc oncogene could reduce or stop the formation of vascular intimal lesions and the use of this drug could benefit to managment of restionosis after a successful percutaneo us transluminal coronary angioplasty.

Key concepts: Vascular smooth muscle, Oncogene, In situ hybridization, Gene expression, Messenger RNA, Intimal hyperplasia, Pathology, Cell

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