Inhibitory Effects Of Warmed Water Extract Of Radix Sophorae On Vascular Restenosis

The Research BackgroundPercutaneous transluminal coronary angioplasty (PTCA) is one of the most efficient way to cure the coronary atherosclerotic heart disease nowadays. However, the rate of suffer restenosis after 6 months adds to 30%~50%,which inhibits the long-term clinical effect, and results in the high medical cost. The mechanism of restenosis is not indentical. Many researches show us the result that restenosis is a recovery reaction of blood vessel respond to PTCA ,which includes reconstruction of blood vessel mediated by inflammatory cell,cytokine and growth factor and induced by genies abnormal expression. They all play a key role in restenosis that contains cell matrix secretion, cleaning disequilibrium, smooth muscle cell immigration and generation.Currently marketed first-generation drug-eluting stents use antiproliferative drugs including rapamycin, its analogues, or paclitaxel. The current antiproliferative strategies are no longer a panacea, however, because this strategy involves potential problems such as impaired endothelial regeneration and an incomplete healing process (excessive inflammation and fibrin deposition) associated with increased risk of stent thrombosis especially lethal Late thrombosis.Sophorae is a commonly prescribed Chinese medicine for many treatments, including as an anti-biotic and for cancer. It has been shown to possess anti-inflammation activity. Recent experimental and clinical studies suggest that inhibition of inflammation (monocyte recruitment and activation) can be a promising next-generation approach for prevention of restenosis. Therefore it is expected that sophorae might play an important role in preventing balloon injury-induced restenosis. The purposeThe research aims at the fact that sophorae can attenuate the TNF (Tumor necrosis factor)expression to depress immune reaction and diminish restenosis, providing materials for preventing and cueing restenosis.The methodThe experiment is divided to two stage. The fist stage is animal experiment that includes the construction of animal model, and administration for the pathematology study. The process contains : the construction of animal model, dividing the test animals to four groups (control, rapamycin, sophorae,model), taking the focus tissue of infection after 2 weeks, making pathological section , comparing and analysising lumina and vessel wall in four groups. The second stage is cell experiment that analyses the sophorae pharmacology mechanism. The process contains: dividing the test animals to four groups (control, rapamycin, sophorae,model), RT-PCR analysis of Rat VSMC TNF- mRNA, Western Blot Analysis of Rat VSMC Tumor Necrosis Factor- proteins expression, comparing and analysising the effect of sophorae to TNF,PCNA,TNF protein expression.The consequenceQuantitative analysis demonstrated a significant reduction (P<0.01) of vascular restenosis (cross-sectional areas of the lumen) in the warmed water extract of Radix Sophorae compared with the model. There were no significant differences in warmed water extract of Radix Sophorae compared with the rapamycin(P>0.05). Semiquantitative analysis demonstrated a significant reduction of expression of tumor necrosis factor- in the warmed water extract of Radix Sophorae compared with the model(P<0.01). Rapamycin also remarkably inhibits expression of tumor necrosis factor- (P<0.01). There were no significant differences in effect of the warmed water extract of Radix Sophorae on expression of tumor necrosis factor- in vascular restenosis compared with effect of rapamycin(P>0.05). But the warmed water extract of Radix Sophorae did not inhibits expression of PCNA protein in vascular restenosis(compared with the model, P>0.05) . In contrast rapamycin still remarkably inhibits expression of PCNA (compared with the model,P<0.05)The conclusionIn a word,our study demonstrated inhibitory effects of warmed water extract of Radix Sophorae on vascular restenosis in a rat carotid model of balloon dilatation injury, and the inhibitory effects are mediated through suppress the expression of TNF.