Differential Study On The Effect Of Blood-activating And Blood-breaking Drugs On TLR4/NF-?B Pathway In ApoE Gene-deficient Mice AS Model

Objective:To observe the effects of different dosages of blood-activating medicines(angelica sinensis and ligusticum wallichii)and blood-breaking medicines(rhizoma sparganii and cureuma zedoary)on Toll-like Receptor4(TLR-4)/nuclear factor-kappa B(NF-?B)pathway of ApoE gene-deficient mouse AS model to provides experimental basis for enriching the scientific meaning of promoting blood circulation and breaking blood and the anti-inflammatory mechanism of Vulnerable plaque(VP).Methods:70 six-week-old male mice with defective ApoE gene were made as atherosclerosis(AS)models and then they were divided into six groups according to random number table:model-control group(model group),atorvastatin calcium group(statin group),high-dose of blood-breaking group(high blood-breaking group),low-dose of blood-breaking group(low blood-breaking group),high-dose of blood-activating group(high blood-activating group),and low-dose of blood-activating group(low blood-activating group).Another 10 C57BL/6J mice without gene defect were set as blank control group(blank group).After 8 weeks of intragastric administration,the animals were put to death.Serum TNF-? concentration was measured by ELISA method,and expression of protein TLR4,My D88 and NF-?B in aortic tissues was detected by Westernblot method.The results were analyzed and compared.Results:Both blood-activating medicines and blood-breaking medicines could significantly reduce the protein expression levels of TLR4,NF-?B,My D88,and affect the synthesis of inflammatory factor TNF-?(P<0.01).The effect of blood-breaking medicines was better than blood-activating medicines with the same dose(P<0.01),and there existed significant dose-effect relationship between the high and low dose blood-activating group and blood-breaking group(P<0.01).Conclusion:Both blood-activating medicines and blood-breaking medicines could reduce the protein expression of TLR4,NF-?B and My D88,and affect the synthesis of inflammatory factor TNF-? by interfering TLR4/NF-?B pathway,and play an antiatherosclerosis role.The effect of blood-breaking medicines was better than blood-activating medicines.