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Objective: To investigate the effect of Qingre Quyu Granule (清热祛瘀颗粒, QRQYG) on stabilizing vulnerable plaques in apolipoprotein E (ApoE) defficient mice. Methods: Seventy-two male ApoE defficient mice were given a high-fat diet from 6 weeks of age. At the 16th week, all the mice were randomized into 3 groups: the QRQYG group, the simvastatin group, and the control group. Sixteen weeks after administration of 0.9 g/kg QRQYG, 3 mg/kg simvastatin or 10 mg/kg sodium chloride per day to the respective groups, the animals were euthanized. The pathological morphologic changes in the vulnerable plaques were evaluated, the matrix metalloprotease-9 (MMP-9) expression was measured by immunohistofluorescence, the soluble intercellular adhesion molecule 1 (ICAM-1) was determined by ELISA, the nuclear factor kappaB (NF-κB) subunit p65 was measured by quantitative RT-PCR, and, finally, thrombospondin-1 (TSP-1) was determined by the immunohistochemical method. Results: The plaque cross-sectional area in the brachiocephalic artery (23.7%, P<0.01), the lipid core of the plaque (43.1%±3.1%), and the number of buried ?brotic caps of the plaque were significantly decreased in the QRQYG group compared to the control group (both P<0.01); furthermore, the thickness of the ?brotic cap of the plaque increased and the intra-plaque hemorrhage of the plaque decreased. The serum soluble ICAM-1 (27.1±5.1 μg/mL), the protein expression of MMP-9 and TSP-1 and the p65 mRNA expression increased in the QRQYG group in comparison with the control group (P<0.05 or P<0.01). Conclusion: QRQYG could stabilize the vulnerable plaque through inhibition of the inflammatory response.
Objective: To investigate the effect of Qingre Quyu Granule (QRQYG) on stabilizing vulnerable plaques in apolipoprotein E (ApoE) defficient mice. Methods: Seventy-two male ApoE defficient mice were given a high-fat diet from 6 weeks At the 16th week, all the mice were randomized into 3 groups: the QRQYG group, the simvastatin group, and the control group. Sixteen weeks after administration of 0.9 g / kg QRQYG, 3 mg / kg simvastatin or 10 mg / kg sodium chloride per day to the respective groups, the animals were euthanized. The pathological morphologic changes in the vulnerable plaques were evaluated, the matrix metalloproteinase-9 (MMP-9) expression was measured by immunohistofluorescence, the soluble intercellular adhesion molecule 1 -1) was determined by ELISA, the nuclear factor kappaB (NF-κB) subunit p65 was measured by quantitative RT-PCR, and, finally, thrombospondin-1 (TSP-1) was determined by the immunohistochemical method. cross-se The number of buried? brotic caps of the plaque were significantly less in the QRQYG group compared to the ctional area in the brachiocephalic artery (23.7%, P <0.01), the lipid core of the plaque (43.1% ± 3.1% The thickness of the? brotic cap of the plaque increased and the intra-plaque hemorrhage of the plaque decreased. the serum soluble ICAM-1 (27.1 ± 5.1 μg / mL), the protein expression of MMP-9 and TSP-1 and the p65 mRNA expression increased in the QRQYG group in comparison with the control group (P <0.05 or P <0.01). Conclusion: QRQYG could stabilize the vulnerable plaque through inhibition of the inflammatory response.