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This study was aimed to determine effect of Bu-Shen Kang-Shuai (BSKS) Tablet on HO-1 mRNA and its associated oxidative stress levels among atherosclerotic rabbits. A total of 56 rabbits were randomly divided into the normal group (8 rabbits) and the experimental group (48 rabbits). Normal diet was given to the normal group. Atherosclerotic rabbits models were established in the experimental group. At the eighth week, rabblits in the experi-mental group were randomly divided into the model group, BSKS Tablet group and simvastatin group. Blood samples were collected before medication, 8-, 12-, 16-week after medication from rabbits of each group. Rabbits were sacri-ficed under aseptic conditions at the last blood collection. Expressions of aortic HO-1 mRNA and PPARα mRNA were measured by Q-PCR method. The level of MMP-9 was measured by immunohistochemical assay. Serum HbCO, COX-2 activity and cGMP level were measured by ELISA assay. The results showed that after the intervention of BSKS Tablet, serum HbCO level decreasd, cGMP was obviously increased. However, there was no obvious change on the COX-2 activity. The immunohistochemical assay showed that BSKS Tablet obviously reduced MMP-9 level of rabbits. There was only small amount of aortic HO-1 mRNA expression in the normal group. However, the expres-sion of aortic HO-1 mRNA in the atherosclerosis group was increased. After intervention of BSKS Tablet, the ex-pression of HO-1 mRNA was increased with statistical significance (P < 0.05). Simvastatin had similar antioxidant effect. It was concluded that the compound preparation of traditional Chinese medicine (TCM) BSKS Tablets had an important antioxidant effect in treatment of atherosclerosis. Its protective mechanism may be through the regulation of HO-1 mRNA gene expression and effects of HO-1/CO-cGMP pathway activities of related enzymes while peroxida-tion stability of atherosclerotic plaque.
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Background Research determined that TLR4 is positively expressed on the macrophages in iris and ciliary in acute endotoxin-induced uveitis(EIU),indicating that TLR4 participated in the pathogenesis of the anterior uveitis.Objective The aim of this study is to observe the expressions of toll-like receptor-4(TLR4),Myeloid differentiation factor 88(MyD88),NF-κB p65 in iris tissue in the eyes with endotoxin-induced acute anterior uveitis.Methods Animal models of acute anterior uveitis were established by a hind footpad injection of 200μg Cholera vibrio LPS in 40 SPF Wistar rats with the age of 6-8 weeks.Other 10 age-matched rats were as normal controls.Ocular inflammation was examined under the slit lamp microscope at the 2-hour interval after the injection and intensity of inflammation was scored according to the standard of Lajavardi[4].Histopathology examination was performed for the evaluation of inflammatory reaction of iris and ciliary tissues by HE staining at 24 hours after LPS injection.Expressions of TLR4,MyD88 and NF-κB p65 in iris and ciliary body tissue were detected through immunohistochemistry.TLR4~+,MyD88~+ and NF-κB p65~+ cells were counted.Results The inflammatory reaction was gradually enhanced after injection of LPS and peaked at 24 hours and allivated 48 hours later.The infiltration of lots of inflammatory cells and fibrinous exudate were exhibited in the anterior chamber,posterior chamber,iris and ciliary tissue under the optical microscope at 24 hours after injection of LPS.No positive expressions of TLR4,MyD88 and NF-κB p65 in iris-ciliary body complex were found in normal control rats.The positive cells for TLR4,MyD88 and NF-κB p65 in iris-ciliary body complex were significantly different among 12 hours group,48 hours group and 72 hours groups(F=46.79,P＜0.05;F=54.37,P＜0.05;F=85.32,P＜0.05),and the positive cells for TLR4,MyD88 and NF-κB p65 peaked at 24 hours after injection of LPS.Conclusion The expression of TLR4 and its downstream signal transduction molecules MyD88,NF-κB p65 vary in uvea during EIU,indicating the potential role of LR4-MyD88 dependent pathway in the pathogenesis of acute anterior uveitis.
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Objective:To observe whether the Simiao Yongan Decoction regulate the nuclear factor-?B(NF-?B) expression and related factors in atherosclerosis(AS)rabbit model,thus restrain the occurrence of atherosclerosis and plaque formation.Methods:56 male Japanese rabbits were randomly divided into normal group,model group,Simvastatin group and Simiao Yongan Decoction group,in addition to the normal group,other groups were established aortic atherosclerotic plaque model.From the1st day of experiment,the corresponding drug intervention began,10 weeks later,the rabbits were killed over the weekend after the anesthesia line access aortic NF-?B immunohistochemical staining,and the experimental dynamic 0,3,6,10 weeks in serum TNF-?,IL-1 and MCP-1 content.Results:The expression of NF-?B p65 subunit in model group was rich,and compared with it,the expression of NF-?B p65 subunit in treatment groups decreased,and the Simiao Yongan Decoction can obviously inhibit the expression of NF-?B p65 subunit.In model group,the expressions of IL-1,TNF-?and MCP-1 in serum increased significantly at different time points(P
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Objective To observe the syndrome manifestations of rabbit atherosclerosis models and explore the syndrome attribution rules of the models.Methods The 24 male Japanese rabbits were randomized into a control group(n=8)and a experimental group(n=16).The control group was given normal feed,and the experimental group was treated with high-fat diet and immune injury and surgical injury through the femoral artery balloon.They were fed totally for 10 weeks.Vascular morphological changes and blood lipid determine were used to evaluate the models.The ear,tongue,eye,and the overall state of rabbits were regularly observed to see the changes of TCM syndromes.Results The rabbits of the experimental group gradually reduced the amount of activity in early stage.When the climate changed,their nasal secretion was increased,and they had wheezing breathing,fever and other common cold symptoms like red auricle.In the medium stage,the fatty plaque or belt around the eyes,cold auricle,and listlessness could be seen,and the blood fat was significantly higher than that of the control group.To the tenth week,the dark tongue with blood spots and purple cold auricle appeared in the rabbits of the experimental group.It was difficult to draw blood from the ear,and the emboli could be seen in the vessels of auricles.Compared with the control group,the oxidized low density lipoprotein and malondialdehyde of the experimental group were significantly increased,and the activity of superoxide dismutase decreased.Conclusion The syndromes of rabbit atherosclerosis models are in the changing state,in early stage they can be manifested as Qi deficiency,in middle stage the manifestation can be Qi deficiency with phlegm retention,and in late stage there will be Qi deficiency with blood stasis.The rule is similar to that of the pathogenesis of atherosclerosis in clinic.