[Effect of Ginkgo biloba Tablet on the Expression of Scavenger Receptor A of the Aortic Wall in Atherosclerotic Rats].

OBJECTIVE: To observe the expression of Ginkgo biloba Tablet (GbT) on scavenger receptor A (SRA) of the aortic wall and changes of serum inflammatory factors in atherosclerotic rats, and to explore its new mechanism for fighting against atherosclerosis (AS). METHODS: Totally 45 male Wistar rats were randomly divided into the control group, the model group, the GbT group, 15 rats in each group. Levels of blood glucose, blood lipids, blood calcium, serum C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (slCAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured in all rats. The expression of SRA in the aortic wall of atherosclerotic rats was observed by immunohistochemical assay. The correlation between the expression of SRA and levels of in-flammatory factors was also observed. RESULTS: Compared with the control group, blood glucose and blood calcium obviously increased (P < 0.05); levels of TG, TC, and LDL-C were significantly elevated (P < 0.01); neointimal areas were significantly thickened, increased intima percentage was significantly enlarged, narrowed lumen index was significantly reduced; levels of CRP, sICAM-1, and sVCAM-1 were significantly elevated in the model group (all P < 0.01). Compared with the model group, blood glucose and blood calcium obviously decreased (P < 0.05); levels of TG, TC, and LDL-C significantly decreased (P < 0.01) in the GbT group. Aortic lumens were obviously narrower in the model group than in the GbT group (P < 0.05). SRA expressed at the aortic wall. The aforesaid 3 indices were significantly improved in the GbT group than in the model group (P < 0.01). Serum levels of CRP, sICAM-1, and sVCAM-1 were significantly decreased in the GbT group than in the model group (P < 0.01). Serum levels of CRP, sICAM-1, and sVCAM-1 were positively correlated with the percentage of SRA positive expression area (r = 0.701, 0.604, 0.581, all P < 0.01). CONCLUSIONS: Serum levels of inflammatory factors in atherosclerotic rats were elevated, and the expression of SRA in the aortic wall was enhanced. The expression of SRA was closely correlated with serum levels of inflammatory factors. GbT could decrease serum levels of inflammatory factors and inhibit the expression of SRA.

[Arterial remodeling at the reference site after angioplasty and the effect of granulocyte-macrophage colony-stimulating factor on remodeling].

OBJECTIVE: To observe the correlation of the arterial remodeling at the reference site and the lesion site and the effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on arterial remodeling. METHODS: 28 healthy New Zealand White rabbits were randomized to 2 equal groups: GM-CSF group receiving subcutaneous injection of GM-CSF (10 microg x kg(-1)xd(-1)) for 7 days, and pure damage group given subcutaneous injection of equivalent normal saline foe 7 days. Seven days later the iliac arteries of all animals were damaged by balloon. The levels of nitrogen monoxide (NO) were detected before and 4 weeks after angioplasty. Histological sections of iliac from rabbits killed 4 weeks after angioplasty were analyzed. Lumen area (LA), external elastic lamina area (EELA), and intimal plus medial areas (I + M) were measured at the lesion(L) and reference(R) sites. RESULTS: The NO levels 4 weeks later of the GM-CSF group was 98 +/- 10 micromol/L, significantly higher than that of the pure damage group (83 +/- 12 micromol/L, P < 0.05). Morphometric analysis showed that the LA(L) of the pure damage group was (0.87 +/- 0.40) mm2, significantly smaller than that of the GM-CSF group [(1.34 +/- 0.52) mm2, P < 0.05]. The I + M(L) of the pure damage group was (2.62 +/- 0.48) mm2, significantly greater than that of the GM-CSF group [(2.26 +/- 0.43) mm2, P < 0.05]. There was no statistical significance in the EEL(L) between the 2 groups [(3.48 +/- 0.80) mm2 versus (3.60 +/- 0.91) mm2, P > 0.05]. Morphometric analysis showed that the LA(R) of the pure damage group was (1.60 +/- 0.48) mm2, significantly smaller than that of the GM-CSF group [(1.99 +/- 0.54) mm2, P < 0.05], whereas there was no statistical significance in the I + M(R) between the 2 groups. In both groups, LA(R) was significantly correlated with LA(L) (r = 0.919, P < 0.001); and EELA(R) was significantly correlated with EELA(L) (r = 0.909, P < 0.001) and I + M(R) (r = 0.685; P < 0.001). CONCLUSION: Remodeling affects both the lesion and the reference sites and appears to occur in parallel and proportionately at both sites. GM-CSF treatment increases re-endothelialization of the injured artery and inhibits unfavorable remodeling.

[Atorvastatin inhibits scavenger receptor A and monocyte chemoattractant protein-1 expressions in foam cell].

OBJECTIVE: To investigate the effects of atorvastatin on expressions of scavenger receptor A and secretion of monocyte chemoattractant protein-1 (MCP-1) in foam cells. METHODS: THP-1 cells were induced to differentiate into macrophages by PMA and treated with 0.1% BSA (control), ox-LDL (100 mg/L) or ox-LDL plus atorvastatin (5, 10, 20 micromol/L) for 24 hours. MCP-1 concentration in cell substratum was measured by ELISA. Scavenger receptor A expression was observed under fluorescent microscope after incubated with DiI-Ac-LDL. The relationship between concentration of MCP-1 and the activity of scavenger receptor A was also analyzed. RESULTS: Compared to the control cells, MCP-1 concentration in ox-LDL treated cells was significantly increased after 6 hours, peaked at 12 hours and was still significantly increased after 24 hours (all P < 0.05 vs. baseline). The activity of scavenger receptor A was also significantly increased in ox-LDL treated cells (P < 0.01 vs. control). The activity of scavenger receptor A proteins correlated positively to the concentration of MCP-1 in ox-LDL treated cells (r = 0.683, P < 0.01). Atorvastatin significantly attenuated these changes in a dose-dependent manner. CONCLUSIONS: Scavenger receptor A and MCP-1 expressions were significantly increased in the course of monocyte lines THP-1 differentiating into macrophages and foam cells. The anti-atherosclerosis effect of atorvastatin might be partly achieved by inhibiting the secretion of MCP-1 and expression of scavenger receptor A in foam cells.

[Change of peripheral blood monocytes derived macrophage scavenger receptors activity in patients with coronary heart disease, and the intervention effect of ginkgo biloba extract].

OBJECTIVE: To observe the activity of peripheral blood monocytes (PBMs) derived macrophage scavenger receptors (MSR) and changes of serum inflammatory factor in peripheral blood in patients with coronary heart disease (CHD), and to evaluate the effect of Ginkgo biloba extract (GBE) on the MSR activity, to explore the relationship between inflammatory factor and scavenger receptors activity as well as the possible mechanism of GBE in stabilizing the atheromatous plaque. METHODS: Ninety-seven CHD patients with normal blood lipids were classified into the stable angina group, the unstable angina group and the acute myocardial infarction group, and 29 healthy persons were taken as control. Levels of C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) in all subjects were determined. And their PBMs were isolated, cultured in vitro, and transferred into macrophage to observe the effect of GBE on the expression of scavenger receptors. RESULTS: The levels of MSR activity, CRP, sICAM-1 and sVCAM-1 in patients with acute myocardial infarction > unstable angina > stable angina > control. CONCLUSION: GBE could down-regulate the MSR activity in CHD patients, which was positively correlated with levels of CRP, sICAM-1 and sVCAM-1. MSR activity could be taken as a monitoring criteria for active degree of vulnerable atherosclerosis plaque. GBE has the effect of suppressing MSR activity.