Preventive effect of Ginkgo biloba (银杏叶) extract on endothelial cells in rat models with atherosclerosis
Hong Ma
Abstract
Hong Ma
Abstract
Objective To examine the effect of Ginkgo biloba (银杏叶) extract (GBE) on the endothelial cells in rat models with atherosclerosis and its mechanism. Methods Fifteen Sprague Dawley (SD) rats were randomly divided into three groups: high lipids (model) group, GBE group and normal control group. The rats in the model group were fed with high lipids and were sacrificed 12 weeks later. Besides fed with high lipids, the animals in GBE group were also administrated intragastricly with GBE aqueous solution (96 mg·kg-1·d-1). The aortas were harvested for histomorphometry and transmission electron microscope observation after 12 weeks. The nuclear factor-κB (NF-κB) activity was measured by electrophoretic mobility shift assays (EMSA) in aortas. The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in serum were measured by radio-immunity method and the level of soluble thrombomodulin (sTM) in serum was measured by enzyme linked immunosorbent assay (ELISA). Results Under electron microscope, the necrosis and apoptosis of aorta endothelial cells were obvious in high lipids group, but the cell damage in GBE group was mild. The level of sTM in the GBE group was significantly higher than that in the normal control group and lower than that in the high lipids group (both P0.05). The activity of NF-κB, the levels of IL-6 and TNF-α were evidently higher in the high lipids group than those in the normal control group, and in the GBE group, they were also elevated, but obviously lower than those in the model group (all P0.05). There were positive linear relationships between the NF-κB activity and each of the following levels: TNF-α, IL-6 and sTM (all P0.05). The level of sTM also had linear relationship with the levels of TNF-α and IL-6 respectively (both P0.05). Conclusion These results indicate that GBE can protect endothelial cells by inhibiting the activity of NF-κB and inflammatory response.
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Objective To examine the effect of Ginkgo biloba (银杏叶) extract (GBE) on the endothelial cells in rat models with atherosclerosis and its mechanism. Methods Fifteen Sprague Dawley (SD) rats were randomly divided into three groups: high lipids (model) group, GBE group and normal control group. The rats in the model group were fed with high lipids and were sacrificed 12 weeks later. Besides fed with high lipids, the animals in GBE group were also administrated intragastricly with GBE aqueous solution (96 mg·kg-1·d-1). The aortas were harvested for histomorphometry and transmission electron microscope observation after 12 weeks. The nuclear factor-κB (NF-κB) activity was measured by electrophoretic mobility shift assays (EMSA) in aortas. The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in serum were measured by radio-immunity method and the level of soluble thrombomodulin (sTM) in serum was measured by enzyme linked immunosorbent assay (ELISA). Results Under electron microscope, the necrosis and apoptosis of aorta endothelial cells were obvious in high lipids group, but the cell damage in GBE group was mild. The level of sTM in the GBE group was significantly higher than that in the normal control group and lower than that in the high lipids group (both P0.05). The activity of NF-κB, the levels of IL-6 and TNF-α were evidently higher in the high lipids group than those in the normal control group, and in the GBE group, they were also elevated, but obviously lower than those in the model group (all P0.05). There were positive linear relationships between the NF-κB activity and each of the following levels: TNF-α, IL-6 and sTM (all P0.05). The level of sTM also had linear relationship with the levels of TNF-α and IL-6 respectively (both P0.05). Conclusion These results indicate that GBE can protect endothelial cells by inhibiting the activity of NF-κB and inflammatory response.
Key concepts: Ginkgo biloba, Tumor necrosis factor alpha, Chemistry, Blood lipids, Apoptosis, Endocrinology, Thrombomodulin, Internal medicine