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Bu-shen-he-mai-fang (HMF) Decoction Inhibits Atherosclerosis by Improving Antioxidant and Anti-Inflammatory Activities in ApoE-deficient Mice
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Objective: To observe the effects of Bu–shen- he- mai- fang (HMF) on experimental atherosclerosis in ApoE-deficient mice. Materials an Methods: Thirty male ApoE-deficient mice were randomly divided into 3 groups (10 mice per group) as follows: one group received the standard high- cholesterol diet (high- cholesterol group, HC); Another group received high- cholesterol diet supplemented with HMF decoction 1.37 g/kg/day; the third group received a high- cholesterol diet, supplemented with atrovastatin 5 mg/kg/day for 8 weeks. The extent of atherosclerosis, the expression of LOX-1 protein and macrophage infiltration were evaluated by H&E, oil red O staining, and immunohistochemical staining. SOD was also measured by a spectrophotometer. Results: The degree of atherosclerosis was significantly lower in HMF group and atrovastatin group than that in high-cholesterol group. The expression of LOX-1 protein and macrophage filtration were significantly lower in HMF group and atrovastatin group than that in high-cholesterol group. Also, the SOD was higher in HMF group and atrovastatin group than that in high-cholesterol group. Conclusion: The results suggested that HMF significantly inhibited early atherosclerotic lesions by inhibiting inflammatory response and decreasing the generation of ROS.
International Association of Biomedical Sciences
Title: Bu-shen-he-mai-fang (HMF) Decoction Inhibits Atherosclerosis by Improving Antioxidant and Anti-Inflammatory Activities in ApoE-deficient Mice
Description:
Objective: To observe the effects of Bu–shen- he- mai- fang (HMF) on experimental atherosclerosis in ApoE-deficient mice.
Materials an Methods: Thirty male ApoE-deficient mice were randomly divided into 3 groups (10 mice per group) as follows: one group received the standard high- cholesterol diet (high- cholesterol group, HC); Another group received high- cholesterol diet supplemented with HMF decoction 1.
37 g/kg/day; the third group received a high- cholesterol diet, supplemented with atrovastatin 5 mg/kg/day for 8 weeks.
The extent of atherosclerosis, the expression of LOX-1 protein and macrophage infiltration were evaluated by H&E, oil red O staining, and immunohistochemical staining.
SOD was also measured by a spectrophotometer.
Results: The degree of atherosclerosis was significantly lower in HMF group and atrovastatin group than that in high-cholesterol group.
The expression of LOX-1 protein and macrophage filtration were significantly lower in HMF group and atrovastatin group than that in high-cholesterol group.
Also, the SOD was higher in HMF group and atrovastatin group than that in high-cholesterol group.
Conclusion: The results suggested that HMF significantly inhibited early atherosclerotic lesions by inhibiting inflammatory response and decreasing the generation of ROS.
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