Guo Jian-En, Mi Shu-Bin, Yan Xiu-Chuan, Xin Si-Yuan, Gao Fei, Liang Guang-He, Li Jing-Hua
Chengde Medical University, Chengde 067000, China.
Graduate School of Tianjin Medical University, Tianjin 300070, China.
Zhongguo Zhong Yao Za Zhi. 2017 Feb;42(4):752-757. doi: 10.19540/j.cnki.cjcmm.20161222.076.
To observe the functions of Gualou Xiebai Banxia decoction（GXBD） on regulating lipid metabolism, anti-oxidation, and interposing ox-LDL/Lox-1 pathway, and to explore its anti-atherosclerosis (AS) mechanisms. AS models were established by using 42 Apo-E-/- male mice with high fat diet. AS model mice were randomly divided into the model group, simvastatin group, and GXBD high and low dose groups. C57BL/6J male mice were used as the normal control group, n=10 and the treatment lasted for 8 weeks. The levels of TC, TG, LDL-C, HDL-C, SOD, MDA, GSH-px, and ox-LDL in blood serum were tested 24 h after the last administration. The changes of aortic tissues structure were observed by HE staining; the expression levels of Lox-1 protein and the expression levels of mRNA were detected by Western blot and PCR respectively.Results showed that the blood lipid levels and MDA, ox-LDL levels in blood serum of model group were significantly higher than those in the normal control group, but SOD, GSH-px levels were significantly lower than those in the normal control group, and the Lox-1 protein and mRNA expression levels were also significantly higher than those in the control group(P<0.05), namely aortic atherosclerosis lesions were obvious in model group.The levels of blood lipid and MDA, ox-LDL of GXBD high and low dose groups and simvastatin group were significantly lower than those in model group, while SOD, GSH-px levels were significantly higher than those in model group, and Lox-1 protein and mRNA expression levels were significantly lower than those in model group(P<0.05), namely the aortic atherosclerosis lesions were significantly relieved. The above results indicated that GXBD was capable of modulating blood lipid, anti-oxidation, and inhibiting the expression of Lox-1, and interposing ox-LDL/Lox-1 pathway in the AS model Apo-E-/- mice, which may be one of the mechanisms of anti-atherosclerosis.
观察瓜蒌薤白半夏汤（GXBD）对调节脂质代谢、抗氧化及干预氧化型低密度脂蛋白/凝集素样氧化低密度脂蛋白受体1（ox-LDL/Lox-1）通路的作用，探讨其抗动脉粥样硬化（AS）机制。采用42只高脂饮食的载脂蛋白E基因敲除（Apo-E-/-）雄性小鼠建立AS模型。将AS模型小鼠随机分为模型组、辛伐他汀组、GXBD高剂量组和低剂量组。以C57BL/6J雄性小鼠作为正常对照组，每组10只，给药持续8周。末次给药24小时后检测血清中总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH-px）及氧化型低密度脂蛋白（ox-LDL）水平。通过苏木精-伊红（HE）染色观察主动脉组织结构变化；分别采用蛋白质免疫印迹法（Western blot）和聚合酶链反应（PCR）检测Lox-1蛋白表达水平及mRNA表达水平。结果显示，模型组血清血脂水平、MDA及ox-LDL水平显著高于正常对照组，而SOD、GSH-px水平显著低于正常对照组，且Lox-1蛋白及mRNA表达水平也显著高于对照组（P<0.05），即模型组主动脉粥样硬化病变明显。GXBD高、低剂量组及辛伐他汀组血脂、MDA及ox-LDL水平显著低于模型组，而SOD、GSH-px水平显著高于模型组，Lox-1蛋白及mRNA表达水平显著低于模型组（P<0.05），即主动脉粥样硬化病变明显减轻。上述结果表明，GXBD在AS模型Apo-E-/-小鼠中具有调节血脂、抗氧化、抑制Lox-1表达及干预ox-LDL/Lox-1通路的作用，这可能是其抗动脉粥样硬化的机制之一。
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