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蜂毒通过抗炎机制减少动脉粥样硬化病变形成。

Bee venom reduces atherosclerotic lesion formation via anti-inflammatory mechanism.

机构信息

Department of Pathology, Catholic University of Daegu, Korea.

出版信息

Am J Chin Med. 2010;38(6):1077-92. doi: 10.1142/S0192415X10008482.

Abstract

The components of bee venom (BV) utilized in the current study were carefully scrutinized with chromatography. Despite its well documented anti-inflammatory property, there are no reports regarding the influence of BV on the expression of cellular adhesion molecules in the vascular endothelium. A great amount of information exists concerning the effects of an atherogenic diet on atherosclerotic changes in the aorta, but little is known about the molecular mechanisms and the levels of gene regulation involved in the anti-inflammatory process induced by BV. The experimental atherosclerosis was induced in mice by a lipopolysaccharide (LPS) injection and an atherogenic diet. The animals were divided into three groups, the NC groups of animals that were fed with a normal diet, the LPS/fat group was fed with the atherogenic diet and received intraperitoneal injections of LPS, and the LPS/fat + BV group was given LPS, an atherogenic diet and intraperitoneal BV injections. At the end of each treatment period, the LPS/fat + BV group had decreased levels of total cholesterol (TC) and triglyceride (TG) in their serum, compared to the LPS/fat group. The LPS/fat group had significant expression of tumor necrosis factor (TNF)-α and interleukin (IL)-1β in the serum, compared with the NC group (p < 0.05). The amount of cytokines reduced consistently in the BV treatment groups compared with those in LPS/fat group. BV significantly reduced the amount of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), transforming growth factor-β1 (TGF-β1) and fibronectin in the aorta, compared with the LPS/fat group (p < 0.05). A similar pattern was also observed in the heart. In conclusion, BV has anti-atherogenic properties via its lipid-lowering and anti-inflammatory mechanisms.

摘要

在当前的研究中,仔细研究了蜜蜂毒液 (BV) 的成分,BV 具有明确的抗炎特性,但没有关于 BV 对血管内皮细胞细胞粘附分子表达的影响的报道。大量信息涉及致动脉粥样硬化饮食对主动脉粥样硬化变化的影响,但关于 BV 诱导的抗炎过程中涉及的分子机制和基因调控水平知之甚少。通过脂多糖 (LPS) 注射和致动脉粥样硬化饮食在小鼠中诱导实验性动脉粥样硬化。将动物分为三组,NC 组动物喂食正常饮食,LPS/脂肪组喂食致动脉粥样硬化饮食并接受腹腔内 LPS 注射,LPS/脂肪+BV 组给予 LPS、致动脉粥样硬化饮食和腹腔内 BV 注射。在每个治疗期结束时,与 LPS/脂肪组相比,LPS/脂肪+BV 组的血清总胆固醇 (TC) 和甘油三酯 (TG) 水平降低。与 NC 组相比,LPS/脂肪组血清中肿瘤坏死因子 (TNF)-α 和白细胞介素 (IL)-1β 的表达显著(p<0.05)。与 LPS/脂肪组相比,BV 治疗组的细胞因子含量一致减少。与 LPS/脂肪组相比,BV 显著降低主动脉中细胞间粘附分子-1 (ICAM-1)、血管细胞粘附分子-1 (VCAM-1)、转化生长因子-β1 (TGF-β1) 和纤维连接蛋白的含量(p<0.05)。在心脏中也观察到类似的模式。总之,BV 通过其降脂和抗炎机制具有抗动脉粥样硬化特性。

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