Ginkgo biloba extracts prevent aortic rupture in angiotensin IIinfused hypercholesterolemic mice
Ginkgo biloba extracts prevent aortic rupture in angiotensin IIinfused hypercholesterolemic mice
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银杏叶提取物预防血管紧张素 II 输注的高胆固醇血症小鼠的主动脉破裂
DOI：
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发表时间：
2019
影响因子：
8.2
通讯作者：
Xie Xiaojie
中科院分区：
文献类型：
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作者：
Huang Xiaofang;Zhang Songzhao;You Yayu;Zhang Na;Lu Hong;Alan Daugherty;Xie Xiaojie
腹主动脉瘤（AAA）是一种以病理性管腔扩张为特征的慢性血管疾病。主动脉破裂是 AAA 的致命后果。银杏叶提取物 (GBE) 是一种广泛用作食品补充剂、药物和化妆品的天然草本提取物，据报道可以抑制氯化钙诱导的小鼠 AAA 的发育。氯化钙诱导的 AAA 不会破裂，而血管紧张素 II (AngII) 诱导的小鼠 AAA 的主动脉破裂率很高，这表明与氯化钙诱导的 AAA 的机制可能不同。本研究旨在确定 GBE 是否会改善 AngII 诱导的 AAA 的主动脉扩张和破裂率。雄性载脂蛋白E（apoE）-/-小鼠被注射AngII并单独或组合施用GBE或其主要活性成分黄酮类化合物和银杏内酯。为了确定GBE对已形成AAA的小鼠的影响，雄性apoE−/−小鼠首先被注射AngII 28天以形成AAA，然后在已形成AAA的小鼠中施用GBE或媒介物，再连续注射AngII 56天。 GBE，而不是两种主要活性成分单独或协同作用，可以预防主动脉破裂，但不能预防主动脉扩张。 GBE 防止主动脉破裂的作用与收缩压、血脂和炎症无关。 GBE 也没有减弱已形成 AAA 的小鼠的主动脉破裂或进行性主动脉扩张。 GBE 也没有减少动脉粥样硬化病变区域。总之，GBE 可预防 AngII 输注的高胆固醇血症小鼠的主动脉破裂，但仅限于疾病发展的早期阶段。
Abdominal aortic aneurysms (AAAs) are a chronic vascular disease characterized by pathological luminal dilation. Aortic rupture is.the fatal consequence of AAAs. Ginkgo biloba extracts (GBEs), a natural herb extract widely used as food supplements, drugs, and.cosmetics, has been reported to suppress development of calcium chloride-induced AAAs in mice. Calcium chloride-induced AAAs.do not rupture, while angiotensin II (AngII)-induced AAAs in mice have high rate of aortic rupture, implicating potentially different.mechanisms from calcium chloride-induced AAAs. This study aimed to determine whether GBE would improve aortic dilation and.rupture rate of AngII-induced AAAs. Male apolipoprotein E (apoE) −/− mice were infused with AngII and administered either GBE or.its major active ingredients, flavonoids and ginkgolides, individually or in combination. To determine the effects of GBE in mice with.established AAAs, male apoE−/− mice were firstly infused with AngII for 28 days to develop AAAs, and then administered either.GBE or vehicle in mice with established AAAs, which were continuously infused with AngII for another 56 days. GBE, but not the two.major active components separately or synergistically, prevented aortic rupture, but not aortic dilation. The protection of GBE from.aortic rupture was independent of systolic blood pressure, lipid, and inflammation. GBE also did not attenuate either aortic rupture.or progressive aortic dilation in mice with established AAAs. GBE did not reduce the atherosclerotic lesion areas, either. In.conclusion, GBE prevents aortic rupture in AngII-infused hypercholesterolemic mice, but only in the early phase of the disease.development.