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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Effects of long-term chloroquine administration on the natural history of aortic aneurysms in mice
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Effects of long-term chloroquine administration on the natural history of aortic aneurysms in mice

机译：长期服用氯喹对小鼠主动脉瘤自然病程的影响

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Autophagy regulates cellular homeostasis and integrates the cellular pro-survival machinery. We investigated the role of autophagy in the natural history of murine abdominal aortic aneurysms (AAA). ApoE(-/-) mice were implanted with saline-or angiotensin II (Ang-II)-filled miniosmotic pumps then treated with either the autophagy inhibitor chloroquine (CQ; 50 mg.(kg body mass)(-1).day(-1), by intraperitoneal injection) or saline. Ang-II-elicited aneurysmal expansion of the suprarenal aorta coupled with thrombus formation were apparent 8 weeks later. CQ had no impact on the incidence (50% for Ang-II compared with 46.2% for Ang-II + CQ; P = NS) and categorical distribution of aneurysms. The markedly reduced survival rate observed with Ang-II (57.1% for Ang-II compared with 100% for saline; P < 0.05) was unaffected by CQ (61.5% for Ang-II + CQ; P = NS compared with Ang-II). CQ did not affect the mean maximum suprarenal aortic diameter (1.91 +/- 0.19 mm for Ang-II compared with 1.97 +/- 0.21 mm for Ang-II + CQ; P = NS). Elastin fragmentation, collagen accumulation, and smooth muscle attrition, which were higher in Ang-II-treated mice, were unaffected by CQ treatment. Long-term CQ administration does not affect the natural history and prognosis of experimental AAA, suggesting that global loss of autophagy is unlikely to be a causal factor in the development of aortic aneurysms. Manipulation of autophagy as a mechanism to reduce AAA may need re-evaluation.
机译：自噬调节细胞稳态并整合细胞的生存机制。我们调查了自噬在小鼠腹主动脉瘤（AAA）的自然史中的作用。将ApoE（-/-）小鼠植入充满生理盐水或血管紧张素II（Ang-II）的微型渗透泵，然后用自噬抑制剂氯喹（CQ; 50 mg。（kg体重）（-1）.day（ -1），腹膜内注射）或生理盐水。 Ang-II引起的肾上动脉的动脉瘤扩张以及血栓形成在8周后可见。 CQ对动脉瘤的分类分布没有影响（Ang-II为50％，Ang-II + CQ为46.2％; P = NS）。 Ang-II的存活率显着降低（Ang-II为57.1％，盐水为100％; P <0.05）不受CQ的影响（Ang-II + CQ为61.5％; P = NS与Ang-II相比） ）。 CQ不会影响平均最大肾上主动脉直径（Ang-II为1.91 +/- 0.19 mm，而Ang-II + CQ为1.97 +/- 0.21 mm; P = NS）。弹性蛋白片段化，胶原蛋白积累和平滑肌磨损（在Ang-II处理的小鼠中更高）不受CQ处理的影响。长期CQ管理不会影响实验性AAA的自然病史和预后，这表明自噬的整体丧失不太可能是主动脉瘤发展的原因。自噬作为减少AAA的机制可能需要重新评估。

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