心血管医学中的口服纳米制剂:动脉粥样硬化治疗的进展

Pharmaceuticals Pub Date : 2024-07-10 DOI:10.3390/ph17070919
Xu Sun, Xushuang Jia, Zhaolin Tan, Dongmei Fan, Meiqi Chen, Ning Cui, Aidong Liu, Da Liu
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引用次数: 0

摘要

动脉粥样硬化(AS)是指动脉壁上形成粥样硬化斑块,导致动脉变窄。如果发生在冠状动脉,血管可能完全堵塞,导致心肌梗塞;如果发生在脑血管,血管可能堵塞,导致脑梗塞,即中风。研究表明,动脉粥样硬化的发病机制涉及炎症、脂质浸润、氧化应激和内皮损伤等过程。SIRT 作为调节氧化应激、炎症和衰老分子机制的关键因子,对斑块形成、进展和易损性的发病机制有着重要影响。统计数据显示,在西方国家,强直性脊柱炎约占死亡人数的 50%。目前,口服药物是治疗强直性脊柱炎的主要手段,但其发展受到副作用、生物利用度低等不利因素的限制。近年来,随着纳米制剂的快速发展,研究人员将他汀类药物和天然产物药物结合到纳米制剂中,以提高其生物利用度。在此基础上,本文总结了强直性脊柱炎的主要发病机制,并提出了脂质体、纳米颗粒、纳米乳剂、纳米胶囊等新型口服纳米制剂,以提高其在强直性脊柱炎治疗中的应用。
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Oral Nanoformulations in Cardiovascular Medicine: Advances in Atherosclerosis Treatment
Atherosclerosis (AS) is the formation of atherosclerotic plaques on the walls of the arteries, causing them to narrow. If this occurs in the coronary arteries, the blood vessels may be completely blocked, resulting in myocardial infarction; if it occurs in the blood vessels of the brain, the blood vessels may be blocked, resulting in cerebral infarction, i.e., stroke. Studies have shown that the pathogenesis of atherosclerosis involves the processes of inflammation, lipid infiltration, oxidative stress, and endothelial damage, etc. SIRT, as a key factor regulating the molecular mechanisms of oxidative stress, inflammation, and aging, has an important impact on the pathogenesis of plaque formation, progression, and vulnerability. Statistics show that AS accounts for about 50 per cent of deaths in Western countries. Currently, oral medication is the mainstay of AS treatment, but its development is limited by side effects, low bioavailability and other unfavourable factors. In recent years, with the rapid development of nano-preparations, researchers have combined statins and natural product drugs within nanopreparations to improve their bioavailability. Based on this, this paper summarises the main pathogenesis of AS and also proposes new oral nanoformulations such as liposomes, nanoparticles, nanoemulsions, and nanocapsules to improve their application in the treatment of AS.
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