ATVB：改良柑橘果胶治疗血管硬化

2012年11月23日 -- 根据美国疾病预防控制中心，今年以来，2.5万人心血管疾病杀了近。随着时间的推移，炎症反应，胶原蛋白沉积和疤痕组织形成导致血管变硬，这个过程被称为血管纤维化。虽然研究人员已经证实激素醛固酮在这个过程中起到了重要作用，但其中机制知之甚少。

现在，一项发表在美国心脏协会Arteriosclerosis, Thrombosis, and Vascular Biology杂志上研究给心血管疾病带来了新的见解。该研究阐明了醛固酮和半乳糖凝集素-3联合如何通过炎症反应、纤维化和胶原沉积过程，共同促进血管重构和充血性心脏衰竭。

研究结果表明，半乳糖凝集素-3对炎症和纤维化反应是必需的，这提示半乳糖凝集素-3在血管纤维化过程中起到关键作用。同样重要的是，研究证明，改良柑橘果胶（MCP），一种来源于柑橘果皮精华的制剂，可以结合半乳糖凝集素-3，控制醛固酮诱导半乳糖凝集素-3水平升高。

果胶是-种复杂的碳水化合物，存在于所有水果和蔬菜的细胞壁中。通常用作果酱和果冻产品的黏合剂。血清中半乳糖凝集素-3与心脏衰竭和转移性肿瘤的高死亡率存在密切联系。研究证实了改良柑橘果胶能减缓肿瘤的进展和转移，阻断炎症反应，有助于防止纤维化。

与硬化相关的拓展阅读：

• Nat Genet：汉族人群肌萎缩侧索硬化疾病易感基因SUSD2及CAMK1G被发现
• JAMA：基于尸检的研究对美军中动脉粥样硬化的发病率进行了检查
• J Hepatol：NSBB治疗降低肝硬化患者肠粘膜通透性
• J. Hepatol.：肝硬化合并肝性脑病患者更易发生颅骨骨折
• The Lancet：依维莫司可明显抑制结节性硬化症的发展
• JCI：血脑屏障的免疫交换或助力多发性硬化症研究
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Galectin-3 Mediates Aldosterone-Induced Vascular Fibrosis

Objective—Aldosterone (Aldo) is involved in arterial stiffness and heart failure, but the mechanisms have remained unclear. Galectin-3 (Gal-3), a β-galactoside-binding lectin, plays an important role in inflammation, fibrosis, and heart failure. We investigated here whether Gal-3 is involved in Aldo-induced vascular fibrosis.

Methods and Results—In rat vascular smooth muscle cells Gal-3 overexpression enhanced specifically collagen type I synthesis. Moreover Gal-3 inhibition by modified citrus pectin or small interfering RNA blocked Aldo-induced collagen type I synthesis. Rats were treated with Aldo-salt combined with spironolactone or modified citrus pectin for 3 weeks. Hypertensive Aldo-treated rats presented vascular hypertrophy, inflammation, fibrosis, and increased aortic Gal-3 expression. Spironolactone or modified citrus pectin treatment reversed all the above effects. Wild-type and Gal-3 knock-out mice were treated with Aldo for 6 hours or 3 weeks. Aldo increased aortic Gal-3 expression, inflammation, and collagen type I in wild-type mice at both the short- and the long-term, whereas no changes occurred in Gal-3 knock-out mice.

Conclusion—Our data indicate that Gal-3 is required for inflammatory and fibrotic responses to Aldo in vascular smooth muscle cells in vitro and in vivo, suggesting a key role for Gal-3 in vascular fibrosis.