Chen Yongfeng, Song Di, Hou Qianqian, Ma Mengrui, Zhao Xiaoyun, Yang Tianzhi, Xie Huichao, Ding Pingtian
School of Pharmacy, Shenyang Pharmaceutical University, Shenyang 110016, China.
School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University, Shenyang 110016, China.
Pharmaceutics. 2022 Feb 1;14(2):343. doi: 10.3390/pharmaceutics14020343.
Venous malformation (VM), which causes severe damage to patients' appearance and organ function, is one of the most common vascular malformations. At present, many drugs in clinical treatment cause various adverse reactions. Herein, we synthesized cationic amphiphilic gelators (TA6, TA8, and TA9) by introducing saturated carbon chains of different lengths to tranexamic acid (TA), which could self-assemble into low-molecular-weight gels (LMWGs) as drug delivery carriers by hydrogen bonds, van der Waals forces, and hydrophobic interactions. The rheological properties, gelation driving force and drug release profiles of TA6, TA8, and TA9 hydrogels were characterized, and the results indicated that the hydrogels prepared in this study possessed the typical characteristics of a gel and could release drugs slowly. More importantly, the TA9 gelator showed significant pharmacological activity, in that it served as both an active drug compound and a drug carrier. The in vitro experiments demonstrated that TA9 induced HUVECs death and hemolysis by destroying cell membranes in a dose-dependent manner, and caused cell death and hemolysis at a concentration of 0.09 µM/mL. Meanwhile, we found TA9 could interact not only with fibrinogen, but also with other endogenous molecules in the blood. After the administration of TA9 hydrogel for 15 days, macroscopic imaging and histological evaluation in mice and rabbits displayed obvious thrombi, inflammatory reactions, and venous embolization, indicating that the mechanism of the TA9 hydrogel in treating VM was involved in two processes. Firstly, the TA9 hydrogel relied on its mechanical strength to physically block veins and continuously release TA9, in situ, for targeted therapy. Then, TA9 destroyed endothelial cells and damaged venous walls critically, causing thrombi. Most excitingly, TA9 was hydrolyzed to TA by enzymes that inhibited the degradation of thrombi by plasmin to prolong the embolization time and to promote venous fibrosis. Compared with other clinically available sclerosants, the degradation of TA9 also empowered a better biocompatibility and biodegradability for the TA9 hydrogel. In conclusion, we synthesized a potentially safe and effective derivative of TA and developed a low-molecular-weight gel as a self-delivery system for TA in treating VM.
静脉畸形(VM)是最常见的血管畸形之一,会对患者的外观和器官功能造成严重损害。目前,临床治疗中的许多药物会引起各种不良反应。在此,我们通过将不同长度的饱和碳链引入氨甲环酸(TA)来合成阳离子两亲性凝胶剂(TA6、TA8和TA9),它们可通过氢键、范德华力和疏水相互作用自组装成低分子量凝胶(LMWG)作为药物递送载体。对TA6、TA8和TA9水凝胶的流变学性质、凝胶化驱动力和药物释放曲线进行了表征,结果表明本研究制备的水凝胶具有典型的凝胶特性且能缓慢释放药物。更重要的是,TA9凝胶剂表现出显著的药理活性,它既是一种活性药物化合物又是一种药物载体。体外实验表明,TA9通过以剂量依赖的方式破坏细胞膜诱导人脐静脉内皮细胞(HUVECs)死亡和溶血,并在浓度为0.09 μM/mL时引起细胞死亡和溶血。同时,我们发现TA9不仅能与纤维蛋白原相互作用,还能与血液中的其他内源性分子相互作用。给小鼠和兔子施用TA9水凝胶15天后,宏观成像和组织学评估显示出明显的血栓、炎症反应和静脉栓塞,表明TA9水凝胶治疗VM的机制涉及两个过程。首先,TA9水凝胶依靠其机械强度物理性阻塞静脉并原位持续释放TA9进行靶向治疗。然后,TA9严重破坏内皮细胞并损伤静脉壁,导致血栓形成。最令人兴奋的是,TA9被酶水解为TA,抑制纤溶酶对血栓的降解,从而延长栓塞时间并促进静脉纤维化。与其他临床可用的硬化剂相比,TA9的降解也赋予了TA9水凝胶更好的生物相容性和生物降解性。总之,我们合成了一种潜在安全有效的TA衍生物,并开发了一种低分子量凝胶作为TA治疗VM的自递送系统。