Wen Xiaodong, Reynolds Lacy, Mulik Rohit S, Kim Soo Young, Van Treuren Tim, Nguyen Liem H, Zhu Hao, Corbin Ian R
Advanced Imaging Research Center, University of Texas Southwestern Medical Center, Dallas, Texas.
Children's Research Institute, Department of Pediatrics and Internal Medicine, Simmons Comprehensive Cancer Center, Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; Internal Medicine Division of Liver and Digestive Diseases, University of Texas Southwestern Medical Center, Dallas, Texas.
Gastroenterology. 2016 Feb;150(2):488-98. doi: 10.1053/j.gastro.2015.10.008. Epub 2015 Oct 17.
BACKGROUND & AIMS: Dietary intake of the natural omega-3 fatty acid docosahexaenoic acid (DHA) has been implicated in protecting patients with viral hepatitis B or C from developing hepatocellular carcinoma (HCC). Little is known about the effects of DHA on established solid tumors. Here we describe a low-density lipoprotein-based nanoparticle that acts as a transporter for unesterified DHA (LDL-DHA) and demonstrates selective cytotoxicity toward HCC cells. We investigated the ability of LDL-DHA to reduce growth of orthotopic hepatomas in rats.
AxC-Irish (ACI) rats were given intrahepatic injections of rat hepatoma cells (H4IIE); 24 tumor-bearing rats (mean tumor diameter, ∼1 cm) were subject to a single hepatic artery injection of LDL nanoparticles (2 mg/kg) loaded with DHA (LDL-DHA), triolein (LDL-TO), or sham surgery controls. Tumor growth was measured by magnetic resonance imaging and other methods; tumor, liver, and serum samples were collected and assessed by histochemical, immunofluorescence, biochemical, and immunoblot analyses.
Three days after administration of LDL-TO or sham surgery, the control rats had large, highly vascularized tumors that contained proliferating cells. However, rats given LDL-DHA had smaller, pale tumors that were devoid of vascular supply and >80% of the tumor tissue was necrotic. Four to 6 days after injection of LDL-DHA, the tumors were 3-fold smaller than those of control rats. The liver tissue that surrounded the tumors showed no histologic or biochemical evidence of injury. Injection of LDL-DHA into the hepatic artery of rats selectively deregulated redox reactions in tumor tissues by increasing levels of reactive oxygen species and lipid peroxidation, depleting and oxidizing glutathione and nicotinamide adenine dinucleotide phosphate, and significantly down-regulating the antioxidant enzyme glutathione peroxidase-4. Remarkably, the redox balance in the surrounding liver was not disrupted.
LDL-DHA nanoparticle selectively kills hepatoma cells and reduces growth of orthotopic liver tumors in rats. It induces tumor-specific necrosis by selectively disrupting redox balance within the cancer cell.
膳食中摄入天然ω-3脂肪酸二十二碳六烯酸(DHA)被认为可保护乙型或丙型病毒性肝炎患者不发生肝细胞癌(HCC)。关于DHA对已形成的实体瘤的影响知之甚少。在此,我们描述了一种基于低密度脂蛋白的纳米颗粒,它可作为未酯化DHA的转运体(LDL-DHA),并对HCC细胞表现出选择性细胞毒性。我们研究了LDL-DHA降低大鼠原位肝癌生长的能力。
将大鼠肝癌细胞(H4IIE)肝内注射到AxC-爱尔兰(ACI)大鼠体内;24只荷瘤大鼠(平均肿瘤直径约1 cm)接受单次肝动脉注射负载DHA的LDL纳米颗粒(2 mg/kg)(LDL-DHA)、三油酸甘油酯(LDL-TO)或假手术对照。通过磁共振成像和其他方法测量肿瘤生长;收集肿瘤、肝脏和血清样本,并通过组织化学、免疫荧光、生化和免疫印迹分析进行评估。
给予LDL-TO或假手术后3天,对照大鼠有大的、血管丰富的肿瘤,其中含有增殖细胞。然而,给予LDL-DHA的大鼠肿瘤较小且颜色苍白,没有血管供应,超过80%的肿瘤组织坏死。注射LDL-DHA后4至6天,肿瘤比对照大鼠的肿瘤小3倍。肿瘤周围的肝组织没有组织学或生化损伤证据。将LDL-DHA注射到大鼠肝动脉中,通过增加活性氧水平和脂质过氧化、消耗和氧化谷胱甘肽及烟酰胺腺嘌呤二核苷酸磷酸,并显著下调抗氧化酶谷胱甘肽过氧化物酶-4,选择性地破坏肿瘤组织中的氧化还原反应。值得注意的是,周围肝脏的氧化还原平衡未被破坏。
LDL-DHA纳米颗粒可选择性杀死肝癌细胞并降低大鼠原位肝肿瘤的生长。它通过选择性破坏癌细胞内的氧化还原平衡诱导肿瘤特异性坏死。