结直肠癌（CRC）被认为是全球主要引发发病率和死亡率的恶性肿瘤。因此，作者研制了新型的聚集β-乳球蛋白涂覆油酸的脂质体（α-LA涂覆脂质体），以期发挥其对CRC的潜在抗肿瘤活性，无论是体外还是在DMH诱导的CRC动物模型中。体外实验结果显示，α-LA涂覆脂质体对正常人细胞具有较高的安全性，同时对Caco-2细胞具有较强的抗肿瘤活性，IC50值为57.01 ± 3.55 µM，并且具有选择性指数为6.92 ± 0.48。这种抗肿瘤活性被认为是通过诱导凋亡机制产生的，通过核团聚和Caco-2细胞在亚G1阶段的停滞来证明。此外，α-LA涂覆脂质体还显著上调p53基因并下调Bcl2基因。此外，体内实验结果显示，在α-LA涂覆脂质体治疗诱导的CRC动物六周后，CRC的症状明显改善。这表现为AFP、CEA、CA19.9、TNF-α、IL-1β、MDA和NO的明显降低，以及SOD、GPx、GSH、CAT和CD4+水平的显著升高。组织病理学研究结果进一步证实了α-LA涂覆脂质体在CRC治疗中的治疗潜力。因此，本研究结果证明了α-LA涂覆脂质体通过恢复受损氧化应激、改善免疫反应和减轻炎症的作用来抑制CRC的抗肿瘤活性。

Colorectal cancer (CRC) is a malignant tumor recognized as a major cause of morbidity and mortality throughout the world. Therefore, novel liposomes of oleic acid coated with camel α-lactalbumin (α-LA coated liposomes) were developed for their potential antitumor activity against CRC, both in vitro and in DMH-induced CRC-modeled animal. In vitro results indicated the high safety of α-LA coated liposomes towards normal human cells with potent antitumor activity against Caco-2 cells at an IC50 value of 57.01 ± 3.55 µM with selectivity index of 6.92 ± 0.48. This antitumor activity has been attributed to induction of the apoptotic mechanism, as demonstrated by nuclear condensation and arrest of Caco-2 cells in sub-G1 populations. α-LA coated liposomes also revealed a significant up-regulation of the p53 gene combined with a down-regulation of the Bcl2 gene. Moreover, in vivo results revealed that treatment of induced-CRC modeled animals with α-LA coated liposomes for six weeks markedly improved the CRC-disorders; this was achieved from the significant reduction in the values of AFP, CEA, CA19.9, TNF-α, IL-1β, MDA, and NO coupled with remarkable rise in SOD, GPx, GSH, CAT, and CD4+ levels. The histopathological findings asserted the therapeutic potential of α-LA coated liposomes in the treatment of CRC. Therefore, the present results proved the antitumor activity of α-LA coated liposomes against CRC through the restoration of impaired oxidative stress, improved immune response, and reduced inflammation.Communicated by Ramaswamy H. Sarma.