目的:ESC或Ehrlich实体癌是一种起源于小鼠自发性乳腺腺癌的肿瘤。它是一种高度侵袭性和快速生长的癌,当插入皮肤下时可以产生固体肿块。它的固体,未分化的形式使其成为研究癌症生物学的理想模型,肿瘤免疫学,并测试各种抗癌治疗方法。此外,arctiin具有多种有益特性,例如抗增殖,抗氧化,抗脂肪,和抗菌。本研究旨在探讨奥克替林对ESC大鼠的潜在抗癌益处,同时分析其对细胞纤维化标志物的影响。肿瘤细胞迁移,和炎性体通路。
方法:通过肌内注射由2×106个细胞组成的大鼠在其左后肢中给予肿瘤。八天后,一些大鼠每天口服30mg/kg的牛磺酸,持续3周。在电子显微镜下观察肌肉样品或用苏木精/伊红染色。此外,Toll样受体4(TLR4)的基因表达和蛋白质水平,NLR家族pyrin结构域含3(NLRP3),信号转导和转录激活因子3(STAT3),转化生长因子(TGF)-β,内皮生长因子(VEGF),和细胞周期蛋白D1在另一部分肌肉样本中进行了评估。
结果:当给予ESC大鼠奥克替林治疗时,他们的平均生存时间增加,肿瘤体积和重量减少。此外,当在电子显微镜下检查肿瘤组织时,它显示出多形性细胞的迹象,坏死,核分裂,细胞质内容物溢出的膜损伤,和细胞连接的丧失。用苏木精/伊红染色的切片显示出致密的细胞团和压缩,退化,肌肉萎缩.然而,用奥克替林治疗改善了所有这些效果。最后,TLR4、NLRP3、STAT3、TGF-β、VEGF,cyclinD1显著降低。
结论:通过使用牛磺酸苷,肿瘤的大小和重量得到了有效的减少,导致大鼠平均存活时间的增加和肌肉结构的改善。另外的研究表明,牛磺酸能够抑制炎症,纤维化,通过抑制STAT3、TGF-β1、TLR4、NLRP3、VEGF、和细胞周期蛋白D1。
OBJECTIVE: ESC or Ehrlich solid carcinoma is a type of tumor originating from a spontaneous mammary adenocarcinoma in mice. It is a highly aggressive and fast-growing carcinoma that can create a solid mass when inserted under the skin. Its solid, undifferentiated form makes it an ideal model for researching cancer biology, tumor immunology, and testing various anti-cancer treatments. Additionally, arctiin has multiple beneficial properties, such as anti-proliferative, anti-oxidative, anti-adipogenic, and anti-bacterial. This study aimed to explore the potential anti-cancer benefits of arctiin in rats with ESC while also analyzing its effects on cell fibrosis markers, tumor cell migration, and inflammasome pathways.
METHODS: Rats were given a tumor in their left hind limb via an intramuscular injection consisting of 2×106 cells. After eight days, some of the rats received a daily oral dose of 30 mg/kg of arctiin for three weeks. Muscle samples were observed under an electron microscope or stained with hematoxylin/eosin. Additionally, gene expression and protein levels of toll-like receptor 4 (TLR4), NLR family pyrin domain containing 3 (NLRP3), signal transducer and activator of transcription 3 (STAT3), transforming growth factor (TGF)-β, endothelial growth factor (VEGF), and cyclin D1 were assessed in another part of the muscle samples.
RESULTS: When ESC rats were given arctiin as a treatment, their mean survival time increased and their tumor volume and weight decreased. Additionally, when tumor tissue was examined under an electron microscope, it showed signs of pleomorphic cells, necrosis, nuclear fragmentation, membrane damage with cytoplasmic content spilling, and loss of cellular junction. The stained sections with hematoxylin/eosin showed a dense cellular mass and compressed, degenerated, and atrophied muscle. However, treatment with arctiin improved all these effects. Finally, the expression of TLR4, NLRP3, STAT3, TGF-β, VEGF, and cyclin D1 was significantly reduced with arctiin treatment.
CONCLUSIONS: Through the use of arctiin, tumor size and weight were effectively reduced, leading to an increase in the average survival time of rats and an improvement in muscle structure. Additional research has shown that arctiin is able to suppress inflammation, fibrosis, and the migration of tumor cells by inhibiting STAT3, TGF-β1, TLR4, NLRP3, VEGF, and cyclin D1.