Britanin是一种生物活性倍半萜内酯,以其有效的抗炎和抗氧化特性而闻名。它还表现出显著的抗肿瘤活性,在体外和体内抑制肿瘤生长。目前对Britanin的研究包括30篇主要与肿瘤有关的论文,其中大多数是胃肠道肿瘤,以前没有总结过。为了推动学术辩论,本文综述了Britanin在胃肠道肿瘤中的现有研究。它还使用与消化系统不直接相关的数据概述了新的研究方向,但可以在未来的胃肠道研究中采用。发现不列颠宁可以抵消肝脏,结直肠,胰腺,和胃肿瘤,通过调节增殖,凋亡,自噬,免疫反应,迁移,和血管生成。正如在胰腺中证实的那样,胃,和肝癌,其最常见的分子效应包括核因子κB和B细胞淋巴瘤2下调,以及Bcl-2相关的X蛋白上调。此外,已发现诱导Akt激酶和叉头盒O1轴,激活AMP激活的蛋白激酶通路,提高白细胞介素-2和过氧化物酶体增殖物激活受体-γ水平,减少白细胞介素-10,以及下调基质金属蛋白酶-9,Twist家族bHLH转录因子1和环氧合酶-2。它还通过中断Ras/RAF/MEK/ERK途径和mTOR/P70S6K/4EBP1信号传导来抑制Myc-HIF1α相互作用和程序性死亡配体1转录。未来的研究应该旨在解开不列颠宁和乙酰胆碱酯酶之间的联系,肥大细胞,骨质溶解,缺血,因为胃肠环境以外的研究提供了令人信服的数据。由于Britanin对非癌细胞的细胞毒性明显低于肿瘤细胞,虽然对后者仍然有效,使用动物模型的进一步深入研究是值得的。该化合物表现出多效的生物活性,并提供了相当大的前景作为抗癌剂,这可以解决目前胃肠道肿瘤患者治疗方案匮乏和死亡率高的问题.
Britanin is a bioactive sesquiterpene lactone known for its potent anti-inflammatory and anti-oxidant properties. It also exhibits significant anti-tumor activity, suppressing tumor growth in vitro and in vivo. The current body of research on Britanin includes thirty papers predominantly related to neoplasms, the majority of which are gastrointestinal tumors that have not been summarized before. To drive academic debate, the present paper reviews the available research on Britanin in gastrointestinal tumors. It also outlines novel research directions using data not directly concerned with the digestive system, but which could be adopted in future gastrointestinal research. Britanin was found to counteract liver, colorectal, pancreatic, and gastric tumors, by regulating proliferation, apoptosis, autophagy, immune response, migration, and angiogenesis. As confirmed in pancreatic, gastric, and liver cancer, its most commonly noted molecular effects include nuclear factor kappa B and B-cell lymphoma 2 downregulation, as well as Bcl-2-associated X protein upregulation. Moreover, it has been found to induce the Akt kinase and Forkhead box O1 axis, activate the AMP-activated protein kinase pathway, elevate interleukin-2 and peroxisome proliferator-activated receptor-γ levels, reduce interleukin-10, as well as downregulate matrix metalloproteinase-9, Twist family bHLH transcription factor 1, and cyclooxygenase-2. It also inhibits Myc-HIF1α interaction and programmed death ligand 1 transcription by interrupting the Ras/ RAF/MEK/ERK pathway and mTOR/P70S6K/4EBP1 signaling. Future research should aim to unravel the link between Britanin and acetylcholinesterase, mast cells, osteolysis, and ischemia, as compelling data have been provided by studies outside the gastrointestinal context. Since the cytotoxicity of Britanin on noncancerous cells is significantly lower than that on tumor cells, while still being effective against the latter, further in-depth studies with the use of animal models are merited. The compound exhibits pleiotropic biological activity and offers considerable promise as an anti-cancer agent, which may address the current paucity of treatment options and high mortality rate among patients with gastrointestinal tumors.