背景:Nigellasativa及其主要生物活性成分,百里香醌,表现出各种药理活性,包括神经保护,肾保护,心脏保护,胃保护,保肝,和抗癌作用。已经进行了许多研究试图阐明介导紫花苜蓿和百里香醌的这些不同药理学性质的分子信号传导途径。因此,这篇综述的目的是说明紫花苜蓿和百里香醌对不同细胞信号通路的影响。
方法:在线数据库Scopus,搜索PubMed和WebofScience,以使用相关关键词列表来识别相关文章,例如Nigellasativa,黑孜然,百里香醌,黑色种子,信号转导,细胞信号,抗氧化剂,Nrf2,NF-κB,PI3K/AKT,凋亡,JAK/STAT,AMPK,MAPK,等。本评论文章仅包含在2022年5月之前以英语发表的文章。
结果:研究表明,紫花苜蓿和百里香醌可提高抗氧化酶活性,有效清除自由基,从而保护细胞免受氧化应激。它们还可以通过Nrf2和NF-κB途径调节对氧化应激和炎症的反应。紫花苜蓿和百里香醌可以通过上调磷酸酶和张力蛋白同源物破坏PI3K/AKT途径来抑制癌细胞增殖。胸腺醌可以调节肿瘤细胞中的活性氧水平,将细胞周期阻滞在G2/M期,并影响包括p53,STAT3在内的分子靶标并触发线粒体凋亡途径。胸腺醌,通过调整AMPK,能调节细胞代谢和能量止血。最后,紫花苜蓿和百里香醌可以提高脑GABA含量,因此,它可以改善癫痫。
结论:综合来看,通过调节Nrf2和NF-κB信号来改善抗氧化状态和预防炎症过程,并通过破坏PI3K/AKT途径来抑制癌细胞增殖,这似乎是参与紫花苜蓿和百里香醌不同药理特性的主要机制。
BACKGROUND: Nigella sativa and its main bioactive ingredient,
thymoquinone, exhibit various pharmacological activities, including neuroprotective, nephroprotective, cardioprotective, gastroprotective, hepatoprotective, and anti-cancer effects. Many studies have been conducted trying to elucidate the molecular signaling pathways that mediate these diverse pharmacological properties of N. sativa and thymoquinone. Accordingly, the goal of this
review is to show the effects of N. sativa and
thymoquinone on different cell signaling pathways.
METHODS: The online databases Scopus, PubMed and Web of Science were searched to identify relevant articles using a list of related keywords such as Nigella sativa, black cumin, thymoquinone, black seed, signal transduction, cell signaling, antioxidant, Nrf2, NF-κB, PI3K/AKT, apoptosis, JAK/STAT, AMPK, MAPK, etc. Only articles published in the English language until May 2022 were included in the present
review article.
RESULTS: Studies indicate that N. sativa and thymoquinone improve antioxidant enzyme activities, effectively scavenges free radicals, and thus protect cells from oxidative stress. They can also regulate responses to oxidative stress and inflammation via Nrf2 and NF-κB pathways. N. sativa and thymoquinone can inhibit cancer cell proliferation through disruption of the PI3K/AKT pathway by upregulating phosphatase and tensin homolog.
Thymoquinone can modulate reactive oxygen species levels in tumor cells, arrest the cell cycle in the G2/M phase as well as affect molecular targets including p53, STAT3 and trigger the mitochondrial apoptosis pathway.
Thymoquinone, by adjusting AMPK, can regulate cellular metabolism and energy hemostasis. Finally, N. sativa and thymoquinone can elevate brain GABA content, and thus it may ameliorate epilepsy.
CONCLUSIONS: Taken together, the improvement of antioxidant status and prevention of inflammatory process by modulating the Nrf2 and NF-κB signaling and inhibition of cancer cell proliferation through disruption of the PI3K/AKT pathway appear to be the main mechanisms involved in different pharmacological properties of N. sativa and thymoquinone.