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乳香酸通过激活抑制性核因子-κB激活来抑制视网膜母细胞瘤细胞生长。

Inhibition of Retinoblastoma Cell Growth by Boswellic Acid Through Activation of the Suppressing Nuclear Factor-κB Activation.

作者信息

Doğan Semih, Tuncer Mehmet Cudi, Özdemir İlhan

机构信息

Department of Ophthalmology, Faculty of Medicine, Beykent University, İstanbul 34398, Turkey.

Department of Anatomy, Faculty of Medicine, Dicle University, Diyarbakır 21280, Turkey.

出版信息

Medicina (Kaunas). 2025 Mar 10;61(3):480. doi: 10.3390/medicina61030480.

DOI:10.3390/medicina61030480
PMID:40142291
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11944177/
Abstract

Despite the development of treatment methods and the emergence of alternative new approaches in recent years, the visual prognosis of retinoblastoma contains deficiencies and this situation increases the need for the development of new treatment approaches. The cytotoxic and apoptosis-inducing effects of the combination of boswellic acid (BA), which has been determined to have significant potential in preclinical and clinical studies of various diseases, and Cisplatin (Cis), a potent chemotherapy agent, were investigated on the human retinoblastoma cell line (Y79). The cytotoxic effect of BA and Cis on Y79 cells was determined by the water soluble tetrazolium-1 (WST-1) test, the apoptotic rate of the cells was determined by annexin V staining, and the gene expressions of , and , which play an important role in apoptosis, were determined by RT-qPCR analysis. Interleukin 1-beta (IL1-β), tumor necrosis factor-α (TNF-α) and interferon γ (IFN-γ) levels were analyzed in cell lysates obtained from the experimental groups. The combination of BA and Cis selectively inhibited the growth of Y79 cells and modulated signaling, potentially through post-translational regulatory mechanisms. Moreover, it induced apoptosis by increasing and expressions, confirming its pro-apoptotic effects. Additionally, the combination treatment was associated with a reduction in inflammatory cytokine levels (TNF-α, IL1-β), suggesting a potential regulatory effect on inflammation-related pathways rather than direct inhibition of activation. These findings suggest that BA combined with Cis inhibits Y79 retinoblastoma cell growth by inducing apoptosis and modulating signaling. While mRNA levels increased, reduced inflammatory cytokines and enhanced apoptosis suggest potential post-translational regulation. Further studies are needed to confirm protein-level effects and in vivo efficacy.

摘要

尽管近年来治疗方法有所发展且出现了替代性新方法,但视网膜母细胞瘤的视觉预后仍存在不足,这种情况增加了开发新治疗方法的必要性。在各种疾病的临床前和临床研究中已确定具有显著潜力的乳香酸(BA)与强效化疗药物顺铂(Cis)联合使用的细胞毒性和诱导凋亡作用,在人视网膜母细胞瘤细胞系(Y79)上进行了研究。通过水溶性四氮唑盐-1(WST-1)试验测定BA和Cis对Y79细胞的细胞毒性作用,通过膜联蛋白V染色测定细胞的凋亡率,并通过RT-qPCR分析测定在凋亡中起重要作用的 、 和 的基因表达。在从实验组获得的细胞裂解物中分析白细胞介素1-β(IL1-β)、肿瘤坏死因子-α(TNF-α)和干扰素γ(IFN-γ)水平。BA和Cis的组合选择性地抑制Y79细胞的生长并调节 信号传导,可能是通过翻译后调节机制。此外,它通过增加 和 的表达诱导凋亡,证实了其促凋亡作用。此外,联合治疗与炎症细胞因子水平(TNF-α、IL1-β)的降低有关,表明对炎症相关途径具有潜在的调节作用,而不是直接抑制 激活。这些发现表明,BA与Cis联合使用通过诱导凋亡和调节 信号传导来抑制Y79视网膜母细胞瘤细胞的生长。虽然 信使核糖核酸水平增加,但炎症细胞因子减少和凋亡增强表明存在潜在的翻译后调节。需要进一步研究来证实 蛋白水平的作用和体内疗效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/9b6133a601ba/medicina-61-00480-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/4376b243f8d4/medicina-61-00480-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/cc726352cbe9/medicina-61-00480-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/74d39d6ef962/medicina-61-00480-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/93d854f10615/medicina-61-00480-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/bea6ed6c6694/medicina-61-00480-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/9b6133a601ba/medicina-61-00480-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/4376b243f8d4/medicina-61-00480-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/cc726352cbe9/medicina-61-00480-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/74d39d6ef962/medicina-61-00480-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/93d854f10615/medicina-61-00480-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/bea6ed6c6694/medicina-61-00480-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91f6/11944177/9b6133a601ba/medicina-61-00480-g006.jpg

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