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Photobiological modulation of hepatoma cell lines and hepatitis B subviral particles secretion in response to 650 nm low level laser treatment
Journal of the Egyptian National Cancer Institute Pub Date : 2023-10-23 , DOI: 10.1186/s43046-023-00190-3
Ghada M Al-Toukhy 1 , Reda A Suef 2 , Sarah Hassan 3 , Mohamed M S Farag 2, 4 , Tarek A El-Tayeb 5 , Mohamed T M Mansour 6, 7
Affiliation  

Chronic hepatitis B virus (HBV) infection is a serious global health concern, with an increased incidence and risk of developing cirrhosis and hepatocellular carcinoma (HCC). Patients chronically infected with HBV are likely to experience chronic oxidative stress, leading to mitochondrial dysfunction. Photobiomodulation is induced by the absorption of low-level laser therapy (LLLT) with a red or infrared laser by cytochrome C oxidase enzyme, resulting in mitochondrial photoactivation. Although it is widely used in clinical practice, the use of LLL as adjuvant therapy for persistent HBV infection is uncommon. This study aimed to investigate the effect of LLLT dosage from 2 J/cm2 to 10 J/cm2 of red diode laser (650 nm) on both hepatoma cell lines (HepG2.2.15 [integrated HBV genome stable cell model] and non-integrated HepG2), with a subsequent impact on HBVsvp production. The present study evaluated the effects of different fluences of low-level laser therapy (LLLT) irradiation on various aspects of hepatoma cell behavior, including morphology, viability, ultrastructure, and its impact on HBVsvp synthesis. In response to LLLT irradiation, we observed a considerable reduction in viability, proliferation, and HBVsvp production in both hepatoma cell lines HepG2.2.15 and HepG2. Ultrastructural modification of mitochondria and nuclear membranes: This effect was dose, cell type, and time-dependent. The use of LLLT may be a promising therapy for HCC and HBV patients by reducing cell proliferation, HBVsvp production, and altering mitochondrial and nuclear structure involved in cellular death inducers. Further research is required to explore its clinical application.

中文翻译:

650 nm 低强度激光治疗对肝癌细胞系和乙型肝炎亚病毒颗粒分泌的光生物学调节

慢性乙型肝炎病毒(HBV)感染是一个严重的全球健康问题,导致肝硬化和肝细胞癌(HCC)的发病率和风险增加。慢性感染乙肝病毒的患者可能会经历慢性氧化应激,导致线粒体功能障碍。光生物调节是通过细胞色素 C 氧化酶吸收红色或红外激光的低强度激光治疗 (LLLT) 来诱导的,从而导致线粒体光活化。尽管 LLL 在临床实践中广泛应用,但使用 LLL 作为持续性 HBV 感染的辅助治疗并不常见。本研究旨在研究 2 J/cm2 至 10 J/cm2 红色二极管激光 (650 nm) 的 LLLT 剂量对两种肝癌细胞系(HepG2.2.15 [整合的 HBV 基因组稳定细胞模型] 和非整合的 HepG2 的影响) ),随后对 HBVsvp 产生产生影响。本研究评估了低强度激光疗法 (LLLT) 照射的不同能量密度对肝癌细胞行为各个方面的影响,包括形态、活力、超微结构及其对 HBVsvp 合成的影响。为了响应 LLLT 照射,我们观察到肝癌细胞系 HepG2.2.15 和 HepG2 的活力、增殖和 HBVsvp 产生显着降低。线粒体和核膜的超微结构修饰:这种效应与剂量、细胞类型和时间有关。LLLT 的使用可能是 HCC 和 HBV 患者的一种有前途的治疗方法,因为它可以减少细胞增殖、HBVsvp 的产生,并改变细胞死亡诱导剂中涉及的线粒体和核结构。需要进一步研究探索其临床应用。
更新日期:2023-10-24
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