靶向MAPK通路诱导胶质母细胞瘤细胞凋亡和自噬抑制的载小檗碱纳米脂质体的合成与表征。

Min Xi, Somayeh Hasani Kia, Hangyu Shi, Xinya Dong, Yongqiang Shi, Luyi Zhang, Bin Jiang
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引用次数: 0

摘要

胶质母细胞瘤(GBM)是最具侵袭性和致死性的原发性脑肿瘤,需要创新的治疗策略来改善患者的预后和生活质量。针对这一迫切需求,我们的研究重点是开发一种装载小檗碱(BBR)的纳米脂质体(NL)作为靶向药物递送系统来对抗GBM。这些纳米脂质体采用薄膜水合法合成,并通过先进的物理和光谱技术对其进行了表征,在提高BBR的治疗效果方面具有很大的潜力。NL配方在粒径为83±12 nm的情况下,负载效率为65.71±1.31%,确保了最佳的给药效果。缓释实验表明,包封的BBR在48小时内持续释放82.65±1.75%,显示出其控释能力。体外实验,包括细胞活力、TUNEL和western blot分析,证实了NL-BBR的有效抗癌作用。该制剂显著破坏了U-87胶质母细胞瘤细胞的代谢,诱导细胞自噬和凋亡增强,最终通过固有的凋亡途径导致细胞死亡。此外,western blot结果表明,NL-BBR有效抑制MAPK信号通路,这是GBM进展的关键驱动因素。本研究强调了将小檗碱纳入纳米脂质体的变革潜力,这不仅提高了其溶解度和生物利用度,而且显著增强了其治疗效果。这些发现为GBM治疗的先进纳米干预铺平了道路,为改善这一具有挑战性的癌症领域的结果提供了一线希望。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Synthesis and characterization of berberine-loaded nanoliposome for targeting of MAPK pathway to induce apoptosis and suppression of autophagy in glioblastoma.

Glioblastoma (GBM), the most aggressive and lethal primary brain tumor, demands innovative therapeutic strategies to improve patient outcomes and quality of life. Addressing this urgent need, our study focuses on developing a berberine (BBR)-loaded nanoliposome (NL) as a targeted drug delivery system to combat GBM. Synthesized using the thin film hydration method and characterized through advanced physical and spectroscopic techniques, these NLs demonstrate promising potential in enhancing BBR's therapeutic efficacy. The NL formulation achieved an impressive loading efficiency of 65.71 ± 1.31% with a particle size of 83 ± 12 nm, ensuring optimal delivery. Sustained release experiments revealed that 82.65 ± 1.75% of the encapsulated BBR was consistently released over 48 h, highlighting its controlled release capabilities.In vitroassays, including cell viability, TUNEL, and western blot analysis, confirmed the potent anti-cancer effects of NL-BBR. The formulation significantly disrupted the metabolism of U-87 glioblastoma cells, inducing enhanced autophagy and apoptosis, ultimately leading to cell death via intrinsic apoptotic pathways. Additionally, western blot results demonstrated that NL-BBR effectively suppressed the mitogen-activated protein kinase signaling pathway, a critical driver of GBM progression. This study underscores the transformative potential of incorporating BBR into NLs, which not only enhances its solubility and bioavailability but also significantly amplifies its therapeutic impact. These findings pave the way for advanced nano-based interventions in GBM treatment, offering a glimmer of hope for improved outcomes in this challenging cancer landscape.

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