马鞭草苷,一种环烯醚萜苷,通过增强线粒体功能,增强抗氧化防御和减少细胞衰老,减轻紫杉醇诱导的骨骼肌毒性。

IF 3.1
Yu-Fan Chuang, Cai-Rong Wu, Wan-Hsuan Chang, Ying-Jung Su, Hung-Te Hsu, Fan-Li Lin, Yi-Ching Lo
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引用次数: 0

摘要

化疗引起的线粒体功能障碍和能量失衡是导致骨骼肌萎缩的关键因素,严重影响癌症患者的生活质量。紫杉醇是一种常用的化疗药物,主要通过损害线粒体功能而促进肌肉萎缩和细胞衰老。在这项研究中,我们研究了马头草苷(一种天然存在的环烯醚萜苷)在预防紫杉醇诱导的骨骼肌细胞损伤中的保护作用。使用C2C12细胞,我们评估了骆马苷是否可以抵消紫杉醇的有害影响。我们的研究结果表明,马甲苷显著提高了细胞活力,保护了线粒体功能,这体现在更好地保存线粒体DNA含量、膜电位和ATP的产生上,同时通过上调PGC-1α、TFAM和NRF1进一步增强了线粒体的生物发生。同时,马头草苷激活代谢调节因子SIRT1和AMPK,同时恢复PDK4的表达,表明能量调节有所改善。此外,糖原水平和肌管形态保持不变,肌球蛋白重链表达持续。马大苷有效降低细胞和线粒体活性氧,增加抗氧化防御,包括超氧化物歧化酶活性和谷胱甘肽水平。值得注意的是,它还能抑制紫杉醇诱导的衰老和炎症,表现为p21表达降低,NFκB磷酸化降低,Cdkn1a和Il6水平降低,SA-β-gal染色降低。总的来说,我们的研究结果表明,马鞭草苷通过保持线粒体功能、支持代谢稳态、减少氧化应激和限制衰老,对紫杉醇诱导的骨骼肌损伤提供全面的保护。这些结果突出了马鞭草苷作为一种预防辅助剂的潜力,以减轻化疗相关的肌肉毒性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Loganin, an Iridoid Glycoside, Alleviates Paclitaxel-Induced Skeletal Muscle Toxicity by Enhancing Mitochondrial Function, Boosting Antioxidant Defenses, and Reducing Cellular Senescence.

Mitochondrial dysfunction and energy imbalance caused by chemotherapy are key contributors to skeletal muscle atrophy, which severely impacts the quality of life in cancer patients. Paclitaxel, a commonly used chemotherapeutic agent, is known to promote muscle wasting and cellular senescence, largely by impairing mitochondrial function. In this study, we investigated the protective role of loganin, a naturally occurring iridoid glycoside, in preventing paclitaxel-induced damage to skeletal muscle cells. Using C2C12 cells, we assessed whether loganin could counteract the harmful effects of paclitaxel. Our results demonstrated that loganin significantly improved cell viability and protected mitochondrial function, as reflected by better preservation of mitochondrial DNA content, membrane potential, and ATP production, while further enhancing mitochondrial biogenesis through upregulation of PGC-1α, TFAM, and NRF1. In parallel, loganin activated metabolic regulators SIRT1 and AMPK, while restoring PDK4 expression, suggesting improved energy regulation. Additionally, glycogen levels and myotube morphology were maintained, alongside sustained myosin heavy chain expression. Loganin effectively reduced both cellular and mitochondrial reactive oxygen species and increased antioxidant defenses, including superoxide dismutase activity and glutathione levels. Notably, it also suppressed paclitaxel-induced senescence and inflammation, as shown by decreased p21 expression, reduced NFκB phosphorylation, and lower levels of Cdkn1a and Il6 as well as reduced SA-β-gal staining. Overall, our findings demonstrate that loganin offers comprehensive protection against paclitaxel-induced skeletal muscle injury by preserving mitochondrial function, supporting metabolic homeostasis, reducing oxidative stress, and limiting senescence. These results highlight the potential of loganin as a preventive adjunctive agent to mitigate chemotherapy-related muscle toxicity.

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