Parishin 通过降低自然衰老小鼠的 CD38 水平缓解肺纤维化

Xinxiu Zhao, Shixian Zhou, Zhaoying Sheng, Linlin Sun, Qin Zhang, Yuanqiang Lu
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摘要

Parishin 是一种天然化合物,在减轻与衰老相关的表型和改善与衰老相关疾病的预后方面具有巨大潜力。鉴于衰老是包括肺纤维化在内的多种慢性疾病的主要风险因素,我们研究了 Parishin 对细胞衰老和肺健康的影响。在我们的研究中,我们用 parishin 处理小鼠肺上皮细胞,观察到细胞衰老标志物减少,同时 sirtuin 1 (SIRT1) 上调。在这些体外研究结果的基础上,我们给自然衰老的小鼠注射了帕利什因。治疗后,肺纤维化减轻,肺组织中的 DNA 损伤减少。值得注意的是,我们发现副主教肽治疗可降低分化集束细胞 38(CD38)的水平,同时增加 SIRT1 的表达。这些研究结果表明,副主教肽可增强老年小鼠的肺功能,这表明它有可能成为治疗与年龄有关的肺部疾病的一种治疗剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Parishin Alleviates Pulmonary Fibrosis by Reducing CD38 Levels in Naturally Aging Mice.

Parishin, a natural compound, has demonstrated significant potential in mitigating age-related phenotypes and improving outcomes in age-associated diseases. Given that aging is a major risk factor for numerous chronic conditions, including pulmonary fibrosis, we investigated parishin's effects on cellular senescence and lung health. In our study, we treated mouse lung epithelial cells with parishin and observed a reduction in cellular senescence markers alongside an upregulation of sirtuin 1 (SIRT1). Building on these in vitro findings, we administered parishin to naturally aged mice. The treatment resulted in decreased pulmonary fibrosis and reduced DNA damage in lung tissue. Notably, we found that parishin treatment led to a reduction in Cluster of differentiation 38 (CD38) levels, concomitant with an increase in SIRT1 expression. These findings indicate that parishin may enhance lung function in aged mice, suggesting its potential as a therapeutic agent for treating age-related pulmonary disorders.

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