基础研究 情报发生 2026-10-31 · 发布于 2026-11-01

百部碱激活 SIRT3 缓解 UVB 诱导的角质形成细胞衰老与光老化

来源:J Biochem Mol Toxicol · PMID 42954650 · DOI 10.1002/jbt.71142 · 来源:IMA 知识库《文献层·文献监控卡片》2026-10-31 期 · 全文级(file_id dmlmcfQeUyzO,实际下载核验) · 全文已获取并通过归属校验

时间标签:数据日期 2026-10-31 · 生成时间 2026-11-01 05:30(Asia/Shanghai)| 检索窗口 PubMed edat 2026/10/28–2026/10/31 | 情报发生日期 2026-10-31

研究问题

Among these, UVB rays (with wavelengths ranging from 280 to 315 nm) are primarily absorbed by the ozone layer in the atmosphere; however, a portion of them still reaches the Earth's surface.;However, research on Stemonine's role in skin protection, particularly against photoaging, remains largely unexplored.;Given its documented anti‐inflammatory and antioxidant properties, we hypothesized that Stemonine may attenuate UVB‐induced keratinocyte senescence by modulating mitochondrial sirtuin signaling.

方法

The knockdown efficiency was validated by western blotting.;Cell viability was assessed using the Cell Counting Kit‐8 (CCK‐8) assay (C0037, Beyotime).;The principle of this assay is that the highly water‐soluble tetrazolium salt WST‐8 is reduced by cellular dehydrogenases to an orange‐colored formazan product, which is soluble in the culture medium.;The quantification of the total protein concentration within the cell supernatant was accomplished through the utilization of the bicinchoninic acid (BCA) Protein Assay Kit sourced from Beyotime, China (P0012S).

核心结论

CCK‐8 results showed that Stemonine had no significant effect on cell viability after 48 h of treatment at concentrations ranging from 0 to 800 μM (Figure ).;Concurrently, the cellular antioxidant defense was compromised, as indicated by significant decreases in GSH content and SOD activity (Figure ).;Stemonine treatment (400 and 800 μM) effectively counteracted these changes, reducing ROS accumulation to 2.3‐fold and 1.7‐fold of the control, respectively, and significantly restoring both GSH levels and SOD activity. ‖ 结论:While these data highlight the potential of targeting mitochondrial SIRT3 against skin photoaging, our findings are currently confined to cell‐based models.

局限

While our loss‐of‐function experiments using lentiviral shRNA confirm that the anti‐senescence efficacy of Stemonine—namely, suppressing acetylated p53/p21, restoring hTERT transcription, and decreasing SA‐β‐Gal positivity—is strictly dependent on SIRT3, the exact upstream molecular interface warrants discussion.;However, several critical limitations must be explicitly acknowledged.;Additionally, the working concentrations of Stemonine employed in vitro (400–800 μmol/L) are relatively high and may be challenging to achieve in epidermal tissue through conventional topical formulation; future studies must assess advanced transdermal nano‐carrier delivery systems or structural analogues effecti

对本项目的价值

★☆☆☆☆ 细胞衰老清除/重编程是项目干预管线的核心支柱之一。

全文来源

PMC JATS 全文(正文 36,414 字符,已过标题/DOI 逐字归属校验)

原文题录

  • 英文标题:Stemonine Alleviates UVB-Induced Keratinocyte Senescence by Activating SIRT3.
  • 期刊与标识:J Biochem Mol Toxicol · PMID 42954650 · DOI 10.1002/jbt.71142

B 级证据分级:B 级(同行评议临床前研究,主要为动物模型)

本文核心结论来自动物模型或体外细胞学,属临床前证据,不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义,与人类临床结局之间仍有距离。

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