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甲基-4可能在调节由表皮生长因子受体抑制剂诱导的CCL5表达中发挥关键作用

Shotaro Goto¹, Shuichi Setoguchi², Daisuke Watase²

¹Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-Ku, Fukuoka, 814-0180, Japan. sgoto@fukuoka-u.ac.jp.

Scientific reports

|December 13, 2023

概括

维生素K2 (menaquinone-4) 和其活性形式menahydroquinone-4 (MKH) 可能减轻EGFR抑制剂引起的皮疹副作用. 这项研究表明,MKH抑制了CCL5,这是药物诱导皮肤损伤的关键因素.

科学领域:

生物化学生物化学
皮肤病学皮肤病学
分子生物学分子生物学

背景情况:

表皮生长因子受体 (EGFR) 抑制剂会引起严重的皮肤皮疹,影响患者的治疗.
维生素K在减轻这些副作用方面表现有前途,但机制尚不清楚.
EGFR抑制剂在皮肤中诱导C-C动机化学因联体5 (CCL5) 的作用.

研究的目的:

为了研究menahydroquinone-4 (MKH) 的机制,维生素K2 (menaquinone-4) 的活性形式,在缓解EGFR抑制剂诱导的皮肤皮疹.
探索MKH在调节CCL5表达中的作用.

主要方法:

使用了人类皮肤细胞系 (HaCaT和HSC-1).
评估EGFR抑制剂和MKH衍生物 (包括MK-4) 对细胞反应的影响.
评估了UBIAD1 (MKH合成酶) 和g-glutamyl carboxylase表达和华法林治疗对CCL5水平的影响.

主要成果:

EGFR抑制剂降低了UBIAD1表达和MKH生物合成的调节.
阻断UBIAD1或γ-谷氨基甲糖酶,和华法林治疗,增加了CCL5表达.
MKH衍生物有效地抑制了EGFR抑制剂诱导的CCL5表达.

结论:

梅纳基-4 (MKH) 在抑制CCL5.5方面发挥着至关重要的作用.
MKH参与缓解EGFR抑制剂引起的皮肤损伤.
这表明MKH在控制EGFR抑制剂相关皮肤病副作用方面具有治疗潜力.

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