通过增强抗氧化剂系统,黄素对氧化压力介导的细胞损伤的保护作用
Pincha Devage Sameera Madushan Fernando1, Dong Ok Ko1, Mei Jing Piao1
1Department of Biochemistry, College of Medicine, and Jeju Research Center for Natural Medicine, Jeju National University, Jeju 63243, Republic of Korea.
Molecular medicine reports
|May 17, 2024
概括
素通过减少活性氧物种 (ROS) 和防止细胞损伤,保护肺纤维细胞免受氧化应激. 这种天然化合物增强了抗氧化防御,并抑制了细胞亡,对过氧化引起的伤害产生细胞保护作用.
科学领域:
- 生物化学 生物化学
- 细胞生物学 细胞生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 生理压力,包括过度的活性氧物种 (ROS) 生产,可以将正常纤维细胞转化为与癌症相关的纤维细胞.
- 与癌症相关的纤维细胞在各种癌症的进展中发挥着重要作用,包括胰腺癌,乳腺癌,肝癌和肺癌.
研究的目的:
- 为了研究白素在肺纤维细胞中对过氧化 (H2O2) 诱导的氧化应激的细胞保护作用.
- 阐明黄素抗氧化和抗亡作用背后的机制.
主要方法:
- 细胞活力,细胞灭绝试验 (G1亚种群,核染色),脂质过氧化和彗星试验被用来评估H2O2诱导的损伤.
- 西方斑点分析评估了与亡相关的蛋白质表达.
- 进行ROS检测 (H2DCFDA,电子自旋共振) 和抗氧化酶活性试验以评估抗氧化作用.
主要成果:
- 素预处理显著降低了细胞内ROS水平,并保护了细胞组件 (脂质,DNA) 免受H2O2诱导的损伤.
- 素增强了细胞活力,通过调节酶和Bcl-2/Bax蛋白水平来抑制细胞亡,并恢复了谷氨水平.
- 氨酸提高了关键抗氧化酶的活性和表达的调节,包括超氧化脱酶,催化酶,谷氨酸过氧化酶和血红素酶-1.
结论:
- 氨酸在肺纤维细胞中对H2O2诱导的氧化应激具有显著的细胞保护作用.
- 保护机制包括ROS清理,抑制细胞灭绝和增强内源抗氧化剂防御系统.
- 丁醇提高抗氧化酶的调节能力表明它作为治疗氧化压力相关肺部疾病的治疗剂的潜力.
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