Nox1-dependent ROS production is crucial for cell signaling, growth, angiogenesis, motility, and blood pressure regulation. ML171 effectively inhibits ROS generation in HT29 cells (IC50=0.129 µM), and only an increased over-expression of Nox1 can counteract the suppression of ROS production by ML171 in a HEK293 cell system outfitted with all elements necessary for Nox1-dependent ROS production. ML171 significantly reduces ROS output, as indicated by carboxy-H2-DCFDA staining, with efficacy comparable to DPI, the positive control. In the HEK293-Nox1 reconstituted cell system, ML171 demonstrates enhanced effectiveness in inhibiting Nox1-dependent ROS generation compared to the original compound[1].
体外研究
Nox1-dependent ROS production is crucial for cell signaling, growth, angiogenesis, motility, and blood pressure regulation. ML171 effectively inhibits ROS generation in HT29 cells (IC50=0.129 µM), and only an increased over-expression of Nox1 can counteract the suppression of ROS production by ML171 in a HEK293 cell system outfitted with all elements necessary for Nox1-dependent ROS production. ML171 significantly reduces ROS output, as indicated by carboxy-H2-DCFDA staining, with efficacy comparable to DPI, the positive control. In the HEK293-Nox1 reconstituted cell system, ML171 demonstrates enhanced effectiveness in inhibiting Nox1-dependent ROS generation compared to the original compound[1].
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