生物活性 | |||
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描述 | Oxidative stress plays an important role in the progression of renal interstitial fibrosis. The nicotinamide adeninedinucleotide phosphate (NADPH) oxidase (Nox) family is considered one of the major sources of reactive oxygen species (ROS)[1]. Fluorofenidone is an effective and novel antifibrotic agent with an IC50 value of 4.18 mM[2]. Fluorofenidone treatment significantly attenuated tubulo-interstitial injury, ECM deposition and oxidative stress in fibrotic rat kidneys. In addition, Fluorofenidone inhibited the expression of ROS, Collagen I (1a), Nox2, p-Akt in Ang II-stimulated NRK-52E cells. Fluorofenidone attenuates the progression of renal interstitial fibrosis partly by suppressing NADPH oxidase and ECM deposition via the PI3K/Akt signalling pathway, suggesting Fluorofenidone is a potential and novel therapeutic agent against renal fibrosis[1]. |
实验方案 | |||
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1mg | 5mg | 10mg | |
1 mM 5 mM 10 mM |
4.92mL 0.98mL 0.49mL |
24.60mL 4.92mL 2.46mL |
49.21mL 9.84mL 4.92mL |
参考文献 |
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