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Am J Med Sci. 2014 Jul;348(1):75-80. doi: 10.1097/MAJ.0000000000000187.

Fluorofenidone attenuates inflammation by inhibiting the NF-кB pathway.

Author information

Division of Nephrology (LH, FZ, YT, JQ, YP, LW, FW, QY, ZP, JL, LT), Department of Internal Medicine, Xiangya Hospital, Central South University; and State Key Laboratory of Medical Genetics of China (LT), Central South University, Changsha, Hunan, China.



Accumulated evidence indicates that inflammation plays a critical role in the progression of many renal diseases. Fluorofenidone (AKF-PD) has been shown to attenuate renal fibrosis in a number of experimental renal fibrosis models. The aim of this study was to assess the anti-inflammatory effect of AKF-PD.


Human proximal tubule (HK-2) cells were stimulated with tumor necrosis factor (TNF)-α in the presence or absence of AKF-PD. Mouse peritoneal macrophages were incubated with necrotic MES-13 cells in the presence or absence of AKF-PD. The production of pro-inflammatory cytokines and chemokines was measured by enzyme-linked immunosorbent assay, and the activation of Nuclear factor κB (NF-κB) pathway was assessed by Western blot analysis.


AKF-PD significantly inhibited TNF-α-induced expression of interleukin-6, monocyte chemoattractant protein-1 and interleukin-8 and nuclear translocation of p65 in HK-2 cells. Addition of AKF-PD also significantly suppressed necrotic cell-induced TNF-α expression and p65 nuclear translocation in mouse peritoneal macrophages.


These results demonstrated that AKF-PD exerts anti-inflammatory effect, at least in part, through inhibition of the NF-κB pathway.

[Indexed for MEDLINE]

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