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Abstract: PO1407

Danhong Injection (DHI) Inhibits Lipopolysaccharide-Enhanced Cell Proliferation of Rat Renal Mesangial Cells via NF-κB Signaling Pathway

Session Information

Category: Glomerular Diseases

  • 1201 Glomerular Diseases: Fibrosis and Extracellular Matrix

Author

  • Liu, Hua, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China
Background

To explore the mechanisms of DHI in the treatment of Mesangioproliferative glomerulonephritis
(MsPGN), we investigated the effects of DHI on LPS-induced NF-κB activation and its downstream inflammatory mediators, such as ICAM-1, TGF-β1, iNOS and FN protein expression in rat MCs.

Methods

The rat MCs treated with different concentrations of DHI (0, 50, 100, 200, 500, 1000, and 2000 uL/L) for 12 h,then incubated with or without 100 ng/ml LPS for another 24 h. Then, cell proliferation was determined by CCK8. The MCs treated with low-dose DHI (250 uL/L), median-dose DHI (500 uL/L) and high-dose DHI (1000 uL/L) for 12 h or PDTC for 30 min before 24h treatment of LPS. Then the activation of NF-κB was detected by Western blot and immunofluorescence. The protein levels of ICAM-1, TGF-β1, iNOS and FN in rat MCs were detected by Western blot.

Results

DHI significantly suppressed LPS-induced cell proliferation by CCk-8 results (Fig 1). LPS stimulation resulted in a significant increment of p65 contents in nucleus and a decrement of p65 contents in cytoplasm in rat MCs compared with NC. PDTC and DHI exerted potent inhibitory effect on increasing expression of p65 in nucleus and decreasing in cytoplasm compared with LPS-treatment group. The inhibitory effect on NF-κB nuclear translocation of DHI was in a dose-dependent manner (Fig 2). The protein level of IκB-α in cytoplasm treated by LPS decreased significantly compared with that in control (Fig 3) and this decrement was significantly reversed by PDTC and DHI. In addition, the protein expression of ICAM-1, TGF-β1, iNOS and FN was also inhibited by PDTC and DHI (Fig 4).

Conclusion

DHI significantly repressed LPS-induced cell proliferation and FN expression in rat MCs through inhibiting the activation of NF-κB signaling pathway also its downstream inflammatory mediators.