AIMS OF THE STUDY: Sodium houttuyfonate (SH) is an addition compound of sodium bisulfite and houttuynin. Houttuynin is one of the main ingredients in the volatile oil of Houttuynia cordata Thunb, which has been widely used in traditional Chinese medicines. In this study, we investigated the effect of SH in membranous glomerulonephritis (MGN) induced by cationic Bovine Serum Albumin (C-BSA) in BALB/c mice. MATERIALS AND METHODS: Mice were divided into four groups, including normal vehicle-treated controls (N group), model (M group), low SH of 60 mg/kg body weight (L group), or high SH of 120 mg/kg body weight (H group). Urine protein quantification was detected by the urine protein strip test. Morphological assessment in kidneys was observed by light microscope and electron microscopy. The level of nuclear factor-kappaB (NF-kappaB) in the nuclear was evaluated by Western blot. Immunohistochemical was used to analyze the expression of MCP-1. RESULTS: SH was shown to reverse C-BSA induced increases in urinary protein, and changes in morphology. Treatment with SH at 60-120 mg/kg (L and H groups, respectively) dose-dependently decreased the level of nuclear NF-kappaB and MCP-1 expression compared to that of the M group. CONCLUSIONS: This study reveals that SH could treat C-BSA induced MGN in BALB/c mice by suppressing NF-kappaB activation and MCP-1 expression. Therefore, the most likely mechanism underlying the biological effects of SH is inhibition of an NF-kappaB mediated-cytokine pathway. (c) 2010 Elsevier Ireland Ltd. All rights reserved.
AIMS OF THE STUDY: Sodium houttuyfonate (SH) is an addition compound of sodium bisulfite and houttuynin. Houttuynin is one of the main ingredients in the volatile oil of Houttuynia cordata Thunb, which has been widely used in traditional Chinese medicines. In this study, we investigated the effect of SH in membranous glomerulonephritis (MGN) induced by cationic Bovine Serum Albumin (C-BSA) in BALB/c mice. MATERIALS AND METHODS:Mice were divided into four groups, including normal vehicle-treated controls (N group), model (M group), low SH of 60 mg/kg body weight (L group), or high SH of 120 mg/kg body weight (H group). Urine protein quantification was detected by the urine protein strip test. Morphological assessment in kidneys was observed by light microscope and electron microscopy. The level of nuclear factor-kappaB (NF-kappaB) in the nuclear was evaluated by Western blot. Immunohistochemical was used to analyze the expression of MCP-1. RESULTS: SH was shown to reverse C-BSA induced increases in urinary protein, and changes in morphology. Treatment with SH at 60-120 mg/kg (L and H groups, respectively) dose-dependently decreased the level of nuclear NF-kappaB and MCP-1 expression compared to that of the M group. CONCLUSIONS: This study reveals that SH could treat C-BSA induced MGN in BALB/c mice by suppressing NF-kappaB activation and MCP-1 expression. Therefore, the most likely mechanism underlying the biological effects of SH is inhibition of an NF-kappaB mediated-cytokine pathway. (c) 2010 Elsevier Ireland Ltd. All rights reserved.