OBJECTIVE: To evaluate the regulatory effects of honokiol on high-glucose (HG)-induced inflammatory responses of human renal mesangial cells (HRMCs). MATERIALS AND METHODS: We performed MTS assays to determine the non-cytotoxic concentration of honokiol for HRMCs. Enzyme-linked immunosorbent assays were performed to analyze the expressions of the proteins interleukin (IL)-1β, IL-18, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β1, monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1α, RANTES, and prostaglandin (PG) E2. The total nitric oxide (NO) concentration was determined using the Griess reaction. RESULTS: Treatment with 50 mmol/L glucose markedly increased the level of IL-1β, IL-18, TNF-α, PGE2, NO, TGF-β1, MCP-1, MIP-1α, and RANTES. Honokiol (~20 μmol/L) treatment inhibited the HG-induced expression of inflammatory cytokines such as IL-1β, IL-18, TNF-α, PGE2, NO, and TGF-β1 in a dose-dependent manner. Moreover, it markedly inhibited the expression of chemokines such as MCP-1, MIP-1α, and RANTES, which are upregulated under HG conditions. CONCLUSION: Honokiol inhibits the HG-induced expression of inflammatory factors in HRMCs. Honokiol may be considered a promising drug with potent anti-inflammatory activities in addition to its strong anti-cancer, anti-angiogenesis, and anti-neurodegenerative effects.
OBJECTIVE: To evaluate the regulatory effects of honokiol on high-glucose (HG)-induced inflammatory responses of human renal mesangial cells (HRMCs). MATERIALS AND METHODS: We performed MTS assays to determine the non-cytotoxic concentration of honokiol for HRMCs. Enzyme-linked immunosorbent assays were performed to analyze the expressions of the proteins interleukin (IL)-1β, IL-18, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β1, monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1α, RANTES, and prostaglandin (PG) E2. The total nitric oxide (NO) concentration was determined using the Griess reaction. RESULTS: Treatment with 50 mmol/L glucose markedly increased the level of IL-1β, IL-18, TNF-α, PGE2, NO, TGF-β1, MCP-1, MIP-1α, and RANTES. Honokiol (~20 μmol/L) treatment inhibited the HG-induced expression of inflammatory cytokines such as IL-1β, IL-18, TNF-α, PGE2, NO, and TGF-β1 in a dose-dependent manner. Moreover, it markedly inhibited the expression of chemokines such as MCP-1, MIP-1α, and RANTES, which are upregulated under HG conditions. CONCLUSION:Honokiol inhibits the HG-induced expression of inflammatory factors in HRMCs. Honokiol may be considered a promising drug with potent anti-inflammatory activities in addition to its strong anti-cancer, anti-angiogenesis, and anti-neurodegenerative effects.
Authors: M Carmen Iglesias-de la Cruz; Fuad N Ziyadeh; Motohide Isono; Martine Kouahou; Dong Cheol Han; Raghu Kalluri; Peter Mundel; Sheldon Chen Journal: Kidney Int Date: 2002-09 Impact factor: 10.612
Authors: Yashpal S Kanwar; Jun Wada; Lin Sun; Ping Xie; Elisabeth I Wallner; Sheldon Chen; Sumant Chugh; Farhad R Danesh Journal: Exp Biol Med (Maywood) Date: 2008-01
Authors: Meei Ling Sheu; Chih Kang Chiang; Keh Sung Tsai; Feng Ming Ho; Te I Weng; Hsiao Yi Wu; Shing Hwa Liu Journal: Free Radic Biol Med Date: 2008-04-03 Impact factor: 7.376