BIHC is a TNF blocker with anti-inflammatory activity. BIHC can significantly inhibit the proliferation of hepatocellular carcinoma (HCC) cells and exhibits potent cytotoxicity against the HepG2 cell line, capable of inducing cell apoptosis, while demonstrating relatively low toxicity towards normal hepatocytes. Additionally, BIHC can be used for research on inflammatory bowel disease (IBD) [1].
In Vivo, BIHC (5 mg/kg; i.p.,Once daily for 5 days) can significantly alleviate dextran sulfate sodium (DSS)-induced colitis in Swiss albino mice, reduce the levels of pro-inflammatory factors TNF-α, IFN-γ, IL-1β, and IL-6, and upregulate the anti-inflammatory factor IL-10[1].
In Vitro, BIHC (5-25 μM; 24-72 h) significantly inhibits the proliferation of hepatocellular carcinoma (HCC) cells with an in vitro anti-HepG2 cell activity IC50 value of 6.4 μM, and inhibits the binding of TNF-α to its antibody in vitro with an IC50 of 16.5 μM[1]. BIHC (25 μM; 24 -72 h) induces apoptosis of liver cancer cells by disrupting the TNF trimer structure, inhibiting the NF-κB signaling pathway and its downstream gene products (such as cyclin D1, Mcl-1, survivin, Bcl-2) in HepG2 cells[1]. BIHC (25 μM; 8 h) also significantly inhibits the invasion of HepG2 cells induced by CXCL12 (20 μM; 2 h)[1].
References:
[1]. Keerthy H K, Mohan C D, Siveen K S, et al. Novel synthetic biscoumarins target tumor necrosis factor-α in hepatocellular carcinoma in vitro and in vivo[J]. Journal of Biological Chemistry, 2014, 289(46): 31879-31890.
In Vivo, BIHC (5 mg/kg; i.p.,Once daily for 5 days) can significantly alleviate dextran sulfate sodium (DSS)-induced colitis in Swiss albino mice, reduce the levels of pro-inflammatory factors TNF-α, IFN-γ, IL-1β, and IL-6, and upregulate the anti-inflammatory factor IL-10[1].
In Vitro, BIHC (5-25 μM; 24-72 h) significantly inhibits the proliferation of hepatocellular carcinoma (HCC) cells with an in vitro anti-HepG2 cell activity IC50 value of 6.4 μM, and inhibits the binding of TNF-α to its antibody in vitro with an IC50 of 16.5 μM[1]. BIHC (25 μM; 24 -72 h) induces apoptosis of liver cancer cells by disrupting the TNF trimer structure, inhibiting the NF-κB signaling pathway and its downstream gene products (such as cyclin D1, Mcl-1, survivin, Bcl-2) in HepG2 cells[1]. BIHC (25 μM; 8 h) also significantly inhibits the invasion of HepG2 cells induced by CXCL12 (20 μM; 2 h)[1].
References:
[1]. Keerthy H K, Mohan C D, Siveen K S, et al. Novel synthetic biscoumarins target tumor necrosis factor-α in hepatocellular carcinoma in vitro and in vivo[J]. Journal of Biological Chemistry, 2014, 289(46): 31879-31890.