κ-Carrageenan, a natural polymer found predominantly in red seaweeds, can serve as an effective drug carrier for delivering curcumin to cancer cells and inducing apoptosis. Additionally, κ-Carrageenan holds promise as a potential inflammatory agent, amplifying existing intestinal inflammation.

κ-Car- Curcumin (Cur) (0-500 μg/mL; 24-72 hours) effectively involves in cancer cell growth inhibition at lower concentrations of 40 μg/mL[1]. The cytotoxicity of the Cur loaded κ-Car has a significantly high apoptotic activity in selected lung cancer cells of A549[1]. κ-Carrageenan (1-60 μg/mL; 0.5-24?hours) enhances LPS-induced IL-8 secretion in HT-29 cells[2]. Cell Viability Assay[1]Cell Line: A549 cells Concentration: 0-500 μg/mL Incubation Time: 24, 48 and 72 hours Result: The dose response effects of cells treated with Cur loaded κ-Car after incubation of 24, 48 and 72 h exhibited a significant IC 50 values of 65, 50 and 40 μg/mL respectively, for 24, 48, 72 h ours.

κ-Carrageenan (1.7-41.7?mg/kg; p.o. for 1 week prior to C. freundii DBS100 treatment) can synergistically activate LPS-induced inflammatory through the Bcl10-NF-κB pathway, as indicated by its aggravation of C. freundii DBS100-induced colitis in mice[2]. κ-Carrageenan enhances the C. freundii DBS100-dependent induction of TLR4 and NF-κB in the intestinal mucosa of infected mice[2]. κ-Carrageenan aggravates the TNBS-induced intestinal inflammation, and such an effect could be associated with the oxidative stress and activation of TLR4-NF-κB and MAPK/ERK1/2 pathway[3]Animal Model: Male and female NIH (s) mice[2]Dosage: 1.7?mg/kg, LOW; 8.3?mg/kg, MED; or 41.7?mg/kg, HIG Administration: Orally administered for 1 week prior to C. freundii DBS100 treatment Result: Enhanced the C. freundii DBS100-dependent induction of TLR4 and NF-κB in the intestinal mucosa of infected mice.