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 inhibits the growth of cancer cells at concentrations as low as 40 μg/mL[1]. The Cur-loaded κ-Car displays significant cytotoxicity, with high apoptotic activity observed in A549 lung cancer cells[1]. In addition, κ-Carrageenan (1-60 μg/mL; 0.5-24 hours) is shown to amplify LPS-induced IL-8 secretion in HT-29 cells[2]. A Cell Viability Assay on the A549 cell line with Cur concentrations ranging from 0-500 μg/mL over 24, 48, and 72 hours demonstrates dose-responsive effects, yielding significant IC 50 values of 65, 50, and 40 μg/mL for 24, 48, and 72 hours, respectively[1].

κ-Carrageenan, administered orally at dosages ranging from 1.7 to 41.7 mg/kg for 1 week prior to Citrobacter freundii DBS100 treatment, markedly enhances LPS-induced inflammation via the Bcl10-NF-κB pathway. This action is evident from the exacerbation of C. freundii DBS100-induced colitis in mice, particularly through the increased induction of TLR4 and NF-κB in the intestinal mucosa of the affected animals. Moreover, κ-Carrageenan intensifies TNBS-induced intestinal inflammation, a process possibly linked to oxidative stress alongside the activation of both the TLR4-NF-κB and MAPK/ERK1/2 pathways. This observation was made in studies utilizing both male and female NIH (s) mice, with the compound being orally administered in low, medium, and high doses, specifically 1.7 mg/kg, 8.3 mg/kg, and 41.7 mg/kg, respectively. The results indicate a heightened induction of TLR4 and NF-κB pathways in the intestinal mucosa of mice infected with C. freundii DBS100.