• Journal of Life Science
• /
• v.34 no.8
• /
• pp.548-557
• /
• 2024

Curcumin, the primary active compound in Curcumae Radix of the ginger family, exhibits a range of therapeutic effects, including blood sugar regulation, immunoregulation, antioxidant, antibacterial, and antitumor activities. However, its poor water solubility and chemical instability result in suboptimal pharmacokinetics with low oral absorption (0.18%) and bioavailability, thus limiting its efficacy. To overcome these limitations, this study aimed to enhance the oral absorption and bioavailability of curcumin by incorporating lysine and β-cyclodextrin. Following oral administration of solubilized cur- cumin, blood samples were collected to assess the oral absorption rate. Solubilized curcumin showed an approximately 1.55-fold increase in absorption at 120 min compared to its non-solubilized form. Furthermore, intravenous administration followed by blood analysis showed a 25-fold increase in bio- availability at 61 min for the solubilized curcumin compared to the non-solubilized variant. In conclusion, employing lysine for dispersion and stabilization, combined with β-cyclodextrin to enhance solubility, significantly improves curcumin's oral absorption and bioavailability. The results of this experiment are expected to lead to the development of herbal medicines and pharmaceuticals that amplify curcumin's anti-inflammatory, anti-tumor, and blood-sugar-regulation effects.

• Radiation Oncology Journal
• /
• v.21 no.3
• /
• pp.207-215
• /
• 2003

Purpose: Extracellular signal-regulated kinase (ERK), which is part of the mitogen-activated protin kinase cascade, opposes initiation of the apoptotic cell death which is programmed by diverse cytotoxic stimuli. In this regard, the inhibition of ERK may be useful in improving the therapeutic efficacy of established anticancer agents. Materials and Methods: Murine hepatocarcinoma, HCa-I is known to be highly radioresistant with a TCD50 (radiation dose yield in $50\%$ cure) of more than 80 Gy. Various anticancer drugs have been found to enhance the radioresponse of this particular tumor but none were successful. The objective of this study was to explore whether the selective inhibition of MEK could potentiate the antitumor efficacy of radiation in vivo, particularly in the case on radioresistant tumor. C3H/HeJ mice hearing $7.5\~8\;mm$ HCa-I, were treated with PD98059(intratumoral injection of $0.16\;\mug/50\;\mul$). Results: Downregulation on ERK by PD98059 was most prominent 1h after the treatment. In the tumor growth delay assay, the drug was found to Increase the effect of the tumor radioresponse with an enhancement factor (EF) of 1.6 and 1.87. Combined treatment of 25 Gy radiation with PD98059 significantly increased radiation induced apoptosis. The peak apoptotic index (number on apoptotic nuclei in 1000 nuclei X100) was $1.2\%$ in the case of radiation treatment alone, $0.9\%$ in the case of drug treatment alone and $4.9\%,\;5.3\%$ in the combination treatment group. An analysis of apoptosis regulating molecules with Western blotting showed upregulation of p53, p$p21^{WAF1/CIP1}\;and\;Bcl-X_s$ in the combination treatment group as compared to their levels in either the radiation alone or drug alone treatment groups. The level of other molecules such as $Bcl-X_L4, Bax and Bcl-2 were changed to a lesser extent. Conclusion: The selective inhibition of MEK in combination with radiation therapy may have potential benefit in cancer treatment.