Summary: | 碩士 === 長榮大學 === 護理學研究所 === 97 === Colorectal cancer is one of the leading causes of malignant death in western countries as well as in Taiwan. Nowadays, medicines and chemotherapy made patients indisposed. The quality of life is low, that made nursing more difficult. Justicidin A is a pure compound isolated from Justicia procumbens, a traditional herbal remedy for treatment of fever, pain, and cancer in Taiwan. Recent reports have demonstrated that justicidin A induced apoptosis in human colorectal cancer HT-29 and HCT 116 cells and suppressed the growth of HT-29 cells transplanted into NOD-SCID mice. In this study, we observed that justicidin A not only increased the expression of autophagic marker LC3-II by immunoblotting and confocol microscopy, but also augmented the formation of acidic vesicular organelles at 3~6 h by flow cytometry. In addition, the expression of p-AKT, p- mTOR, p-p70S6k were inhibited in justicidin A-treated HT-29 cells demonstrated by western blotting. However, the expression of Type III PI3K and beclin 1 were increased in the cells demonstrated by western blotting. These results suggest that justicidin A-induced autophagic signaling pathways were via inhibition of AKT/mTOR signaling pathway and induction of Type III PI3K/beclin 1 signaling pathway. Annexin V-FITC and PI double staining followed by flow cytometry further revealed that induction of early apoptosis was displayed at 12 h, that was later than the induction of autophagy. Administration of autophagy inhibitor 3-MA further demonstrated that autophagy promoted apoptosis in justicidin A-treated HT-29 cells since 3-MA inhibited the percentage of early apoptotic cells determined by flow cytometry. Taken together, induction of autophagy leading to apoptotic death of the cells suggests chemotherapeutic potential of justicidin A on human colorectal cancer. The purpose of the present study was to discover a drug with selective to enhance quality of nursing.
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