A monoclonal antibody (MAb) 1C1 against artemisinin was prepared by a cell fusion with splenocytes and aminopterin-sensitive myeloma cells, SP2/0. An artesunate-BSA conjugate was used as immunogen to raise antibodies specific to artemisinin. The prepared anti-artemisinin MAb-1C1 have a novel characteristic which shows a specificity to compounds that are structurally related to artemisinin such as artesunate (630%) and dihydroartemisinin (29.9%). By using MAb-1C1, a specific and reliable ELISA was developed for the detection of compounds structurally related to artemisinin. The system shows a full measuring range from 2 to 20 microg/mL in the case of artemisinin and from 4 to 125 ng/mL in the case of artesunate in the competitive ELISA, and was validated to be of use for surveying and breeding of Artemisia annua containing a high amount of artemisinin as well as for the characterization of the pharmacokinetics of artemisinin and its derivatives.
Currently, only gemcitabine plus platinum demonstrates the considerable activity for cholangiocarcinoma. The anticancer effect of Delta (9)-tetrahydrocannabinol (THC), the principal active component of cannabinoids has been demonstrated in various kinds of cancers. We therefore evaluate the antitumor effects of THC on cholangiocarcinoma cells. Both cholangiocarcinoma cell lines and surgical specimens from cholangiocarcinoma patients expressed cannabinoid receptors. THC inhibited cell proliferation, migration and invasion, and induced cell apoptosis. THC also decreased actin polymerization and reduced tumor cell survival in anoikis assay. pMEK1/2 and pAkt demonstrated the lower extent than untreated cells. Consequently, THC is potentially used to retard cholangiocarcinoma cell growth and metastasis.
Currently, only gemcitabine plus platinum demonstrates the considerable activity for cholangiocarcinoma. The anticancer effect of Delta (9)-tetrahydrocannabinol (THC), the principal active component of cannabinoids has been demonstrated in various kinds of cancers. We therefore evaluate the antitumor effects of THC on cholangiocarcinoma cells. Both cholangiocarcinoma cell lines and surgical specimens from cholangiocarcinoma patients expressed cannabinoid receptors. THC inhibited cell proliferation, migration and invasion, and induced cell apoptosis. THC also decreased actin polymerization and reduced tumor cell survival in anoikis assay. pMEK1/2 and pAkt demonstrated the lower extent than untreated cells. Consequently, THC is potentially used to retard cholangiocarcinoma cell growth and metastasis.
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