RESUMO
This study aimed to investigate the absorption mechanism of three curcumin constituents in rat small intestines. Self-emulsification was used to solubilize the three curcumin constituents, and the rat in situ intestinal perfusion method was used to study factors on drug absorption, including drug mass concentration, absorption site, and the different types and concentrations of absorption inhibitors. Within the scope of experimental concentrations, three curcumin constituents were absorbed in rat small intestines through the active transport mechanism.
Assuntos
Adjuvantes Farmacêuticos/farmacologia , Curcumina/análogos & derivados , Curcumina/farmacocinética , Inibidores Enzimáticos/farmacocinética , Absorção Intestinal , Intestino Delgado/metabolismo , 2,4-Dinitrofenol/farmacocinética , Transportadores de Cassetes de Ligação de ATP/antagonistas & inibidores , Animais , Cromatografia Líquida de Alta Pressão/métodos , Curcumina/química , Diarileptanoides , Emulsões , Feminino , Absorção Intestinal/efeitos dos fármacos , Intestino Delgado/efeitos dos fármacos , Masculino , Proteína 2 Associada à Farmacorresistência Múltipla , Proteínas Associadas à Resistência a Múltiplos Medicamentos/análise , Proteínas Associadas à Resistência a Múltiplos Medicamentos/antagonistas & inibidores , Imagem de Perfusão/métodos , Probenecid/farmacologia , Ratos Sprague-Dawley , Valores de Referência , Reprodutibilidade dos Testes , Fatores de Tempo , Desacopladores/farmacologia , Verapamil/farmacologiaRESUMO
This study aimed to investigate the absorption mechanism of three curcumin constituents in rat small intestines. Self-emulsification was used to solubilize the three curcumin constituents, and the rat in situ intestinal perfusion method was used to study factors on drug absorption, including drug mass concentration, absorption site, and the different types and concentrations of absorption inhibitors. Within the scope of experimental concentrations, three curcumin constituents were absorbed in rat small intestines through the active transport mechanism.
Assuntos
Animais , Masculino , Feminino , Adjuvantes Farmacêuticos/farmacologia , Curcumina/análogos & derivados , Curcumina/farmacocinética , Inibidores Enzimáticos/farmacocinética , Absorção Intestinal , Intestino Delgado/metabolismo , Valores de Referência , Fatores de Tempo , Desacopladores/farmacologia , Verapamil/farmacologia , Probenecid/farmacologia , Reprodutibilidade dos Testes , Cromatografia Líquida de Alta Pressão/métodos , Ratos Sprague-Dawley , Transportadores de Cassetes de Ligação de ATP/antagonistas & inibidores , 2,4-Dinitrofenol/farmacocinética , Curcumina/química , Proteínas Associadas à Resistência a Múltiplos Medicamentos/análise , Proteínas Associadas à Resistência a Múltiplos Medicamentos/antagonistas & inibidores , Emulsões , Imagem de Perfusão/métodos , Absorção Intestinal/efeitos dos fármacos , Intestino Delgado/efeitos dos fármacosRESUMO
Glargine is widely used as a long-acting insulin analogue in the treatment of diabetes mellitus. However, this insulin analogue has been recently suspected to be associated with an increased risk of cancer. The aim of this study was to investigate the influence of glargine on proliferation of breast adenocarcinoma cell line (MCF-7) and its possible mechanism. Effects of glargine and regular human insulin on the cell proliferation were tested in ER-positive MCF-7 cells by MTT assay. Apoptosis in MCF-7 cells was measured by flow cytometry. The protein levels of p-AKT, Bcl-2, and Bax were also determined by Western blotting and immunohistochemistry, respectively. The result showed that glargine (100, 200 nmol/l) stimulated proliferation of ER-positive MCF-7 cells compared with regular human insulin. At the same time, glargine decreased the percentage of early apoptosis in MCF-7 cells. Otherwise, glargine (100 nmol/l) stimulated the p-AKT in a time-dependent manner in MCF-7 cells. Furthermore, we found that glargine downregulated the level of Bax protein and upregulated that of Bcl-2 (p <0.05). These data show that glargine promote the proliferation of breast adenocarcinoma cells in vitro, probably by preventing apoptosis.
