RESUMO
Hepatocyte nuclear factor (HNF-6) is a liver-specific protein and a key component in the differentiation process during the development of mature liver. The immunohistochemical staining and RT-PCR techniques were employed to examine the expression of HNF-6 and proliferation of Ki-67+ cells during the early regeneration of the liver on postsurgery in 3, 6, 12, and 24 h in original model of partial hepatectomy in rats. The earliest proliferating (Ki-67+) cells were observed in 3 h after surgery in liver sinusoids (liver macrophages) and then in liver parenchyma. Expression of HNF-6 in hepatocytes and epithelial cells of the bile ducts attained maximum in 6 h after surgery. At later terms, this parameter somewhat decreased, but still surpassed the control level.
Assuntos
Fator 6 Nuclear de Hepatócito/genética , Hepatócitos/metabolismo , Células de Kupffer/metabolismo , Regeneração Hepática/genética , Fígado/metabolismo , Animais , Ductos Biliares/metabolismo , Ductos Biliares/cirurgia , Proliferação de Células , Feminino , Regulação da Expressão Gênica , Hepatectomia/métodos , Fator 6 Nuclear de Hepatócito/metabolismo , Hepatócitos/citologia , Antígeno Ki-67/genética , Antígeno Ki-67/metabolismo , Células de Kupffer/citologia , Fígado/cirurgia , Masculino , Ratos , Ratos Sprague-DawleyRESUMO
OBJECTIVE: To investigate the effects and mechanisms of sesquiterpene (+)-chabranol on proliferation of a panel of four human tumour cell lines (BGC-823, SGC-7901, SSMC-7721 and HepG2). METHODS: Cell viability was assessed using a standard methyltetrazolium assay; cell-cycle analysis of BGC-823 cells was performed by flow cytometry. Transmission electron microscopy (TEM) was used to examine the ultrastructure of BGC-823 cells exposed to (+)-chabranol. Apoptosis was investigated by evaluating DNA laddering, using gel electrophoresis. RESULTS: (+)-Chabranol had a marked time- and concentration-dependent inhibitory effect on BGC-823 cell proliferation. The effect was less marked in SGC-7901, SSMC-7721 and HepG2 cells. Exposure of BGC-823 cells to (+)-chabranol arrested the cell cycle at G(1). Evidence of apoptosis and autophagy was observed by TEM; DNA laddering in BGC-823 cells supported the presence of apoptosis. CONCLUSIONS: This study suggested that (+)-chabranol has antitumour activity against BGC-823 cells, and may exert its action by inhibition of proliferation and induction of apoptosis and autophagy. With further development, (+)-chabranol may represent a potential novel treatment for poorly differentiated gastric cancer.
