Résumé
Aim To explore the mechanism of tetram-ethypyrazine ( TMP) in the inhibition of cancer cell in-vasion and metastasis, by investigating the effect of TMP on cell migration, cell invasion and cytoskeleton of HepG2 cells. Methods Using HepG2 cells as tar-get cells, cell migration of different concentrations of TMP on HepG2 cells was assayed by the scratch wound healing assay. Matrigel cell invasion assay was used to detect the effect of TMP on the invasion of HepG2 cells. The effect of TMP on cytoskeleton of HepG2 cells was detected by high content screening ( HCS ) . Results TMP inhibited the migration of HepG2 cells, and showed a time-dependent and dose-dependent manner. Moreover, TMP significantly inhibited the in-vasion of HepG2 cells ( P<0. 01 ) , and showed a cer-tain time-dependence. Furthermore, compared with control group, a significant decrease in HepG2 cy-toskeleton area was found in a dose-dependent manner ( P<0. 01 ) . Conclusion TMP can inhibit the migra-tion and invasion of HepG2 cells, and it has the poten-tial to resist tumor metastasis, and the mechanism may be associated with TMP significantly decreasing the number and area of cytoskeleton, and inhibiting the re-arrangement of cytoskeleton.
Résumé
@#The purpose of the present study was to investigate the anti-proliferative and apoptotic effects of tetramethypyrazine(TMP)on HepG2 and to elucidate the underlying mechanisms. CCK-8 was introduced to analyze the HepG2 cells proliferation. Cell apoptosis, mitochondrial membrane potential(ΔΨm)and cytochrome C were measured by high content screening(HCS). Cleaved-caspases protein expression was detected by Western blot. CCK-8 assay indicated that TMP significantly inhibited HepG2 cells proliferation in dose-dependent manner compared with the control group. Moreover, it was found that TMP could also induce HepG2 cell apoptosis, directly increase the release of cytochrome C, decrease ΔΨm and increase cleaved-caspase-3 and cleaved-caspase-9 protein expression. TMP may inhibit cell proliferation and induce cell apoptosis by stimulating the mitochondrial pathway apoptosis in HepG2 cells.
Résumé
AIM To investigate the protective effects and mechanisms of TMP on accelerated anti-glomerulus basement membrane(GBM) antibody nephritis of rats. METHODS Model of accelerated anti-GBM nephritis was established in rats and TMP was administrated 120 mg?kg -1 ?d -1 by ip since the day before the model established, consecutively for 15 days. Content of 24h urine protein was detected after model established and rats were killed on d 7 and d 14. Contents of blood urine nitrogen (BUN) and serum creatinine (SCr) were detected. Renal cortex cytoplasm and mitochondria were produced and change of content of lipid peroxidation products malondialdehyde(MDA), activities of glutathione peroxidase(GSH-Px) and catalase(CAT) and superoxide dismutase(SOD) were investigated. RESULTS Compared with model group, TMP group showed significant inhibition in changes of proteinuria and BUN, SCr(P