RESUMO
AIM:To investigate the effects of nodosin extracted from Chinese traditional medicine on the pro-liferation of HepG2 cells cultured in vitro and to detect the protein expression of Bcl-2 and Bax in HepG2 cells.METH-ODS:HepG2 cells were treated with different concentrations (1.25, 2.5, 5, 10 and 20 μmol/L) of nodosin for 24 h. The morphological changes of HepG2 cells were observed under inverted microscope.The inhibitory rates of HepG2 cell growth were detected by MTT assay.The apoptotic rates and the protein expression of Bcl-2 and Bax were analyzed by flow cytometry.RESULTS:Shrunken and suspended HepG2 cells increased with the increases in the concentrations of nodo-sin.The apoptotic rates and the expression of Bax increased with the increases in the doses of nodosin, while the expression of Bcl-2 decreased.CONCLUSION:Nodosin inhibits the growth of HepG2 cells in a dose-dependent manner.The inhibi-tion of HepG2 cell growth is induced by decreasing Bcl-2 and increasing Bax, thus promoting cell apoptosis.
RESUMO
AIM:The present study was designed to establish H2O2-induced NRK52E cell apoptotic model and to investigate the effects and the mechanism of nmhaFGF on the NRK52E cell apoptosis induced by H2O2. METHODS: In vitro experiment, a apoptotic model of normal rat kidney epithelium (NRK52E) was made by MTT method, Hoechst33342 dyeing and flow cytosorting (FCR). NRK52E cells were cultured with different concentrations of nmhaFGF and haFGF for 24 h before H2O2 was added. The apoptotic rate was detected with FCR method. RESULTS: H2O2 at concentration of 0.4 mmol/L, the optimal condition to establish the apoptotic model, was used to treat NRK52E cells for 18h. Different doses of nmhaFGF (0.01, 0.03, 0.10, 0.30, 1.00 mg/L) reduced the apoptotic rates with the dose rising. However, the decreasing tends of apoptotic rates with dose increasing for haFGF was not so obvious. CONCLUSION: nmhaFGF protects the NRK52E cells against apoptosis. The mechanism might be connected with its non-mitogenic property.
RESUMO
AIM: To investigate the effect of non-mitogenic human acidic fibroblast growth factor(nm-haFGF) on renal ischemia-reperfusion injury in rats.METHODS: Rat renal ischemia-reperfusion(I/R) injury was produced by removing the left kidney and subsequently clamping the right renal artery for 60 min followed by reperfusion for 24 h.5 min after reperfusion,different doses of nm-haFGF and haFGF(as positive control) were injected by lingual vein.24 h later,the samples of blood,urine and kidney were collected and the contents of malondialdehyde(MDA),blood urea nitrogen(BUN),creatinine(Cr) and superoxide dismutase(SOD) activity were detected.Histopathological changes were also observed.RESULTS: In the serum,SOD activity of all the nm-haFGF groups and the haFGF group increased significantly while the content of MDA decreased dramatically compared with the model group;The content of BUN and Cr also decreased wherever in serum or in urine;In renal tissue,SOD activity in nm-haFGF 20 ?g/kg group,40 ?g/kg group and haFGF group rose significantly compared with the model group,while MDA decreased dramatically.Histological examination showed that nm-haFGF markedly attenuates the renal edema,brush border's defluvium and cell necrosis induced by ischemia-reperfusion.CONCLUSION: nm-haFDF could resist the renal injury induced by ischemia-reperfusion in rats.