ABSTRACT
AIM: To study the preventive effect of fibronectin on hepatic failure induced by endotoxin in mice.METHODS: The survival rate was observed in endotoxemia mice injected with fibronectin from human plasma. The tissue damage and expression of TNF?, IL-1?, IL-6 mRNA in hepatocyte were detected by the methods of histology, ultrastructure, DNA fragementation and RT-PCR. RESULTS: ①Fibronectin obviously reduced the mortality of endotoxemia mice sensitized by D-galactosamine(GalN). ②Histopathology showed that less necrosis occurred on the hepatocyte of endotoxemia mice injected with fibronectin, compared with saline control. ③Ultrastructure and DNA fragmentation showed fibronectin suppressed hepatocyte apoptosis induced by LPS. ④Fibronectin down-regulated the overexpression of TNF?, IL-1?, IL-6 mRNA on hepatocyte induced by LPS. CONCLUSION: Fibronectin supports endotoxemia mice surrival by down-regulating the expression of TNF?, IL-?, IL-6, it may be a potent therapy for endotoxemia.
ABSTRACT
AIM: To observe the effect of antisense bcl-2 oligodeoxynucleotides(AS-PS-ODN) on bcl-2 mRNA and protein expression, cell proliferation,viability and apoptosis in a small-cell lung cancer cell line NCI-H446. METHODS: Semi-quantitative RT-PCR was performed to detect the bcl-2 mRNA expression, the Bcl-2 protein was determined by immunocytochemistry and flow cytometry analysis, and the effect of bcl-2 AS-PS-ODN on cell proliferation, viability and apoptosis were investigated by colony assay , cell count, DNA content analysis and TUNEL. RESULTS: ① 1 ?mol/L bcl-2 AS-PS-ODN significantly down-regulated the expression of bcl-2 mRNA and protein. The inhibition rate of mRNA and protein were 69.5% and 62.7%, respectively. ② bcl-2 AS-PS-ODN decreased cell proliferation and viability , induced cell apoptosis.The apoptosis rate was 22.3%-32.7% in cells treated with 1?mol/L bcl-2 AS-PS-ODN. CONCLUSION: bcl-2 AS-PS-ODN down-regulated expression of bcl-2 mRNA and protein, inhibited cell proliferation and induced apoptosis in a small cell lung cancer cell line, NCI-H446.
ABSTRACT
Aim To investigate the effects of allicin on the proliferation and apoptosis of HL-60 cells,and to explore the underlying mechanism.Methods The cell viability and colony formation were detected by MTT assay.Apoptotic cells were tested by means of TUNEL labeling.RT-PCR was used to analyze the bcl-2 mRNA expressions.Results HL-60 cell growth was significantly inhibited by allicin in dose and time dependent manners.Cell colony formation obviously decreased.The typical hypo-diploid pea J apoptotic peaJ appeared in each dose group.Apoptosis occured in a dose-dependent manner.And its later stages were identified by TUNEL labeling methods respectively,and bcl-2/bax was decreased.The expression of bcl-2 mRNA was down-regulated in a time-dependent manner after treatment with allicin at different time points.Conclusion Allicin effectively inhibits growth and induces apoptosis on HL-60 cells,which may be related with the down-regulation of expressions of bcl-2.