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Objective To investigate the effects of different dialysates on expression of protein kinase C-δ (PKCδ) and apoptosis of U937 cell line. Methods Different dialysates were added into culture fluid with U937 cell line at exponential phase of growth, and groups were divided: fluid A+fluid B group (dialysate A+dialysate B), fluid A+fluid B+rottlerin (PKCδ specific inhibitor)group, fluid A+powder B group (dialysate A+powder B) and fluid A+powder B + rottlerin group. Besides, blank control group and normal control group were established. Cells were harvested 24 h and 48 h after treatment, morphological changes were observed by Hoechst33258 fluorescence staining, cell apoptosis was measured by Annexin-V-FITC/PI double staining, and expression of PKCδ mRNA and protein was detected by RT-PCR and Western blotting, respectively. Results Cell apoptosis significantly increased in fluid A+powder B group, with typical morphology of apoptosis. After treatment for 24 h and 48 h, cell apoptosis rates in fluid A+powder B group were significantly higher than those at corresponding time points in blank control group , normal control group and fluid A+powder B+rottlerin group (P<0.05). Compared with normal control group, blank control group and fluid A+powder B+rottlerin group, the expression of PKCδ mRNA and protein of U937 cells in fluid A+powder B group were significantly increased (P<0.05). There was no significant difference in cell apoptosis rates and expression of PKCδ mRNA and protein between fluid A+fluid B group and blank control group, normal control group and fluid A+fluid B+rottlerin group (P＞0.05). Conclusion Fluid A+powder B can significantly increase apoptosis of U937 cell line, the mechanism of which may be associated with the up-regulation of expression of PKCδ. Compared with fluid A+powder B, fluid A+fluid B is superior in reducing apoptosis of peripheral blood monouclear cells.
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The human La protein is recently identified as a host factor potentially involved in the post-transcriptional regulation of hepatitis B virus (HBV) RNA. The La binding site is mapped to a predicted stem-loop structure within a region shared by all HBV RNAs, and it is known that human La protein protected HBV RNA against Rnase-mediated degradation. HLa mutants lost the ability of binding and protecting HBV RNA, which make it easy for HBV RNA to degrade and the virus replication to terminate. This review summarizes the latest investigation about the interaction of La protein,HBV RNA and Nuclear RNases, and discusses the possible mechanisms of HBV RNA degradation, the effect of La protein and its mutants on the translation initiation of HBV RNA, and the replication of the virus.
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Objective:To prove whether La protein could effect the replications of the HBV in cultured cells.Methods:Three specific SiRNAs for human La protein was obtained by transcription in vitro. After transfection with the SiRNAs into HepG2.2.15 cell, the levels of La protein mRNA and HBV DNA were detected by real-time PCR.Results:The HBV DNA secreted by the cell transfected with the SiRNAs was reduced with reduction of the mRNA of the La protein.Conclusion:The La protein can protect the replications of the HBV in cultured cells.
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The Campylobacter carrier rate of the bile was 23. 64%,14. 29%,7. 14%,6. 64%,5.88%, 5.55% and 3. 63% in the quails, cats, dogs, pigs, chickens, ducks and oxen respectively. The survival time of Campylobacter in the bile in vitro ranged from 4 to 7 weeks. The Campylobacter carrier rate of the intestinal content was higher than that of the bile in all the domestic animals and fowls. It is believed that the domestic animals and fowls may be an important source of Campylobacter infection in human beings according to our findings.
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0.05).It is concluded that furazolidone in small doses is as efficacious as Denol in the treatment of duodenal ulcer and the clearance of H.pylori,and it be a safe substitute for the routine dose of furazolidone for the treatment of duodenal ulcer.