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Objective To study the effects of different hypertonic saline (4.5%and 7.5%) in fluid resuscitation on hemodynamics in traumatic rabbits with hemorrhagic shock.Methods Thirty-two healthy rabbits ( male or female, 2.0-3.0 kg body weight) were divided into 4 groups randomly:SHAM group, SWT group ( shock without treatment) , 4.5%group (resuscitation with 4.5% hypertonic saline), and 7.5% group ( resuscitation with 7.5% hypertonic saline), 8 rabbits in each group.The rabbit model of uncontrolled hemorrhagic shock was established after anesthesia.The fluid used in the two methods of fluid resuscitation was infused into the rabbits at designed times.The hemodynamic data including the left intraventricular systolic pressure ( LVSP) and maximal change rate of left intraventricular pressure ( ±dp/dtmax) were determined at 0 min, 30 min, 60 min, and 90 min.Results (1) The rabbit models of uncontrolled hemorrhagic shock were generated successfully.At 30 min, data of SWT in the 4.5%and 7.5%groups had no significant difference through pairwise comparison (P>0.05).(2) The hemodynamic parameters changed similarly during the experiment.At 60 min, the values of the 7.5%group ( LVSP=115.00 ±8.37 mmHg, +dp/dtmax=4.29 ±0.50 mmHg/ms, -dp/dtmax=-3.25 ±0.25 mmHg/ms) were significantly higher than those in the 4.5%group ( ( LVSP=104.14 ±7.73 mmHg, +dp/dtmax=3.35 ±0.39 mmHg/ms, -dp/dtmax=-2.27 ±0.12 mmHg/ms) (P0.05 ) .Conclusions Fluid resuscitation can improve the hemodynamic function in traumatic rabbits with uncontrolled hemorrhagic shock.Comparing with the 4.5%hypertonic saline, 7.5% hypertonic saline can improve the hemodynamic function more apparently.Our results may provide an experimental support for the treatment of clinical patients with uncontrolled hemorrhagic shock.
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Objective To investigate the effect of periplocin of cortex periplocae (CPP) on Stat3 signaling and its probable molecular mechanism of inducing apoptosis and anti-tumor activity. Methods Cell proliferation was detected by MTT. Cell apoptosis and cell cycle were investigated by flow cytometry. Expression of Stat3 protein in SMMC-7721 cells was analyzed by Western blot. Mcl-1, Survivin and XIAP mRNA expressions were measured by RT-PCR. Results CPP inhibited the proliferation of SMMC-7721 cells significantly, induced their apoptosis and arrested their cell cycle at G2/M phase. Decreased expression of Stat3 protein in the cell nucleus was observed after CPP treatment, but no significant changes were found in cytoplasma. Mcl-1, Survivin and XIAP mRNA expression levels were decreased in a time-dependent manner. Conclusion CPP inhibits cell proliferation and induces apoptosis by inhibiting Stat3 signal transduction in human hepatocellular carcinoma cell line SMMC-7721.
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Objective To investigate the effects of inhibition of STAT5 gene expression by RNA interference technology on apoptosis of human hepatocellular carcinoma cell line SMMC-7721. Methods Three siRNA eukaryotic expression vectors against STAT5 were constructed and transfected with lipofectamineTM 2000 into SMMC-7721 cells. The changes in STAT5 expression were detected by semi-quantitative RT-PCR and Western blot. Cell apoptosis was assayed by flow cytometry (FCM). Results The sequence-specific siRNA could effectively and specifically inhibit STAT5 gene expression at both mRNA and protein levels. The inhibition rates of STAT5 mRNA expression were 70.43%, 43.02%, and 45.07%, respectively. The inhibition rates of STAT5 protein expression were 67.45%, 37.36%, and 41.86%, respectively. At 48 h after transfection, apoptosis rate was 25.61%. Conclusion siRNA against STAT5 can inhibit STAT5 gene expression in SMMC-7721 cells effectively and specifically and induce apoptosis of SMMC-7721 cells. siRNA targeting STAT5 has a great potential value in gene therapy of hepatocellular carcinoma.
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0.05);the TAV of the drug plus radiation dose of 20,25Gy groups were much smaller than that of the radiation alone groups (P