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@#Objective To summarize the mid-term follow-up results and postoperative aortic remodeling of treating blunt aortic injuries (BAI) with thoracic endovascular aortic repair (TEVAR). Methods A retrospective study was conducted on BAI patients treated with TEVAR, who were admitted into the Department of Vascular Surgery in Zhongshan Hospital, Affiliated to Fudan University between September 2003 and December 2015. There were 15 males and 9 females at an average age of 45.6±14.0 years. The mechanism of BAI was mainly auto car crash. Totally 25 entry tears were detected and most of them were located at the aortic isthmus. Results Twenty-four BAI patients survived and eventually went through TEVAR. One patient died of pulmonary embolism 1 week post-TEVAR. Rate of technical success, clinical success and perioperative mortality was 100.0%, 95.8%, and 4.2%, respectively. Nineteen patients were followed up with a mean time of 35.1(13-87) months. All of them survived this period. Based on the follow-up imaging of CTA, 18 of them revealed no endoleak or stent migration, and 1 patient of transection still had perfusion of distal false lumen at the abdominal aorta. None of the aortic segments measured in this study showed expansion of ≥5 mm during follow-up. The aorta remodeled well in 94.7% of them. Conclusion TEVAR for treating BAI appears feasible with high rates of technical and clinical success rates. The mid-term follow-up results seems satisfying, but the long-term results are yet to be assessed with further follow-up.
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This study is to investigate the cytoprotective role of NaNO2 preconditioning against ethanol induced damage in human hepatoma SMMC-7721 cells. The cells were preconditioned with NaNO2 (0.25 mmol x L(-1)) for 24 hours or 4 weeks, and then exposed to ethanol (200 mmol x L(-1)) for additional 12 h and untreated cells served as control. Both temporal and chronic NaNO2 preconditioning could prevent ethanol elicited cytotoxicity as evidenced by thiazolyl blue (MTT). NaNO2 preconditioning also could inhibit ethanol-induced apoptosis, which was confirmed by FITC-Annexin V/PI flow cytometer and Hoechst 33258 and PI staining. Further, simultaneous NaNO2 preconditioning treatment along with ethanol showed protection against ethanol mediated cellular damage as indicated by significantly decreased levels of malondialdehyde (MDA) and elevated activities of superoxide dismutase (SOD) and catalase (CAT). Western blotting analysis revealed that in ethanol treated cells preconditioned with NaNO2, the HIF-1alpha and Bcl-2 increased obviously, while the expression of pro-apoptotic proteins, including Bax, Caspase-9, Caspase-3 decreased. The results showed that low doses of NaNO2 preconditioning resistant to ethanol-induced human hepatoma SMMC-7721 cells apoptosis, which mechanism may be related to increased expression of HIF-1alpha in the cells.
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This study is to observe the effect of N-(3-phenylallylidene)-6-fluoro-1, 8-(2, 1-propoxy)-7-(4-methylpiperazin-1-yl)-quinolin-4(1H)-one-3-carbonyl hyarazine (FQ16) on apoptosis of hepatocarcinoma SMMC-7721 cells in vitro. With different concentrations of FQ16 at different times used to treat SMMC-7721 cells in vitro, the proliferation of the cells and the inhibition effect of FQ16 on the cell proliferation were examined by MTT assay. Cell apoptosis was determined by Hoechst 33258/PI fluorescence staining, TUNEL and agarose gel electrophoresis method. The effect of FQ16 on topoisomerase II activity was measured by agarose gel electrophoresis using Plasmid pBR322 DNA as the substrate. Mitochondrial membrane potential (MMP, delta psi m) was measured by high content screening image system. The reverse transcriptase-polymerase chain reaction (RT-PCR) was used to detect the expression changes of Bcl-2 mRNA and Bax mRNA. The caspase-9, caspase-8, caspase-3, p53, Bcl-2 and Bax protein expressions were detected by Western blotting analysis. The results showed that the cell proliferation was inhibited by FQ16 at 0.625 - 10 micromol L(-1) in a time-dose dependent manner. Treatment of SMMC-7721 cells with different concentrations of FQ16 for 24 h increased the percentage of the apoptosis cells obviously (P<0.05), the typical ladder DNA in apoptotic cells and a concomitant dissipation of the mitochondrial membrane potential. Compared with control group, FQ16 influenced obviously DNA topoisomerase II activity, stimulated DNA cleavage and inhibited DNA reunion mediated by topoisomerase II. In addition, FQ16 (3 - 7.39 micromol L(-1)) increased mRNA expression of Bax and protein expression of p53, Bax, caspase-9, caspase-3, separately, and induced cytosolic accumulation of activities caspase-9 and caspase-3, whereas the mRNA and protein expression of Bcl-2 decreased with no change of caspase-8. Therefore it can be concluded that the effects of inhibited topoisomerase II and mitochondrial-dependent pathways were involved in FQ16 induction of apoptosis of SMMC-7721 cells.