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[ ABSTRACT] AIM:To investigate the inhibitory effect of Am80 on neointima hyperplasia in carotid arteries after balloon injury and to observe the interaction between Krüppel-like factor 4 (KLF4) and retinoic acid receptorα(RARα). METHODS:Neointima hyperplasia in carotid arteries was observed by hemotoxylin and eosin staining.The expression of KLF4 and cyclin D1 was examined by immunostaining and Western blotting analysis.To detect the interaction between KLF4 and RARαin the vascular tissue, the injured arteries were harvested, and the protein extracts were prepared and subjected to co-immunoprecipitation assay.RESULTS:Compared with injured group, Am80 significantly reduced neointi-mal hyperplasia and the thickness ratio of intima to media.Am80 not only up-regulated KLF4 or RARαexpression in caro-tid arteries, but also increased the interaction between KLF4 and RARαat tissue levels.CONCLUSION:Am80 inhibits neointima hyperplasia in carotid arteries after balloon injury by promoting the interaction between KLF4 and RARα.
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AIM:To discover the effect of MCPH1 on the DNA damage induced by ionizing radiation in esoph-ageal cancer cells.METHODS:ECA109 cancer cells were radiated at dose of 8 Gy.The nuclear foci of relevant factors were detected 1 h after irradiation in the ECA109 cells after silence of MDC1 gene.A cell line was established that was sta-ble low expression of MCPH1.The nuclear foci induced by ionizing radiation after silence of MCPH1 were determined.RE-SULTS:The MCPH1 gene silenced ECA109 cell line was successfully constructed.A strong relationship between MDC1, MCPH1 andγ-H2AX was observed 1 h after 8 Gy irradiation.Silence of MDC1 did not affect the nuclear foci formation ofγ-H2AX and MCPH1.The nuclear foci of MDC1 but notγ-H2AX significantly reduced after silencing of MCPH1.CON-CLUSION:MCPH1 is located in the downstream of H2AX and upstream formation of MDC1, and regulates the nuclear fo-ci formation of MDC1 during DNA damage response.
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<p><b>OBJECTIVE</b>To study whether previously intravenous injection of anisodamine can prevent endotoxemia of heat stroke of rats.</p><p><b>METHODS</b>Experimental animals were randomly divided into two groups, their average artery pressure, heart rate, survival time, survival rate and rectal temperature were measured at an environmental temperature of 38 degrees C-40 degrees C and 50%-60% retative humidity. Blood samples for endotoxins analyses were taken both before and after heat-stress.</p><p><b>RESULTS</b>During heat stress, the animals of rectal temperature of the experimental and control groups continuously increased and two hours later, separately to (42.7 +/- 0.6) degree C and (43.1 +/- 0.5) degree C, without statistic difference(P > 0.05), and to (44.6 +/- 0.4) degree C and (44.2 +/- 0.3) degree C prior to death, with statistic difference(P < 0.05). Before the experiment, the contents of endotoxins of portal vein blood were (45.7 +/- 5.2) pg/ml and (42.6 +/- 5.4) pg/ml, and that of systemic blood was (14.8 +/- 4.5) pg/ml and (13.9 +/- 7.2) pg/ml, without statistic difference(P > 0.05). Two hours later, the contents of portal vein blood separately increased to (122.2 +/- 16.7) pg/ml and (49.7 +/- 10.2) pg/ml, obviously higher than that before heat-stress(P < 0.01). And there were clear statistic difference between the two groups(P < 0.01). The changing tendency of the heart rhythm is almost the same in two groups, that is, first rose and then fell. But it is without statistic difference before and two hours later(P > 0.05): before heat-stress, the average artery pressures were (13.3 +/- 0.6) kPa and (13.6 +/- 0.5) kPa, without statistic difference(P > 0.05), and two hours later, were (9.6 +/- 0.5) kPa and (8.6 +/- 0.6) kPa, with obvious statistic difference(P < 0.01). The survival time of the animals were (166.5 +/- 16.9) min and (144.5 +/- 18.2) min with obvious statistic difference(P < 0.01), the survival rate of heat stressed rats in the experimental group were obviously higher than control group(P < 0.01 or P < 0.05).</p><p><b>CONCLUSIONS</b>Anisodamine can prevent endotoxemia in rats suffering heat stroke.</p>