Background Cardiomyocyte apoptosis is a primary cause for coronary microembolization （CME）-induced cardiac dysfunction, p53induces cell growth retardation and apoptosis through stress pathway. The present study inve...Background Cardiomyocyte apoptosis is a primary cause for coronary microembolization （CME）-induced cardiac dysfunction, p53induces cell growth retardation and apoptosis through stress pathway. The present study investigated the mechanism of p53-induced myocar-dial apoptosis and cardiac dysfunction by activating the mitochondrion apoptotic pathway following CME. Methods Forty SD rats wereequally divided into microembolization （CME）, sham operation （sham）, CME＋siRNA-p53, and CME＋control-p53 groups. The CME ratmodel was established by injecting microembolization spheres via the left ventricle. Cardiac ultrasound, TUNEL, fluorescence quantitativePCR, and Western blot were used to assess the cardiac function indicators, cardiomyocyte apoptosis, and the expressions of mRNA and pro-tein in myocardial tissues, respectively. Results Echocardiography revealed a significantly reduced cardiac function of the CME group thanthe sham group while the CME-induced cardiac dysfunction was improved in the CME＋siRNA-p53 group. The indicators of myocardialapoptosis in the CME group increased significantly than the sham group; those of the CME＋siRNA-p53 group decreased significantly thanthe CME group. Fluorescence quantitative PCR and Western blot demonstrated that p53, Bbc3 （PUMA）, and cleaved caspase-3 expressionswere significantly increased, and BCL-2 expression was declined in myocardial tissues of the CME group compared to the sham group. Acontrasting result was observed in the CME＋siRNA-p53 group as compared to the CME group. Conclusions P53 is involved in theCME-induced cardiac dysfunction, which may up-regulate Bbc3 to activate BCL-2/caspase3 mitochondrial apoptotic pathway and inducemyocardial apoptosis. Inhibiting the p53 expression can effectively suppress this pathway, thereby reducing myocardial apoptosis and car-diac dysftmction.展开更多
Background Nicorandil （NIC） is a vasodilatory drug used to treat angina. However, its efficacy of cardioprotection in coronary mi- croembolization （CME） is largely unknown. This study was undertaken to determine w...Background Nicorandil （NIC） is a vasodilatory drug used to treat angina. However, its efficacy of cardioprotection in coronary mi- croembolization （CME） is largely unknown. This study was undertaken to determine whether nicorandil pretreatment could attenuate myo- cardial apoptosis and improve cardiac function after CME in rats. Methods Forty-five rats were randomly divided into a Sham group, a CME group and a CME ＋ NIC （NIC） group （n = 15 per group）. CME was established by injecting plastic microspheres （42 pm in diameter） into the left ventricle of the rats in all of the groups except the Sham group. The NIC group received nicorandil at 3 mg/kg per day for seven days before the operation. Cardiac fimction was assessed by echocardiography, the expression levels of cleaved caspase-9/8/3 were detected by Western blot, microinfarction area was measured by haematoxylin-basic fuchsin picric acid staining, and myocardial apoptosis was de- tected by TUNEL staining. Results Compared to that in the Sham group, cardiac fimction in the CME group was significantly decreased （P 〈 0.05）. However, compared to the CME group, the NIC group showed improved cardiac function （P 〈 0.05）. The expression levels of cleaved caspase-9/8/3 protein and myocardial apoptosis were dramatically increased in the CME group compared to those in the Sham group （P 〈 0.05）, while the NIC pretreatment group had significantly decreased expression levels of cleaved caspase-9/8/3 protein as well as a de- creased apoptotic rate （P 〈 0.05）. Conclusions NIC pretreatment inhibited CME-induced myocardial apoptosis and improved cardiac func- tion through blockade of the mitochondrial and death receptor-mediated apoptotic pathways.展开更多
Background Myocardial injury caused by microvascular obstruction(MVO)is characterized by persistent ischemia/hypoxia(IH)of cardiomyocytes after microembolization.Autophagy and Egr-1 were closely associated with variou...Background Myocardial injury caused by microvascular obstruction(MVO)is characterized by persistent ischemia/hypoxia(IH)of cardiomyocytes after microembolization.Autophagy and Egr-1 were closely associated with various cardiovascular diseases,including MVO.Bim and Beclin-1 are the important genes for autophagy and apoptosis.We aimed to explore whether the Egr-1/Bim/Beclin-1 pathway is involved in regulating autophagy and apoptosis in IH-exposed cardiomyocytes.Methods Neonatal rat cardiomyocytes exposed to the IH environment in vitro were transfected with lentivirus expressing Egr-1 or Egr-1 sh RNA,or further treated with 3-methyladenine(3-MA).The expressions of autophagy and apoptosis-associated genes were evaluated using RT-q PCR and Western blots assays.Autophagic vacuoles and autophagic flux were detected by transmission electron microscopy(TEM)and confocal microscope,respectively.Cell injury was assessed by lactate dehydrogenase(LDH)leakage,and apoptosis was determined by flow cytometry.Results IH exposure elevated Egr-1 and Bim expressions,and decreased Beclin-1 expression in rat cardiomyocytes.Egr-1 overexpression in IH-exposed cardiomyocytes significantly up-regulated the levels of Egr-1 and Bim,and down-regulated the level of Beclin-1.Egr-1 knockdown resulted in down-regulated expressions of Egr-1 and Bim,as well as up-regulated expression of Beclin-1.In addition,Egr-1 knockdown induced autophagy was suppressed by 3-MA treatments.TEM and autophagic flux experiments also confirmed that Egr-1 inhibited autophagy progression in IH-exposed cardiomyocytes.Egr-1 suppression protected cardiomyocytes from IH-induced injury,as evidenced by the positive correlations between Egr-1 expression and LDH leakage or apoptosis index in IH-exposed cardiomyocytes.Conclusions IH-induced cardiomyocyte autophagy and apoptosis are regulated by the Egr-1/Bim/Beclin-1 pathway,which is a potential target for treating cardiomyocyte injury caused by MVO in the IH environment.展开更多
Monochloroacetic acid(MCAA)is identified as a highly carcinogenic disinfection by-product in chlorinated drinking water.In this study,a series of CeO_(2)-supported Pd catalysts(Pd/MCeO_(2))were synthesized through one...Monochloroacetic acid(MCAA)is identified as a highly carcinogenic disinfection by-product in chlorinated drinking water.In this study,a series of CeO_(2)-supported Pd catalysts(Pd/MCeO_(2))were synthesized through one-step calcination of Pd-loaded Ce-UiO-66-BDC(CeMOF),and the liquid-phase catalytic hydrodechlorination of MCA A was explored using these catalysts.For comparison,Pd/CeO_(2)catalysts were additionally synthesized using the conventional impregnation method.The characterization results reveal that the catalysts exhibit strong metal-support interaction,leading to high Pd dispersion and Pd^(n+)content.Additionally,the calcination temperature significantly influences catalytic performance,with the catalyst calcined at 500℃(Pd/MCeO_(2)-500)demonstrating the highest catalytic activity and achieving complete dechlorination of MCA A within 50 min.Furthermore,it is found that the catalytic MCAA hydrodechlorination using the catalysts adheres to the Langmuir-Hinshelwood model.Accordingly,low reaction pH is favorable for the catalytic hydrodechlorination of MCAA,enhancing MCAA adsorption on the catalyst surface due to the electrostatic interaction between MCAA and the catalyst surface.Theoretical results suggest that the presence of Pd^(n+)efficiently facilitates MCAA adsorption and C-Cl cleavage,thus significantly enhancing the liquid-phase catalytic hydrodechlorination.展开更多
In order to study and popularize clones from the introduced Robinia pseudoacacia, morphological charac- teristics and leaf nutrition of samples of a three-year-old stand were observed and analyzed during its growing s...In order to study and popularize clones from the introduced Robinia pseudoacacia, morphological charac- teristics and leaf nutrition of samples of a three-year-old stand were observed and analyzed during its growing season. Combined with data on rooting ability, height and basal diameter, comparisons were made on morphological characteris- tics, growth traits and leaf nutrition of 11 introduced R. pseudoacacia clones （two from Hungary and nine from South Ko- rea） and two domestic clones, The results show that there are significant differences in growth and morphological char- acteristics among the 13 clones, but no significant differences in the contents of crude protein and crude fibers in the leaves （p 〉 0.05）. Height and basal diameter growth of clones B and G were recorded as the fastest, while clone H1 was the slowest. Clone H2 had the largest leaflets, three times as large as other clones, while K4 had the heaviest dry weight per 100 leaflets because of its thick leaves. The 13 clones can be divided into four classes based on the number of leaf- lets per compound leaf, i.e., 1-3, 13-17, 15-23 and 21-25. There were significant differences in thorn size： H2, with the largest leaflets had the smallest thorns. While of course all clones produced roots, there were significant differences; clones 2N, K5 and B had many adventitious roots, while clones K3, K4 and H1 had few. Correlation between content of crude protein and （length x width of leaf） was positive （p 〈 0.05）, while correlations of the content of crude protein, with the number of leaflets per compound leaf, petiole length of compound leaf and thorn length were negative （p 〈 0.01）. Plant height and basal diameter were positively correlated with each other （p 〈 0.01） and negatively correlated with base width of thorns （p 〈 0.05）.展开更多
文摘Background Cardiomyocyte apoptosis is a primary cause for coronary microembolization （CME）-induced cardiac dysfunction, p53induces cell growth retardation and apoptosis through stress pathway. The present study investigated the mechanism of p53-induced myocar-dial apoptosis and cardiac dysfunction by activating the mitochondrion apoptotic pathway following CME. Methods Forty SD rats wereequally divided into microembolization （CME）, sham operation （sham）, CME＋siRNA-p53, and CME＋control-p53 groups. The CME ratmodel was established by injecting microembolization spheres via the left ventricle. Cardiac ultrasound, TUNEL, fluorescence quantitativePCR, and Western blot were used to assess the cardiac function indicators, cardiomyocyte apoptosis, and the expressions of mRNA and pro-tein in myocardial tissues, respectively. Results Echocardiography revealed a significantly reduced cardiac function of the CME group thanthe sham group while the CME-induced cardiac dysfunction was improved in the CME＋siRNA-p53 group. The indicators of myocardialapoptosis in the CME group increased significantly than the sham group; those of the CME＋siRNA-p53 group decreased significantly thanthe CME group. Fluorescence quantitative PCR and Western blot demonstrated that p53, Bbc3 （PUMA）, and cleaved caspase-3 expressionswere significantly increased, and BCL-2 expression was declined in myocardial tissues of the CME group compared to the sham group. Acontrasting result was observed in the CME＋siRNA-p53 group as compared to the CME group. Conclusions P53 is involved in theCME-induced cardiac dysfunction, which may up-regulate Bbc3 to activate BCL-2/caspase3 mitochondrial apoptotic pathway and inducemyocardial apoptosis. Inhibiting the p53 expression can effectively suppress this pathway, thereby reducing myocardial apoptosis and car-diac dysftmction.
基金This work received the support of the National Natural Science Foundation of China （Grant No. 81600283） and the Guangxi Natural Science Foundation （Grant No. 2016 GXNSFBA380022）.
文摘Background Nicorandil （NIC） is a vasodilatory drug used to treat angina. However, its efficacy of cardioprotection in coronary mi- croembolization （CME） is largely unknown. This study was undertaken to determine whether nicorandil pretreatment could attenuate myo- cardial apoptosis and improve cardiac function after CME in rats. Methods Forty-five rats were randomly divided into a Sham group, a CME group and a CME ＋ NIC （NIC） group （n = 15 per group）. CME was established by injecting plastic microspheres （42 pm in diameter） into the left ventricle of the rats in all of the groups except the Sham group. The NIC group received nicorandil at 3 mg/kg per day for seven days before the operation. Cardiac fimction was assessed by echocardiography, the expression levels of cleaved caspase-9/8/3 were detected by Western blot, microinfarction area was measured by haematoxylin-basic fuchsin picric acid staining, and myocardial apoptosis was de- tected by TUNEL staining. Results Compared to that in the Sham group, cardiac fimction in the CME group was significantly decreased （P 〈 0.05）. However, compared to the CME group, the NIC group showed improved cardiac function （P 〈 0.05）. The expression levels of cleaved caspase-9/8/3 protein and myocardial apoptosis were dramatically increased in the CME group compared to those in the Sham group （P 〈 0.05）, while the NIC pretreatment group had significantly decreased expression levels of cleaved caspase-9/8/3 protein as well as a de- creased apoptotic rate （P 〈 0.05）. Conclusions NIC pretreatment inhibited CME-induced myocardial apoptosis and improved cardiac func- tion through blockade of the mitochondrial and death receptor-mediated apoptotic pathways.
基金supported by the National Natural Science Foundation of China(Grant No.81770346)the Innovation Project of Guangxi Graduate Education(Grant No.YCBZ2019040)。
文摘Background Myocardial injury caused by microvascular obstruction(MVO)is characterized by persistent ischemia/hypoxia(IH)of cardiomyocytes after microembolization.Autophagy and Egr-1 were closely associated with various cardiovascular diseases,including MVO.Bim and Beclin-1 are the important genes for autophagy and apoptosis.We aimed to explore whether the Egr-1/Bim/Beclin-1 pathway is involved in regulating autophagy and apoptosis in IH-exposed cardiomyocytes.Methods Neonatal rat cardiomyocytes exposed to the IH environment in vitro were transfected with lentivirus expressing Egr-1 or Egr-1 sh RNA,or further treated with 3-methyladenine(3-MA).The expressions of autophagy and apoptosis-associated genes were evaluated using RT-q PCR and Western blots assays.Autophagic vacuoles and autophagic flux were detected by transmission electron microscopy(TEM)and confocal microscope,respectively.Cell injury was assessed by lactate dehydrogenase(LDH)leakage,and apoptosis was determined by flow cytometry.Results IH exposure elevated Egr-1 and Bim expressions,and decreased Beclin-1 expression in rat cardiomyocytes.Egr-1 overexpression in IH-exposed cardiomyocytes significantly up-regulated the levels of Egr-1 and Bim,and down-regulated the level of Beclin-1.Egr-1 knockdown resulted in down-regulated expressions of Egr-1 and Bim,as well as up-regulated expression of Beclin-1.In addition,Egr-1 knockdown induced autophagy was suppressed by 3-MA treatments.TEM and autophagic flux experiments also confirmed that Egr-1 inhibited autophagy progression in IH-exposed cardiomyocytes.Egr-1 suppression protected cardiomyocytes from IH-induced injury,as evidenced by the positive correlations between Egr-1 expression and LDH leakage or apoptosis index in IH-exposed cardiomyocytes.Conclusions IH-induced cardiomyocyte autophagy and apoptosis are regulated by the Egr-1/Bim/Beclin-1 pathway,which is a potential target for treating cardiomyocyte injury caused by MVO in the IH environment.
基金financially supported by the National Natural Science Foundation of China(Nos.21976086 and 22002059)。
文摘Monochloroacetic acid(MCAA)is identified as a highly carcinogenic disinfection by-product in chlorinated drinking water.In this study,a series of CeO_(2)-supported Pd catalysts(Pd/MCeO_(2))were synthesized through one-step calcination of Pd-loaded Ce-UiO-66-BDC(CeMOF),and the liquid-phase catalytic hydrodechlorination of MCA A was explored using these catalysts.For comparison,Pd/CeO_(2)catalysts were additionally synthesized using the conventional impregnation method.The characterization results reveal that the catalysts exhibit strong metal-support interaction,leading to high Pd dispersion and Pd^(n+)content.Additionally,the calcination temperature significantly influences catalytic performance,with the catalyst calcined at 500℃(Pd/MCeO_(2)-500)demonstrating the highest catalytic activity and achieving complete dechlorination of MCA A within 50 min.Furthermore,it is found that the catalytic MCAA hydrodechlorination using the catalysts adheres to the Langmuir-Hinshelwood model.Accordingly,low reaction pH is favorable for the catalytic hydrodechlorination of MCAA,enhancing MCAA adsorption on the catalyst surface due to the electrostatic interaction between MCAA and the catalyst surface.Theoretical results suggest that the presence of Pd^(n+)efficiently facilitates MCAA adsorption and C-Cl cleavage,thus significantly enhancing the liquid-phase catalytic hydrodechlorination.
基金financially supported by the National Key Technology R&D Program (No. 2006BAD01A1601)the National High Technology Research and Development Program of China (863 Program, No. 2007AA100105)+1 种基金the Special Fund for Agro-scientific Research in the Public Interest (No. 200803034)the Key ResearchProgram of the State Forestry Administration of China (No. 2004-04)
文摘In order to study and popularize clones from the introduced Robinia pseudoacacia, morphological charac- teristics and leaf nutrition of samples of a three-year-old stand were observed and analyzed during its growing season. Combined with data on rooting ability, height and basal diameter, comparisons were made on morphological characteris- tics, growth traits and leaf nutrition of 11 introduced R. pseudoacacia clones （two from Hungary and nine from South Ko- rea） and two domestic clones, The results show that there are significant differences in growth and morphological char- acteristics among the 13 clones, but no significant differences in the contents of crude protein and crude fibers in the leaves （p 〉 0.05）. Height and basal diameter growth of clones B and G were recorded as the fastest, while clone H1 was the slowest. Clone H2 had the largest leaflets, three times as large as other clones, while K4 had the heaviest dry weight per 100 leaflets because of its thick leaves. The 13 clones can be divided into four classes based on the number of leaf- lets per compound leaf, i.e., 1-3, 13-17, 15-23 and 21-25. There were significant differences in thorn size： H2, with the largest leaflets had the smallest thorns. While of course all clones produced roots, there were significant differences; clones 2N, K5 and B had many adventitious roots, while clones K3, K4 and H1 had few. Correlation between content of crude protein and （length x width of leaf） was positive （p 〈 0.05）, while correlations of the content of crude protein, with the number of leaflets per compound leaf, petiole length of compound leaf and thorn length were negative （p 〈 0.01）. Plant height and basal diameter were positively correlated with each other （p 〈 0.01） and negatively correlated with base width of thorns （p 〈 0.05）.
