排序方式： 共有109条查询结果，搜索用时 187 毫秒
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HEI Zi-qing WU Wei-kang SUN Hui-lan HUANG He-qing TAN Hong-mei LUO Han-chuan 《园艺学报》2003,19(3):345-347
AIM:To observe the effects of Sini decoction on atherosclerosis(AS) and ceramide content of aorta in rabbits. METHODS:28 rabbits were randomly divided into three groups. Control group was fed with a normal diet; High cholesterol group was fed 1% cholesterol and 5% fat diet; Sini decotion+ high cholesterol group was fed 1% cholesterol and 5% fat diet plus Sini decotion (4.2 g·kg-1·d-1). At the end of study, the plaque area were measured, the atorta ceramide and cell apoptosis were also detected. RESULTS:Sini decotion diminished lipid plaque area on the aortic endothelium, reduced the levels of aorta ceramide and the apoptosis index. CONCLUSION:Sini decoction has an inhibitory effect on AS, the mechanism may be that Sini decotion reduces concentration of ceramide in aorta. 相似文献
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HUANG Zeng-yan HUANG Man-ping PENG Chun-li LIU Yong-yuan LI Chun-yan LIANG Dong-hui 《园艺学报》2021,37(1):34-40
AIM To observe effects of emotional stimulation on expression of stromal cell-derived factor-1（SDF-1） and CXC chemokine receptor 4 （CXCR4） in plasma, platelets, aortas, hippocampus and bone marrow of apolipoprotein E gene knockout （ApoE -/-） mice, and to reveal the possible mechanism of the aggravated atherosclerotic plaque vulnerability by emotional stimulation. METHODS Thirty 8-week-old male ApoE -/- mice were randomly divided into normal control group, high fat group, and emotional stimulation group. Ten 8-week-old inbred C57BL/6J mice served as blank control group. After 12 weeks of intervention, the serum levels of SDF-1 and CXCR4 were investigated by ELISA. The protein levels of SDF-1 and CXCR4 in platelets, aortas, hippocampus and bone marrow were determined by Western blot. The pathological damage of aortas was observed by oil red O staining. RESULTS Compared with blank control group, normal control group and high fat group, the mice subjected to emotional stimulation showed more serious atherosclerosis in aortas detected by oil red O staining, and increased levels of SDF-1 and CXCR4 in the plasma and aortas were also observed （P <0.05）. The results of Western blot showed that the protein levels of SDF-1 and CXCR4 in platelets, aortas and hippocampus were increased in the mice subjected emotional stimulation, but the expression of SDF-1 and CXCR4 in the bone marrow was decreased （P <0.05）. CONCLUSION Imbalance of SDF-1/CXCR4 may be the key target by which emotional stimulation accelerates the progression of atherosclerosis. 相似文献
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ZHANG Qiong WAN Chang-wu YU Yan-ni XIA-Bing LIU Jiang-jin ZHANG Qiao-jun LI Zhu WANG Cheng-fei DAI Jia-lin WANG Jie 《园艺学报》2021,36(12):2133-2138
AIM To explore the possible mechanism of cathepsin C （CTSC） and tumor necrosis factor-α （TNF-α） in coronary heart disease （CHD） by detecting the protein expression of CTSC and TNF-α in human coronary artery tissue. METHODS The coronary artery tissues from 52 cases of CHD and 25 cases of accidental death without any heart disease in the Forensic Judicial Expertise Center of Guizhou Medical University from October 2018 to December 2019 were collected as CHD group and control group, respectively. The coronary artery stenosis and intimal plaque formation were examined by histopathology, the protein expression of CTSC and TNF-α was determined by Western blot, and the intracellular expression of CTSC and TNF-α was analyzed by immunohistochemical staining. RESULTS The results of HE staining showed that the intima of coronary artery in control group was smooth, and no thickening or stenosis was observed. In CHD group, the intima thickened irregularly, atherosclerotic plaques formed, the intima became thinner and the lumen showed eccentric stenosis in varying degrees （P <0.05）. The results of Western blot showed that the expression of CTSC and TNF-α in CHD group was significantly higher than that in control group （P <0.05）. Immunohistochemical staining showed that both CTSC and TNF-α were expressed in the cytoplasm of foam cells, and their positive expression was significantly higher than that in control group （P <0.05）. The results of Pearson moment correlation analysis showed that there was positive correlation between the expression of CTSC and TNF-α in CHD （r2 =0.743, P <0.05）. CONCLUSION The up-regulated expression of CTSC in coronary artery tissue may promote the expression of TNF-α and affect the occurrence and development of CHD. 相似文献
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YU Si-yang WANG Yan ZENG Gao-feng LIU Yang XU Jian-qiang ZENG Meng-ya TANG Ye-hua ZENG Zhi-ying SHI Xiao-qiao CHEN Ying ZHAO Guo-jun 《园艺学报》2016,32(5):863-868
AIM: To explore the role of nucleotide-binding oligomerization domain-like receptor protein 1 (NLRP1) inflammasome in atorvastatin-induced reduction of interleukin-1β (IL-1β) and interleukin-18 (IL-18) releases from the THP-1 macrophages. METHODS: Lipopolysaccharide (LPS, 10 μg/L) was used to trigger the secretion of IL-1β and IL-18 in the THP-1 macrophages. The cells were incubated with different concentrations of atorvastatin (1, 10 and 20 μmol/L) for 24 h, or treated with 10 μmol/L atorvastatin for different time (12 h, 24 h and 48 h). NLRP1 siRNA was transfected into the THP-1 cells. The mRNA expression of NLRP1 inflammasome was detected by RT-PCR. The protein expression of NLRP1 inflammasome was determined by Western blot. The secretion of proinflammatory cytokines IL-1β and IL-18 was quantified by ELISA. RESULTS: Atorvastatin inhibited the mRNA and protein expression of NLRP1 inflammasome in the THP-1 macrophages in a dose- and time-dependent manner. Transfection of NLRP1 siRNA significantly decreased the protein expression of NLRP1 and promoted the suppressive effect of atorvastatin on IL-1β and IL-18 secretion in the THP-1 macrophages. CONCLUSION: Atorvastatin inhibits the production of IL-1β and IL-18 in the macrophages through decreasing NLRP1 inflammasome expression, possibly contributing to the anti-inflammatory effect of atorvastatin on atherosclerosis. 相似文献
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AIM: To observe the changes of transient receptor potential channel 5 (TRPC5) in vascular smooth muscle cells (VSMCs) of apolipoprotein E-knockout (ApoE-/-) mice and the effect of atorvastatin interference, and to investigate the mechanism of atorvastatin therapy. METHODS: Male ApoE-/- mice at 6 weeks of age were used to establish the atherosclerosis model by feeding with hyperlipidic diet. The mice were randomly divided into model group and atorvastatin group. The mice in atorvastatin group were lavaged with atorvastatin at 20 mg·kg-1·d-1, while the mice in model group received normal saline. The healthy C57BL/6J mice with the same age and the same genetic background, feeding with ordinary food, served as control group. At the time points of 14 and 24 weeks, the mice were sacrificed. The serum was collected for detecting the lipid levels. The aortic roots of the heart were taken to make paraffin sections with HE staining for measuring and comparing the relative atherosclerotic plaque area in each section. The expression of TRPC5 in VSMCs was examined with immunohistochemical staining. The mRNA levels of TRPC5 in the serum and the thoracoabdominal aorta were measured by real-time PCR. RESULTS: Compared with model group, blood lipids in atorvastatin group were significantly decreased, and the formation of plaque under aorta intima also decreased. The protein expression of TRPC5 in atorvastatin group decreased significantly compared with model group. Compared with 20-week model group, TRPC5 in 30-week model group showed increasing tendency, but has no statistical significance. Compared with 20-week atorvastatin group, TRPC5 of 30-week atorvastatin group declined. CONCLUSION: Atorvastatin suppresses TRPC5 expression, thus attenuating atherosclerotic development in ApoE-/- mice. 相似文献
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AIM: To study the protective effect of brain-derived neurotrophic factor (BDNF) on vascular endothelial cells with H2O2-induced oxidative injury. METHODS: Human umbilical vein endothelial cells (HUVECs) were cultured in vitro, and the oxidation injury model of HUVECs was established by treatment with H2O2. The oxidatively injured HUVECs were cultured with different concentrations (1, 10 and 100 μg/L) of BDNF. At the same time, the control group (no injury), PBS treatment after H2O2 injury group and TrkB inhibitor group (with 100 μg/L BDNF and 1: 1 000 TrkB inhibitor) were also set up. The viability of the HUVECs was detected by MTT assay. The levels of LDH, MDA, SOD and GSH were measured. The releases of NO, ET-1 and ICAM-1 were analyzed by ELISA. The changes of ROS production and cell apoptosis were evaluated by flow cytometry. The protein levels of TrkB, p-TrkB, cleaved caspase-3, Bcl-2 and Bax were determined by Western blot. RESULTS: Compared with uninjured control group, in H2O2 oxidative injury plus PBS treatment group, the viability of the cells was decreased significantly, the LDH and MDA levels were increased significantly and the activities of SOD and GSH were decreased significantly. The NO secretion was decreased, and the ET-1 and ICAM-1 concentrations were increased significantly. The ROS content and apoptotic rate were increased significantly. The protein levels of cleaved caspase-3 and Bax were increased but Bcl-2 protein expression was decreased significantly. Compared with PBS treatment group, in H2O2-injured HUVECs treated with different concentrations of BDNF, the cell viability was gradually increased, the LDH and MDA levels were decreased and the activities of SOD and GSH were increased gradually. The secretion of NO was increased but ET-1 and ICAM-1 were decreased gradually. The ROS content and apoptotic rate were decreased significantly. The TrkB and p-TrkB levels were significantly increased significantly, the protein expression of cleaved-caspase 3 and Bax was decreased gradually and the Bcl-2 protein expression increased gradually. The role of BDNF was inhibited by TrkB inhibitor. CONCLUSION: BDNF protects HUVECs from oxidative injury by binding with TrkB to activate the BDNF-TrkB signaling pathways. 相似文献
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LI Fei WANG Jing-feng NIE Ru-qiong LUO Nian-sang GENG Deng-feng YUAN Wo-liang XIE Shuang-lun LIN Yong-qing ZHAO Wen-jie 《园艺学报》2008,24(5):909-914
AIM: To investigate the effects of ox-LDL on TLR2 and TLR4 expression and production of TNF-α, IL-10, IL-12, NO and MDA in macrophages and to observe intervention effect of GW1929 in above procedure. METHODS: The mouse peritoneal macrophages were pretreated with ox-LDL (50 mg/L, 100 mg/L) and GW1929 (20 μmol/L) respectively for 24 h. The concentrations of MDA, NO-2/NO-3, TNF-α, IL-10 and IL-12 in the culture fluid were detected. Flow cytometry was used to observe TLR2 and TLR4 expressions after the mouse peritoneal macrophages were pretreated with ox-LDL (50 mg/L) and GW1929 (20 μmol/L) respectively for 6 h, 12 h, and 24 h. RESULTS: The concentrations of MDA, NO-2/NO-3, TNF-α and IL-10 in ox-LDL (50 mg/L, 100 mg/L) group were higher than those in control and GW1929 group obviously, but the concentrations of above index in ox-LDL (50 mg/L, 100 mg/L)+GW1929 group were lower than those in ox-LDL (50 mg/L, 100 mg/L) group apparently. No IL-12 in every group was detected. Expressions of TLR-2 in ox-LDL+GW1929 (6 h, 12 h, 24 h) group were lower than those in ox-LDL (6 h, 12 h, 24 h) group respectively. TLR-4 expressions in ox-LDL+GW1929 (12 h) were lower than those in ox-LDL (12 h) apparently. CONCLUSION: ox-LDL up-regulates TLR2 and TLR4 expressions and promotes the production of ROX, NO, TNF-α and IL-10 in macrophages. GW1929 is capable of inhibiting the above ox-LDL effects. 相似文献
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