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OBJECTIVE： To study the effects of Tiaopi huxin prescription （TPHXP） on the atherosclerosis （AS） of ApoE－/－ mice， and to investigate its mechanism. METHODS： Forty male ApoE－/－ mice were divided into blank group， model group， simvastatin group （positive control， 5 mg/kg） and TPHXP low-dose and high-dose groups （50， 150 mg/kg）， with 8 mice in each group. Except that blank group was given common diet， other groups were given high-lipid diet to induce AS model. After modeling， administration groups were given relevant medicine intragastrically， and blank group and model group were given constant volume of normal saline intragastrically， once a day， for consecutive 12 weeks. After last medication， the serum levels of TC， TG， LDL-C and HDL-C were determined by spectrophotometry. The serum level of NO was detected by nitrate reduction method. The serum levels of IL-6 and VCAM-1 were determined by ELISA. After separating thoracic aorta， HE staining was used to observe the formation of plaque in the thoracic aorta of mice in each group， and the corrected plaque area was calculated. Western blotting was conducted to determine the expression of NF-κB p65， Cav-1 and eNOS. RESULTS： Compared with blank group， the serum levels of TC， TG， LDL-C， IL-6 and VCAM-1 were increased significantly in model group， while the levels of HDL-C and NO were decreased significantly （P＜0.01）. The plaque of thoracic aorta was obvious and the corrected plaque area were increased significantly （P＜0.01）. The relative expression of NF-κB p65 and Cav-1 were increased significantly， while the relative expression of eNOS was decreased significantly （P＜0.01）. Compared with model group， the serum levels of TC， TG and LDL-C in administration groups， the serum levels of IL-6 and VCAM-1 in simvastatin group and TPHXP high-dose group were decreased significantly， while the serum levels of HDL-C and NO were increased significantly in administration groups （P＜0.05 or P＜0.01）. In administration groups， the plaques of thoracic aorta were reduced and the corrected plaque area was decreased significantly （P＜0.05 or P＜0.01）； the relative expression of NF-κB p65 and Cav-1 were decreased significantly， while the relative expression of eNOS was increased significantly （P＜0.05 or P＜0.01）. CONCLUSIONS： TPHXP can regulate the level of blood lipid， decrease the level of inflammatory factors and inhibit the formation of AS plaque， the mechanism of which may be associated with inhibiting Cav-1/NF-κB pathway.
RESUMO
OBJECTIVE： To systematically evaluate the difference in therapeutic efficacy， safety and cardiac function of Chinese patent medicine injection for promoting blood circulation and removing blood stasis combined with routine treatment after percutaneous coronary intervention （PCI）， and to provide evidence-based reference for clinical drug use. METHODS： Retrieved from Cochrane library， PubMed， Embase， CNKI， Wanfang database and Chinese sci-tech periodicals database， RCTs about different Chinese patent medicine injection for promoting blood circulation and removing blood stasis combined with routine treatment （trial group） versus routine treatment （control group） after PCI were collected. After screening the literature and extracting the data， the quality of the included studies was evaluated by modified Jadad scale. Bayesian network Meta- analysis was performed by using Stata 14.0 software and Markov Chain-Monte Carlo method. RESULTS： A total of 15 RCTs involving 1 364 patients were included， involving Salvia miltiorrhiza injection， Puerarin injection， Yiqi fumai injection， Xuebijing injection， Shenfu injection， Shuxuetong injection， Salvia miltiorrhiza and ligustrazine injection， Rhodiola wallichiana injection， Danhong injection. Results of Meta-analysis showed that in the aspect of improving total response rate of ECG， 8 kinds of intervention measures were involved；compared with control group， 7 kinds of intervention measures could improve the total response rate of ECG of trial group except for Shenfu injection （P＞0.05）； network Meta-analysis ranking showed that S. miltiorrhiza injection＞Puerarin injection＞Shenfu injection＞S. miltiorrhiza and ligustrazine injection＞Shuxuetong injection＞R. wallichiana injection＞ Danhong injection＞routine treatment. In terms of reducing adverse cardiovascular events （MACE） incidence，8 kinds of intervention measures were involved； compared with control group， 7 kinds of intervention measures could reduce the MACE incidence of trial group except for Puerarin injection （P＞0.05）； network Meta-analysis ranking showed that S. miltiorrhiza and ligustrazine injection＞Danhong injection＞Xuebijing injection＞Shuxuetong injection＞S. miltiorrhiza injection＞R. wallichiana injection＞ Puerarin injection＞routine treatment. In terms of improving left ventricular ejection fraction （LVEF） after treatment， 8 kinds of intervention measures were involved； compared with control group， 7 intervention measures could significantly improve LVEF after treatment of trial group except for R. wallichiana injection (P＞0.05）； network Meta-analysis ranking showed that S. miltiorrhiza and ligustrazine injection＞Yiqi fumai injection＞Danhong injection＞Shenfu injection＞S. miltiorrhiza injection＞Shuxuetong injection＞R. wallichiana injection＞routine treatment. CONCLUSIONS： Compared with routine treatment， S. miltiorrhiza injection is the best in improving total response rate of ECG； S. miltiorrhiza and ligustrazine injection is the best in reducing MACE incidence and improving LVEF after treatment.
RESUMO
OBJECTIVE： To explore the component， target and pathway of Panax notoginseng for coronary heart disease （CHD） and its potential molecular mechanism. METHODS： Based on network pharmacology， active components of P. notoginseng were retrieved with TCMSP platform. The targets of P. notoginseng for CHD were screened by using DRAR-CPI server， GeneCards and DisGeNET databases. Cytoscape 3.6.0 software was used to form the effective components-CHD targets network of P. notoginseng. String database was used to draw target interaction network. Network Analyzer tool was used to calculate target connectivity， and potential core targets were screened. Molecular docking between the core targets and the effective components of P. notoginseng was performed by Systems Dock Web Site server. KEGG pathway enrichment analysis and gene ontology （GO） enrichment analysis were also carried out to explore the important signal pathway and molecular function of P. notoginseng for CHD. “Effective component-target-signal pathway”network of important signal pathway were constructed. RESULTS： Five effective components （stigmasterol， β-sitosterol， ginsenoside rh2， quercetin， notoginsenoside r1） were screened from P. notoginseng for CHD， which acted on 96 targets and had 134 functional relationships. Five core targets were protein kinase B （AKT）， interleukin 6 （IL-6）， vascular endothelial growth factor A （VEGFA）， c-JUN protein （c-JUN） and heparin binding epidermal growth factor （HB-EGF）， which played an important role in the treatment of CHD by altering protein binding and regulating signaling pathways as phosphatidylinositol-3 kinase-protein/kinase B （PI3K/AKT）， hypoxia-inducible factor-1 （HIF-1） and mitogen-activated protein kinase （MAPK）. CONCLUSIONS： P. notoginseng in the treatment of CHD is not only play a variety of effects through the role of multiple targets， but also produce complex network regulation effect through the interaction between targets.