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Heart failure is the terminal stage of various cardiovascular diseases and a leading cause of death. For a long time, natural medicines have been used to treat heart failure（HF） with remarkable effects. In this paper, the Traditional Chinese Medicine compound patents in the national patent database were mined, common Traditional Chinese Medicines for the clinical treatment of HF were selected, and the single active ingredient contained in them was analyzed, which provided some valuable tips for the development of drugs for the treatment of heart failure.
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Metabolic homeostasis is a basic function necessary for the survival of the organism. α1-acid glycoprotein (AGP) is an acute phase protein with a glycosylation degree of up to 45%. It has high affinity and low capacity. Although the biological role of AGP is not fully understood, it has been proven that it can regulate immunity and metabolism, and play an important role in transporting drugs and maintaining capillary barrier function. In this review, the structural characteristics, biochemical characteristics and the regulation of AGP expression were reviewed, with emphasis on the regulatory role of AGP in metabolism, suggesting that AGP may be a potential key factor in metabolic pathways, which provides a new research direction for metabolic diseases.
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Objective:To analyze the influence of micro-course guided by mind mapping on the examination results, critical thinking ability and learning efficiency of interns in internal medicine department of traditional Chinese medicine.Methods:A total of 86 interns rotated in the internal medicine department of traditional Chinese medicine from July 2018 to November 2019 were randomized into two groups, namely the control group ( n=43) and the research group ( n=43). The control group received traditional teaching, and the research group adopted micro-course guided by mind mapping to carry out teaching activities. SPSS 21.0 was used to conduct t test and chi-square test to compare the evaluation results of assessment, critical thinking ability, learning efficiency and comprehensive ability. Results:The scores of theory and skill practice in the research group were higher than those in the control group ( P<0.05). After intervention, the evaluation results of critical thinking ability in the two groups were better than before intervention ( P<0.05), and the evaluation results of critical thinking ability in the research group were better than those in the control group ( P<0.05). The total effective rate of the research group was significantly higher than that of the control group ( P<0.05). The evaluation results of comprehensive ability in the research group were significantly higher than those in the control group ( P<0.05). Conclusion:The application of micro-course guided by mind mapping in practice teaching of internal medicine department of traditional Chinese medicine has a positive impact on the cultivation of interns' critical thinking ability and comprehensive ability, with excellent examination results and high learning efficiency.
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Objective To evaluate the MRI features of erythromycin eye ointment entered into the orbital soft tissue of guinea pigs.Methods MRI was performed dynamically to observe the signal changes 1 day,1 week,2 weeks ,3 weeks and 4 weeks after erythromycin eye ointment was successfully injected into orbital soft tissue of guinea pigs ,as well as HE stainings to monitor retrob-ulbar soft tissue specimens at each time point were obtained.Results After the injection of erythromycin eye ointment 1 day,1 week,2 weeks,3 weeks and 4 weeks later,the signal intensity of erythromycin eye ointment was resemble to the surrounding soft tissue and indistinguishable on T2 WI.On T1 WI,the signal intensity of erythromycin eye ointment was higher than that of contralat-eral adipose body of orbit at 1day and 1 week,and slightly higher than the contralateral adipose body of orbit at 2 weeks and 3 weeks,but resemblance at 4 weeks.HE staining showed that inflammatory cell infiltration and tissue necrosis at 1 day,the presence of foreign body macrophages and fibroblasts at 2 weeks,and the inflammatory cells surrounding the optic nerve gradually subsided at 3 weeks and 4 weeks.Conclusion Fat-suppressed T1 WI is the best sequence to observe erythromycin eye ointment.Abnormal signal changes on T1 WI can reflect the histopathological changes after erythromycin eye ointment into the tissue.
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OBJECTIVE@#To determine the effect of Gingkgo biloba leaf extract (EGb761) induced delayed preconditioning on cytochrome c oxidase (CcO) expression during myocardial ischemia-reperfusion in rats.@*METHODS@#Four groups (10 in each) of Sprague-Dawley male rats were studied. In the sham group, the rats received no treatment. Rats in the ischemia-reperfusion (IR) group were treated with NS (1.0 mL/kg intravenously) 24 h before ischemia. Rats in the M group were treated with EGb761 (100 mg/kg intravenously) 24 h before the ischemia. In the D group , EGb761-treated rats that received the 5-hydroxydecanoate (5-HD), an inhibitor of mitochondrial KATP channels 15 min before the ischemia. The IR, M, and D groups were subjected to ischemia by 30 min of coronary artery occlusion before 2 h of reperfusion. At the end of the reperfusion, myocardial infarct size was measured. CcO was measured by Western blot. The myocardial ultrastructure was observed under the electron microscope.@*RESULTS@#The infarct size was significantly smaller in the M group [(23.78 ± 4.82)%] than in the I/R group [(37.87 ± 5.92)%] (P0.05).@*CONCLUSION@#EGb761 induced delayed preconditioning attenuates myocardial ischemia-reperfusion injury possibly through up-regulating CcO expression in rats.
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Animais , Masculino , Ratos , Medicamentos de Ervas Chinesas , Farmacologia , Usos Terapêuticos , Complexo IV da Cadeia de Transporte de Elétrons , Metabolismo , Ginkgo biloba , Química , Pós-Condicionamento Isquêmico , Métodos , Precondicionamento Isquêmico Miocárdico , Métodos , Isquemia Miocárdica , Traumatismo por Reperfusão Miocárdica , Metabolismo , Fitoterapia , Folhas de Planta , Química , Ratos Sprague-DawleyRESUMO
AIM: To investigate the signal transduction mechanism of Chlamydia pneumoniae (Cpn) in down-regulating the expression of ATP binding cassette A1 (ABCA1) and ATP binding cassette G1 (ABCG1),the key molecules in cholesterol efflux and atherogenesis,from THP-1-derived macrophages. METHODS: Cpn was propagated in Hep-2 cells. THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate (PMA) for 48 h,and were randomly allocated into 4 groups to incubate continually: control group,50 mg/L low density lipoprotein (LDL); Cpn infection group,Cpn (1×10~6 IFU) and 50 mg/L LDL; Cpn and SP600125 (a special JNK inhibiter) group,THP-1 macrophages were previously treated with different concentrations (1-20 μmol/L) of SP600125 for 1 h,and then infected with Cpn (1×10~6 IFU) and 50 mg/L LDL; SP600125 group,SP600125(20 μmol/L)and 50 mg/L LDL. The expressions of ABCA1/ABCG1 and peroxisome proliferator-activated receptor γ (PPARγ) from each group were detected then. The cholesterol efflux was detected by enzyme-fluorescence. The expressions of ABCA1/ABCG1 and PPARγ mRNA and protein were determined by RT-PCR and Western blotting,respectively. RESULTS: Cpn not only down-regulated the ABCA1/ABCG1 expression,but also down-regulated the expression of PPARγ,which regulated the ABCA1/ABCG1 genes transcriptions. However,the mentioned effects of Cpn infection were restrained by the special JNK inhibitor SP600125 in a dose-dependent manner. CONCLUSION: Chlamydia pneumoniae may down-regulate ABCA1/ABCG1 expression from THP-1-derived macrophages via JNK-PPARγ signal transduction pathway.
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Objective To study the influence of arachidonic acid (AA) on L-type calcium channel in rabbits sin-gle cardiomyocyte and its mechanism of antiarrhythmia. Method The single ventricular cardiomyocyte was isolat-ed by using enzyme dispersion method and whole-cell clamp-patch technique was used to record L-type calcium current.All data were analyzed using ANOVA. Results AA inhibited Ica-L in a concentration-dependent manner. The application of 3 μmol/L, 10 μmol/L and 20 μmol/L arachidonic acid reduced the density of peak Ica-L from (10.79±0.93)pA/pF to (8.99±0.43)pA/pF to (7.60±0.35)pA/pF and to (5.60±0.30)pA/pF, respctive-ly (n=7, P<0. O1 ). The Ica-Lpartially resumed after washout. The AA up-shifted the I-V curves of Ica-L without changes of their shape,peak and reverse potentials. The AA also markedly shifted the inactivation curve to left, and prolonged the recorvery time from inactivation,but did not change the curve of calcium channel activation. Con-clustions By acceleration of L-type calcium channel inactivation and prolongation of recorvery time from inactiva-fion,arachidonic acid can reduce the calcium ion influe and prolong effective refractory period, playing the role of antiarrhythmia.
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Objective To investigate the role of c-Jun N-terminal kinase (JNK) signal transduction pathway on the up-regulation of the expression of acyl-coenzyme A: cholesterol acyltransferasel (ACAT1) induced by Chlamydia pneumoniae (C. pn), and to discuss the mechanism of macrophages-derived foam cell formation induced by C. pn. Methods C. pn was propagated in Hep-2 cells. THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA) for 48 h, and were randomly allocated into four groups to be incubated continually: control group, C. pn infection group, C. pn and SP600125 (a special JNK inhibitor)group and SP600125 group. Lipid droplets in cytoplasm were observed by oil red O staining. The contents of intracellular cholesterol ester were detected by enzyme fluorescence analysis. The expressions of ACAT1 mRNA and protein were determined by reverse transcriptase polymerase chain reaction(RT-PCR) and Western blot, respectively. Results Compared with the control group, the expressions of ACAT1 mRNA and protein were up-regulated in C. pn infection group [(4.16±0.26) vs. (2.17±0.18), (1.20±0.10)vs. (0.61±0.03), both P<0.05], and C. pn-induced foam cell formation was observed. The expressions of ACAT1 mRNA and protein and the foam cell formation were inhibited by SP600125 in a concentration-dependent manner (r = - 0.92, P<0.05; r= - 0. 96, P<0.05, respectively). Conclusions The up-regulation of ACAT1 expression is induced by C. pn via JNK signal transduction pathway, which is involved in the mechanism of C. pn-induced macrophage-derived foam cell formation.
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Objective:To investigate the effects of Chlamydia pneumoniae(Cpn) on SR-A1 and CD36 expression in THP-1-derived macrophages and role of c-Jun NH_2-terminal signal transduction pathway in the process.Methods:Cpn was propagated in Hep-2 cells.THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA)for 48h,and were randomly allocated into four groups to be incubated continually: control group;Cpn infection group;Cpn and SP600125(a JNK inhibiter)group and SP600125 group.Lipid droplets in cytoplasm were observed by oil red O staining.The contents of intracellular cholesterol ester were detected by enzyme-fluorescence.The expression of SR-A1 and CD36mRNA and protein were determined by RT-PCR and Western blot, respectively. Results:THP-1-derived macrophages infected with Cpn resulted in large accumulation of lipid droplets and foam cell formation when co-cultured with LDL.Meanwhile,the expression of SR-A1 mRNA and protein were up-regulated by Cpn infection (P<0.05).However,the expressions of CD36 mRNA and protein in THP-1-derived macrophages infected with Cpn were unchanged.Moreover,the up-regulation of SR-A1 and foam cell formation induced by Cpn could be restrained by the JNK inhibiter SP600125 in a dose-dependent manner,and SP600125 had little impact on the expression of CD36 in THP-1-derived macrophages infected with Cpn.Conclusion:The up-regulation of SR-A1 but not CD36 expression is involved in mechanisms of Cpn inducing foam cell formation.And Chlamydia pneumoniae up-regulates the expression of SR-A1 via the JNK signal transduction pathway.This may be a novel mechanism for the foam cell formation induced by Cpn.
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The effect of atorvastatin on warfarin-induced aortic medial calcification and systolic blood pressure (SBP) of rats induced by warfarin was studied. Thirty healthy and adult rats were randomly divided into Warfarin group (n=10), Atorvastatin group (n=10) and normal control group (n=10). Caudal arterial pressure of rats was measured once a week, and 4 weeks later, aorta was obtained. Elastic fiber, collagen fiber and calcium accumulation in tunica media of cells were measured by Von Kossa staining. The results showed that warfarin treatment led to elevation of systolic blood pressure and aortic medial calcification. The chronic treatment also increased collagen, but decreased elastin in the aorta. However, the atorvastatin treatment had adverse effects. It was concluded that treatment with atorvastatin presented evidence of blood pressure lowing and calcification reducing. These data demonstrate that atorvastatin protected aortic media from warfarin-induced calcification and elevation of systolic blood pressure.