Mechanism of Callerya nitida var.hirsutissima in treatment of breast cancer based on network pharmacology / 中国药理学通报

Aim To explore the mechanism of action of the active ingredients of Callerya nitida var.hirsutissima corresponding to the target gene in the treatment of triple-negative breast cancer(TNBC), using network pharmacology, molecular docking technology and in vitro experimental verification.Methods Based on literature research and combined with database screening, the main active components of Callerya nitida var.hirsutissima and the related targets of TNBC were obtained.Intersection genes were found to construct a protein interaction(PPI)network diagram, and core targets were screened according to the size of the correlation.A core target interaction network model of "Traditional Chinese Medicine-Ingredients-Targets-Disease" was constructed.The intersection targets were analyzed for gene GO function and KEGG pathway enrichment analysis.Finally, molecular docking and in vitro experimental verification of the selected components and the target were carried out.Results A total of 38 active components of Callerya nitida var.hirsutissima were collected, as well as 388 related potential targets, 3 919 TNBC targets, and 277 Callerya nitida var.hirsutissima therapeutic targets for TNBC.It mainly acted on multiple targets such as PIK3R1, PIK3CA, MAPK1, AKT1, SRC, etc.In in vitro experiments, it could be seen that the chloroform fraction of Callerya nitida var.hirsutissima and the monomer compounds luteolin and betulin had certain inhibitory effects on cell proliferation.All groups could inhibit the expression of VEGFA, AKT, PIK3CA, CDK1, CDK4 within the range of administration concentration.Conclusions Based on network pharmacology and molecular docking methods, this study explores the possible targets and signaling pathways of Callerya nitida var.hirsutissima in the treatment of TNBC, and conducts in vitro verification experiments to further verify the prediction of network pharmacology.

Expression of vascular endothelial growth factor (VEGF) and VEGF-C in serum and tissue of Wilms tumor / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Angiogenesis and lymphogenesis which were promoted by vascular endothelial growth factor (VEGF) and VEGF-C are important in the growth and metastasis of solid tumors. The high level of VEGF and VEGF-C were distributed in numerous types of cancers, but their distribution and expression in Wilms tumor, the most common pediatric tumor of the kidney, was unclear.</p><p><b>METHODS</b>To learn about the distribution, mass spectroscopy and immunohistochemistry were used to measure the level of VEGF and VEGF-C in serum and tissue of Wilms tumor.</p><p><b>RESULTS</b>The expression level of VEGF in serum of Wilms tumor was the same as in pre-surgery and control, so it was the same case of VEGF-C. Both of these factors were chiefly located in Wilms tumor tissue, but not in borderline and normal. In addition, the higher clinical staging and histopathologic grading were important elements in high expression of VEGF and VEGF-C. Gender, age and the size of tumor have not certainly been implicated in expression level of VEGF and VEGF-C.</p><p><b>CONCLUSIONS</b>The lymph node metastasis and growth of tumors resulted from angiogenesis and lymphogenesis which were promoted by VEGF and VEGF-C in Wilms tumor. The autocrine and paracrine process of VEGF and VEGF-C were the principal contributor to specific tissues of Wilms tumor but not to the entire body.</p>

Effect of Guanxinkang on ATP-sensitive potassium channel in myocardial cells of rat with ischemic/ reperfusion injury / 中国中西医结合杂志

<p><b>UNLABELLED</b>OBJECTIVE To investigate the effect of Guanxinkang (GXK) on ATP-sensitive potassium channel in myocardial cells of rat with ischemic/reperfusion injury and its possible mechanism for cardiac vascular protection and anti-myocardial ischemia.</p><p><b>METHODS</b>Wistar rats were established into I/R injured models by 10 min perfusion--30 min no-flow ischemia--45 min reperfusion, and divided into 5 groups: the I/R model group and 4 treatment groups treated respectively with glibenclamide, pinacidil, GXK and GXK+glibenclamide. Rats' heart were isolated for detecting Ca(2+)-Mg(2+)-ATPase, Na(+)-K(+)-ATPase activity in myocardial cells, and the changes of current in ATP-sensive potassium channel (K(ATP)) was recorded by whole patch clamp technique. Data were controlled by those taken from normal rats in a control group.</p><p><b>RESULTS</b>K(ATP) in the GXK treated group were higher than that in the I/R model group; and similar to that in the pinacidil treated group (P > 0.05). As compared with the model group, activities of Ca(2+)-Mg(2+)-ATPase and Na(+)-K(+)-ATPase in the GXK treated group were increased significantly (P < 0.05).</p><p><b>CONCLUSION</b>GXK shows definite intervention effect on myocardial I/R injury; which is possibly by way of furthering the opening of K(ATP) channel, decreasing Ca2+ influx, and inhibiting Ca2+ overload.</p>

Endothelial function evaluation in salt-sensitive normotensive and mild hypertensive subjects and effects of potassium supplement / 中华心血管病杂志

<p><b>OBJECTIVE</b>Salt-sensitivity plays an important role in essential hypertension and is associated with more severe target organ injury and higher mortality in patients with essential hypertension. However, the pathologic mechanism of salt-sensitivity is poorly understood and endothelial dysfunction might be involved in salt-sensitive hypertension. We, therefore, observed the endothelial function changes by measuring plasma and urine nitric oxide (NO) concentrations in salt-sensitive (SS) normotensive and mild hypertensive subjects underwent various salt loading protocols and the effects of potassium supplement.</p><p><b>METHODS</b>Thirty-nine normotensive and mild hypertensive subjects (< 160/100 mm Hg), aged 16-60, were enrolled and the study protocol is as follows: 3 days baseline investigation, 1 week low-salt loading (3 g/day), 1 week. high-salt loading (18 g/day) and 1 week high-salt loading plus potassium chloride (4.5 g/day).</p><p><b>RESULTS</b>Plasma and urine NO levels were significantly lower in SS (n = 8) subjects at baseline, low-salt and high-salt loading phases compared with salt-resistant subjects (SR, n = 31) and oral potassium supplement to SS subjects with high salt loading significantly increased plasma and urine NO levels.</p><p><b>CONCLUSION</b>Endothelial function is impaired in normotensive and mild hypertensive SS subjects. Oral potassium supplement could improve endothelial function in normotensive and mild hypertensive SS subjects.</p>

Application of Serum Protein Markers in Hirschsprung′s Disease / 实用儿科临床杂志

Objective To check serum protein of children′s Hirschsprung′s disease(HD) and sift specific protein marker which was used in constructing of HD screening and early diagnosis of serum protein fingerprint model.Methods Surface-enhanced laser desorption/ionization time of flight mass spectrometry(SELDI-TOF-MS) was applied to detect protein mass spectrometry of serum specimens in 82 cases(HD group 42 cases,20 cases of other types of obstruction,healthy control group 20 cases) and data were analyzed by bioinformatics methods(support vector machine).Results 1.For HD group and healthy control group:selected 3 M/Z in 3 221.7,5 639.2,6 884.2 protein markers were selected,HD early screening and diagnostic model was established,3 markers in HD low expression,the expressions of them in HD group and healthy control group were 378.29?273.34,295.65?159.38,444.13?254.06 and 1 428.18?1 192.61,1 039.60?785.64,1 115.72?680.48,respectively.There were significant differences in two groups(Pa0.05).Conclusions The establishment of serum protein fingerprint model of HD by SELDI-TOF-MS support vector machine could screen and diagnose HD early,which is a new method of better specificity,high sensitivity and is worthy of further research and application.