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Exploring the mechanism of icariin in regulat⁃ing cardiac microvascular endothelial cells based on network pharmacology,molecular docking and in vitro experiments

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中国药理学与毒理学杂志 2023年第S1期37卷 25-26页

作者： CAO Ce LI Li WANG Ziyan LI Haoran LIU Jianxun Institute of Chinese Medicine Sciences Guang-dong Pharmaceutical UniversityGuangzhou 510006China National Clinical Research Center of Traditional Chinese Medicine for Cardio-vascular Diseases China Academy of Chinese Medical SciencesBeijing Key Laboratory of Chinese Materia PharmacologyInstitute of Basic Medical Sciences of Xiyuan HospitalBeijing 100091China

OBJECTIVE To investigate the regulatory effects of icariin(ICA)on cardiac micro⁃vascular endothelial cells(CMEC)after oxygenglucose deprivation reperfusion(OGD/R)*** CMEC were subjected to OGD/R treatment to construct a myocardial ischemiareperfusion model,and were divided into normal,model,low(10μmol·L^(-1)),medium(20μmol·L^(-1))and high(40μmol·L^(-1))ICA group,and high ICA+inhibitor group(40μmol·L^(-1)+20 nmol·L^(-1)).CCK-8 assay was used to assess the protective ability of ICA against CMEC,and cell migration assay and tube-formation assay were used to detect the migration and generation ability of *** TCMSP database,Swiss-Target database and literature mining methods were used to col⁃lect ICA-related targets,the GeneCards data⁃base was used to collect target genes related to myocardial ischemia/reperfusion,and Cytoscape 3.8.0 software was used to construct a"drug-tar⁃get-disease"*** potential targets were imported into STRING 11.5 database to obtain the PPI *** and KEGG enrichment analyses were performed on the potential targets using the DAVID *** docking was performed using AutoDock-vina 1.1.2 soft⁃*** blot detected the expression of related *** After CMEC was subjected to OGD/R treatment,ICA had a protec⁃tive effect at 10^(-1)60μmol·L^(-1);the results of the cell migration assay showed that each group of ICA could promote the migratory effect of CMEC(P<0.01,P<0.01);and the results of tube-for⁃mation assay showed that each group of ICA could significantly promote the generation of branches(P<0.01)and the capillary length exten⁃sion(P<0.05).Network pharmacology collected a total of 23 ICA action targets,1500 disease tar⁃gets and 12 key *** function enrichment analysis found 85 *** pathway enrich⁃ment analysis found 53 results,involving AGERAGE signaling pathway,sphingolipid signaling pathway and VEGF signaling ***⁃lar docking results showed that ICA had better binding

关键词： icariin myocardial ischemia-reperfusion injury cardiac microvascular endothelial cells network pharmacology molecular docking

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Tongxinluo Reverses the Hypoxia-suppressed Claudin-9 in cardiac microvascular endothelial cells

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Chinese Medical Journal 2016年第4期129卷 442-447页

作者： Kun Liu Xiu-Juan Wang Yan-Ning Li Bin Li Jin-Sheng Qi Jing Zhang Yu Wang Department of Biochemistry Hebei Key Laboratory of Medical Biotechnology Hebei Medical University Shijiazhuang Hebei 050017 China Department of Molecular Biology Hebei Key Lab of Laboratory Animal Hebei Medical University Shijiazhuang Hebei 050017 China

Background： Claudin-5, claudin-9, and claudin-11 are expressed in endothelial cells to constitute tight junctions, and their deficiency may lead to hyperpermeability, which is the initiating process and pathological basis of cardiovascular *** tongxinluo （TXL） has satisfactory antianginal effects, whether and how it modulates claudin-5, claudin-9, and claudin-1 1 in hypoxia-stimulated human cardiac microvascular endothelial cells （HCMECs） have not been ***： In this study, HCMECs were stimulated with CoCl2 to mimic hypoxia and treated with ***, the messenger RNA （mRNA） expression of claudin-5, claudin-9, and claudin-l 1 was ***, the protein content and distribution of claudin-9, as well as cell morphological changes were evaluated after TXL ***, the distribution and content histone H3K9 acetylation （H3K9ac） in the claudin-9 gene promoter, which guarantees transcriptional activation, were examined to explore the underlying mechanism, by which TXL up-regulates claudin-9 in hypoxia-stimulated ***： We found that hypoxia-suppressed claudin-9 gene expression in HCMECs （F=7.244;P =0.011） and the hypoxia-suppressed claudin-9 could be reversed by TXL （F=61.911;P =0.000）, which was verified by its protein content changes （F=29.142;P =0.000）.Moreover, high-dose TXL promoted the cytomembrane localization of claudin-9 in hypoxia-stimulated HCMECs, with attenuation of cell ***, high-dose TXL elevated the hypoxia-inhibited H3K9ac in the claudin-9 gene promoter （F=37.766;P =0.000）, activating claudin-9 ***： The results manifested that TXL reversed the hypoxia-suppressed claudin-9 by elevating H3K9ac in its gene promoter, playing protective roles in HCMECs.

关键词： cardiac microvascular endothelial cells Claudin-9 H3K9 Acetylation Hypoxia Tongxinluo

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Gene Expression Profiling of the Proliferative Effect of Periplocin on Mouse cardiac microvascular endothelial cells

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Chinese Journal of Integrative Medicine 2010年第1期16卷 33-40页

作者：王小莹高秀梅刘虹张晗刘洋姜民胡利民张伯礼 Institute of Traditional Chinese Medicine Research Tianjin University of Traditional Chinese Medicine Key Laboratory of Pharmacology of Traditional Chinese Medical Formulae Ministry of Education Key Laboratory of Traditional Chinese Medicine Pharmacology Tianjin

Objective： Periplocin is an active digitalis-like component from Cortex Periplocae, which has been widely used in the treatment of heart diseases in China for many years. According to the recommendations on the cardiovascular effect of periplocin from in vivo experiments, subsequent in vitro experiments are greatly needed for the global assessment of periplocin. The objective of this study is to investigate the cell proliferation effect and the mechanism of periplocin on endothelial cells. Methods： The proliferative activity of periplocin （0.4, 2, 10, 50, 250 pmol/L; 6, 12, 24, 48, 72 h） was investigated by a comparison with the well-reported cardiac glycoside, ouabain, on mouse cardiac microvascular endothelial cells （CMEC）. 3-（4,5-dimethylthiazolyl）- 2,5-diphenyltetrazolium bromide （MTT）, lactate dehydrogenase （LDH） and 5-bromo-2-deoxyuridine （BrdU） assays were used to evaluate cell proliferation and viability. Subsequently, cDNA microarray experiments were performed on periplocin- （50 pmol/L） and ouabain- （50 pmol/L） treated cells, and data was analyzed by ArrayTrack software. Results： Periplocin could increase cell viability to a level lower than ouabain in the MIF analysis, but decrease LDH release simultaneously. The BrdU incorporation assay showed an increase in cell proliferation with 2-50 μmol/L periplocin. Genes related to protein serine/threonine kinase were the most significantly enriched in the 160 genes identified in periplocin versus the control. In the 165 genes regulated by periplocin versus ouabain, GTP-binding was the most altered term. Conclusions： The results demonstrated the proliferation action of periplocin on CMEC. Meanwhile, its lower cytotoxicity compared to ouabain provides a new insight into the treatment of heart failure.

关键词： periplocin cardiac microvascular endothelial cells proliferation protein serine/threonine kinase GTP-binding

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