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Objective The molecular biology mechanism of cerebral ischemia animal models be analyzed from acupuncture experimental literatures by using data mining methods as a tentative exploration. Methods Retrieve the literatures of acupuncture animal experiments during 1978-2015, and screen the literatures about acupuncture effect on cerebral ischemia animal model of gene protein expression. Acupoint and gene/protein targets were extracted and normalized, and then the frequency statistics, association rule, calculation of complex networks were analyzed and visually displayed.Results A total of 350 papers were included. Seventy-nine acupoints were summarized, and the most frequent acupoint wasbaihui; A total of 180 genes/proteins were found, and the most frequent genes/proteins was BCL2. The most common group acuppointszusanli and quchifor the association rule results. The results of complex networks analysis showed the HSP70, BCL2, CASP3, Bax were more closely associated with cerebral ischemia injury or rehabilitation mechanism. Conclusions The mechanism of acupuncture treatment for cerebral ischemia was that acupuncture adjusting ischemic brain damage and improve the nervous system disorders from many channels and multiple targets.
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AIM: To investigate the antiplatelet aggregation of naringenin and its possible mechanism . METHODS:The effects of naringenin at different concentrations on adenosine diphosphate ( ADP)-induced platelet aggre-gation and platelet spreading on immobilized fibrinogen were detected by aggregational detector and observed under fluores -cence microscope, respectively.The expression of phosphoinositide 3-kinase (PI3K) and the phosphorylation of Akt were analyzed by Western blot .RESULTS:Naringenin significantly inhibited ADP-induced platelet aggregation in a dose-de-pendent manner in vitro and in vivo, and inhibited platelet ' s spreading on immobilized fibrinogen in vitro.Further studies indicated that naringenin inhibited platelet activation accompanied by attenuating not only the activation of PI 3K, but also the phosphorylation of Akt .Moreover, naringenin combined with LY294002 additively inhibited the ADP-induced platelet aggregation.CONCLUSION:Naringenin may inhibit platelet activation by regulation of PI 3K/Akt signaling pathway.
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AIM: To investigate effect of naringenin on ADP-induced platelet aggregation and its possible mechanism.METHODS: The levels of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) were measured in the platelets with ADP stimulation using ELISA in the presence or absence of different concentrations of naringenin.The effect of naringenin at different concentrations on the change of phosphodiesterase (PDE) activity was measured by high efficiency liquid chromatography.The effects of naringenin at different concentrations on phosphorylation of vasodilator-stimulated phosphoprotein (VASP) at positions Ser157 and Ser239 in washed platelets with ADP stimulation were analyzed by Western blot.The phosphorylation of VASP at Ser239 was also analyzed in the presence of protein kinase A (PKA), protein kinase G (PKG), or protein kinase C (PKC) inhibitors before incubation with naringenin.The platelet aggregation was measured in the presence of PKA or PKG inhibitors before incubation with naringenin.RESULTS: Naringenin elevated cGMP levels significantly but not cAMP levels in the platelets with ADP stimulation in a dose-dependent manner.Naringenin inhibited PDE activity.Naringenin increased the phosphorylation of VASP at Ser239 in a dose-dependent manner in the platelets with ADP stimulation but only modest changes in the phosphorylation at position Ser157.The phosphorylation level of VASP at Ser239 position was inhibited when the platelets were treated with PKA inhibitor before incubation with naringenin.Incubation of platelets with neither PKG nor PKC inhibitors before treatment with naringenin affect the phosphorylation of VASP at Ser239.Pretreatment with PKA inhibitor but not PKG inhibitor significantly reversed the antiplatelet aggregation by naringenin in ADP-stimulated platelets.CONCLUSION: Naringenin may inhibit platelet activation through the elevation of cGMP-and PKA-mediated VASP phosphorylation.
ABSTRACT
This paper was aimed to study the molecular mechanism of acupoint biology effect on acupuncture experiment articles.The acupuncture experiment articles in CNKI,Wanfang Data Resource Library and the China Biomedical Literature Database (CBM) were searched.The literature on acupoint and related genes were selected according to the literature inclusion criteria and exclusion criteria.The acupoint and corresponding genes in the literature were collected and analyzed by software written in Python,Cytoscape 3.3.0 and MECODE algorithm.The results showed that 2136 articles were collected,with 233 acupoints and 793 genes.Acupoints in the top 10 frequency were ST36 (Zusanli),GV20 (Baihui),PC6 (Neiguan),GV26 (Shuigou),GV14 (Dazhui),SP6 (Sanyinjiao),BL23 (Shenshu),LI11 (Quchi),GV16 (Fengfu) and GB34 (Yanglingquan).Genes in the top 10 frequency were BCL2,FOS,BDNF,Bax,CASP3,TNFA,GFAP,NGF,HSP70 and IL1B.Acupoint-groups in the top 5 frequency were GV14 (Dazhui)-GV20 (Baihui),GV26 (Shuigou)-GV20 (Baihui),GV20 (Baihui)-ST36 (Zusanli),SP6 (Sanyinjiao)-ST36 (Zusandi),PC6 (Neiguan)-GV26 (Shuigou).ST36 (Zusanli) was in the center of the acupoint-gene network.Through module analyzing,there were some genes belong to different pathways and some acupoints in one network module.It was concluded that ST36 (Zusanli) was the core acupoint in the acupoint experiment study,the stomach meridian of foot Yangming may be closely related with the metabolic pathway.This finding may provide new research ideas for clinical and experimental research.