RESUMEN
In the long course of traditional Chinese medicine (TCM) development history,generations of physicians in their long-term medical practice,have paid attention to assimilate and apply new technology and new theory,constantly enrich and perfect the medical technologies,methods and theory systems.It is particularly important to promote the innovation of TCM theory and guide the clinical application of TCM through the learning and absorption of advantages from modern technologies and biomedicine to transform as part of TCM,and then,to expatiate with TCM language.It is especially important in the promotion of TCM theory innovation and clinical guidance of TCM practice.This paper overviewed the common points between TCM and modern medicine from the aspects of balance and steady state of organism,zangfu-organ relationship,etiology and pathogenesis,syndrome differentiation methods,compatibility of Chinese herbal medicine and formula,medicinal properties and pharmacology,etc.The feasibility of applying modern medicine in the interpretation of TCM and its development prospects was expatiated.It provided new ideas and new methods in TCM development.
RESUMEN
This study was aimed to predict active compounds,drug targets and potential diseases of Yi-Guan decoction (YGD) by network pharmacological technology,and to clarify molecular mechanisms of YGD efficiency on different diseases with liver and kidney yin deficiency syndrome (LKYDS).Chemistry compounds,targets and related diseases from YGD were collected from TCMSP,TCM Database@Taiwan,TCMID,HIT,Drugbank,PubChem and TTD databases.The YGD compounds-targets-diseases network was constructed.The network topology was analyzed by Cytoscape software.The analysis of GO biological processes and KEGG pathways enrichment were performed by DAVID website.The results showed that 849 chemical compounds were identified from Beishashen,Maidong,Danggui,Shengdihuang,Chuanlianzi and Gouqizi.There were 49 active CHM compounds that were both oral bioavailability (OB) ≥ 30％ and drug-likeness (DL) ≥ 0.18,corresponding to 200 target proteins and 264 diseases.The top three GO biological processes were response to organic substance,regulation of cell proliferation,and response to endogenous stimulus,respectively.The top three KEGG pathways were pathways in cancer,hepatitis B,and prostate cancer,respectively.It was concluded that the analysis on YGD was conducted based on network pharmacology,and the compound-target-disease network was built,which may help to clarify the mechanisms of YGD efficiency on different diseases with LKYDS.It can provide clues to find new potential clinical adaptation of disease and new drugs.
RESUMEN
<p><b>OBJECTIVE</b>To investigate the changes in the functional activity of glycogen synthase kinase-3 (GSK-3) in the hepatic tissue after endotoxin (lipopolysaccharide, LPS) tolerance and explore the effects of LPS-induced GSK-3 inhibition on glycogen metabolism in the liver.</p><p><b>METHODS</b>Male SD rats were randomly divided into normal control, endotoxin pretreatment and GSK-3 inhibitor (lithium chloride) groups with corresponding pretreatments prior to a large dose of LPS challenge (10 mg/kg) to induce liver injury. Glycogen deposition and content in the hepatic tissue was detected using periodic acid-Schiff (PAS) staining and a glycogen quantification kit, respectively. Western blotting was performed for semi-quantitative analysis of protein level and inhibitory phosphorylation of GSK-3, and a Coomassie brilliant blue G-250-based colorimetric assay was used to detect calpain activity in the liver.</p><p><b>RESULTS</b>Glycogen content in the liver decreased significantly after LPS challenge in all the 3 groups (P<0.05) but showed no significant difference among the groups (P>0.05). Both LPS and lithium chloride pretreatments caused a significant increase of liver glycogen content (P<0.05). LPS pretreatment induced inhibitory phosphorylation of GSK-3β (P<0.05) and partial cleavage of GSK-3α but did not affect the expression of GSK-3 protein (P>0.05). Large-dose LPS challenge significantly increased the activity of calpain in the liver tissue (P<0.05) to a comparable level in the 3 groups (P>0.05).</p><p><b>CONCLUSION</b>Endotoxin pretreatment induces inhibitory phosphorylation of GSK-3β and partial cleavage of GSK-3α and promotes the deposition of liver glycogen but does not affect the activity of calpain, which may contribute to an increased glycogen reserve for energy supply in the event of large-dose LPS challenge.</p>