ABSTRACT
Aim To evaluate the efficacy of the combination of leonurine(SCM),polygonatum polysaccharide(PSP)and deoxynojirimycin(DNJ)in hypoglycemic and antithrombotic aspects by establishing and using zebrafish type II diabetes combined with thrombosis model. Methods On the basis of the zebrafish type II diabetes model established by streptozotocin,phenylhydrazine(PH),arachidonic acid(AA)and ponatinib(PT)were used respectively to establish thrombosis models,which were divided into control group,model group,metformin+aspirin group,and the high,medium and low concentration groups of the combination drugs. After drug intervention in the experimental group,the thrombosis of tail vein was observed. Kit was used to determine the sugar content of juvenile fish tissues in each group. Quantitative analysis of cardiac erythrocytes by o-dianisidine staining method was used to calculate the inhibition rate of thrombus. Quantitative real-time polymerase chain reaction(qRT-PCR)was used to detect the mRNA expressions of related genes in zebrafish. Results Compared with the model group,the combined drug could significantly increase the staining intensity of erythrocytes in zebrafish hearts,inhibit thrombosis,down-regulate the expression of thrombosis-related genes,and reduce tissue glucose content. Conclusions The combined use of the three drugs can effectively reduce the tissue sugar content and have antithrombotic effect,which show great potential in the development of drugs for the treatment of type II diabetes and thrombosis.
ABSTRACT
<p><b>OBJECTIVE</b>To study the effect of crocin on rat experimental hyperlipemia and its mechanisms.</p><p><b>METHOD</b>Hyperlipemia model was established by feeding heavy cholesterol for 2 months and the effect of crocin on blood lipid in experimental hyperlipemia rats was observed. Aortic smooth muscle cells were cultured in different culture media and proliferation was measured by MTT assay. Western blotting was used to detect the effect of crocin on phosphorylation of p38 MAPK.</p><p><b>RESULT</b>Crocin not only decreased greatly the content of cholesterol, triglyceride and density lipoprotein in blood, but also increased the content of high density lipoprotein. In addition, the proliferation of smooth muscle cells and the activation of p38MAPK were inhibited by Crocin.</p><p><b>CONCLUSION</b>Crocin prevents atherosclerosis in hyperlipemia, which may be mediated by the inhibition of both proliferation of smooth muscle cells and activation of p38MAPK.</p>
Subject(s)
Animals , Male , Rats , Aorta, Thoracic , Cell Biology , Carotenoids , Pharmacology , Cell Proliferation , Cholesterol , Blood , Crocus , Chemistry , Hyperlipidemias , Metabolism , Pathology , Hypolipidemic Agents , Pharmacology , Lipoproteins, HDL , Blood , Lipoproteins, LDL , Blood , Myocytes, Smooth Muscle , Cell Biology , Plants, Medicinal , Chemistry , Rats, Sprague-Dawley , Triglycerides , Blood , p38 Mitogen-Activated Protein Kinases , MetabolismABSTRACT
<p><b>AIM</b>To investigate the effect of epigallocatechingallate (EGCG) on acute lung injury induced by oleic acid in mice and the possible mechanism.</p><p><b>METHODS</b>Acute lung injury was induced by oleic acid in mice. Light microscopy and electron microscopy were used to examine histological changes and lung index as well as wet to dry weight ratio was calculated. Serum TNF-a level was measured by enzyme linked immunosorbent assay (ELISA) and the phosphorylation of p38 MAPK was determined by Western blotting.</p><p><b>RESULTS</b>Pretreatment of EGCG significantly alleviated oleic acid induced lung injury accompanied by reduction of lung index and wet to dry weight ratio, decreased of TNF-a level in serum and inhibition of phosphorylation of p38 MAPK.</p><p><b>CONCLUSION</b>EGCG showed beneficial effect on acute lung injury induced by oleic acid in mice. The ultimate reduction of TNF-alpha in serum caused by inhibition of phosphorylated p38 MAPK is involved in the mechanism of action of EGCG.</p>