Objective:To establish criteria of commonly-seen TCM syndromes of depression.Methods:Consultation of specialists,clinical epidemiological survey,scores of syndrome degree rating and statistical analysis of multiple factors were adopted to establish the criteria for main syndrome differentiation of 5 commonly-seen TCM syndromes of depression.Results:Of 1977 cases of depression,1731 cases were stagnation of the liver-Qi,stagnation of the liver-Qi and deficiency of the spleen,stagnation of the liver-Qi and phlegm,deficiency of both the heart and spleen,and Yin-deficiency of both the liver and kidney.And according to statistical analysis,the criteria for main syndrome differentiation of the 5 syndromes were established.Conclusion:Commonly-seen syndromes of depression have common cause of disease and pathogenesis.Stagnation of the liver-Qi is basic syndrome,and in clinical manifestation of various syndromes emotional depression is common main syndrome,but various syndromes still have other main syndrome.

Objective To explore the molecule mechanisms of migraine with hyperactivity of liver-yang related proteins. Methods Animal model of migraine with hyperactivity of liver-yang was established through electrical trigeminal ganglion stimulation,and by administering orally with Fuzi decoction. The total proteins of splenic lymphocytes in the rats were separated by immobilized pH gradient-based two-dimensional gel electrophoresis. With coomassie blue staining,the 2-DE images were analyzed by PDQuest 7.0 software. Matrix-Assisted Laser Desorption/Ionization-Time of Flight Mass Spectrometry (MALDI-TOF-MS) and database were used to identify the differential proteins. Result Ten differential spots protein were identified,and they were chloride intracellular channel 1,thioredoxin peroxidase Ⅰ,thioredoxin peroxidase Ⅱ,sequence 7 from patent WO9709348,Rho GDP dissociation inhibitor (GDI) alpha,actin related protein 2/3 complex neurofilament light polypeptide,proteasome subunit beta type and heat shock protein-27,annexin A1. Conclusion These protein may be involved in the development of migraine with hyperactivity of liver-yang. These data provide useful clues for elucidating the mechanisms of migraine with hyperactivity of liver-yang.

Objective To explore the molecule mechanisms of ping-gan qianyang therapy on migraine rat model with the hyperactivity of liver-yang.Methods An animal model of migraine with hyperactivity of liver-yang was established through electrical trigeminal ganglion stimulation and administering orally with Fuzi decoction.The total proteins of adrenal#and in the rats were separated by immobilized PH gradient-based two-dimensional gel electrophoresis, and the 2-DE images Was analyzed by PDQuest 7.0 software.Matrix-Assisted Laser Desorption/Ionization-Time Of Flight Mass Spectrometry(MALDI-TOF-MS)and SWISS-PORT and MSDB database were used to identify differential proteins.Result The well-resolution and reproducible 2-DE patterns of rat adrenal glands in normal group,model group and therapy group were obtained.A total of 8 differentially expressed proteins were identified.Conclusion Ping-gan qianyang therapy may effect on migraine by regulating the expression of proteins related to energy metabolism and ubiquitin.

Objective To explore the molecular mechanism of the formulae for calming the liver and suppressing YANG in migraine rat model with syndrome of hyperactivity of the liver-YANG.Methods A rat model of migraine with hyperactivity of liver-YANG was established through electrical trigeminal ganglion stimulation and syndrome of oral administration of Fuzi decoction. The total proteins of the lymphocyte in the rats were separated by immobilized pH gradient-based 2-dimensional gel electrophoresis(2-DE), and the 2-DE image was analyzed by PDQuest 7.0 software. Matrix-assisted laser desorption/ionzation-time of flight mass spectrometry (MALDI-TOF-MS) and the SWISS-PORT and MSDB database were used to identify differential proteins.Results The formulae for calming the liver and suppressing YANG could also improve headache. Well-resolution and reproducible 2-DE patterns of rat lymphocyte from normal, model, and therapy tissues were obtained. Eleven of the total 13 differential protein spots were successfully identified by MALDI-TOF-MS. These proteins were alcohol dehydrogenase 3(ADH3), glycogen phosphorylase, ATP synthase D chain, annexin-3, ubiquitin, neutrophil defensin 4 precursor, melanoma-associated antigen E2, heat shock protein-27, annexin-A1, peroxirdoxin-Ⅱ, MU class glutathione S-transferase (Fragment)(GSH). Conclusion Differences occur in the expression of lymphocyte proteins in migraine rats with syndrome of hyperactivity of liver-YANG after treatment with the formulae for calming the liver and suppressing YANG, and the 11 identified protein spots may be associated with its mechanism.

Objectives:Fenofibric acid is extracted from the widely used hypolipemic fenofibrate,nowadays being approved for marketing around numerous nations and regions,nonetheless not in China.Present trial evaluated the efficacy and safety in the Chinese hypertriglyceridemia population. Methods:This is a multi-center,randomized,double-blind,placebo-controlled phase Ⅲ clinical trial.Patients from 3 different cohorts,including severe hypertriglyceridemia(HTG),moderate HTG and mixed-dyslipidemia(MD),were randomized at 1:1 ratio to receive fenofibric acid 135 mg or placebo daily for 12 weeks.The primary endpoint was the percentage change of triglyceridemia(TG)from baseline at week 12.Secondary endpoints were the percentage changes of other blood lipid indexes.At the same time,the incidence of medical adverse events was observed. Results:Among the three cohorts of patients with severe HTG(n=52),moderate HTG(n=23)and MD(n=52),the TG levels in the fenofibric acid-treated group decreased by(49.12±29.19)%,(49.95±25.19)%and(49.79±19.28)%,respectively from baseline to 12 weeks,while the corresponding placebo groups decreased by(18.88±40.69)%,(8.11±29.86)%and increased by(10.42±73.04)%,respectively from baseline to 12 weeks.The differences between treatment and placebo groups were statistically significant(P<0.017 for severe HTG cohort,P<0.05 for moderate and MD cohort).The high-density lipoprotein cholesterol(HDL-C)in the fenofibric acid-treated group increased by(25.51±21.45)%,(24.55±24.73)%,and(23.60±27.38)%,and the placebo group increased by(1.91±20.42)%,(2.40±9.32)%and(7.13±19.12)%,respectively,the differences between the two groups were statistically significant(all P<0.05).In the fenofibric acid group,adverse events with incidence>5%included upper respiratory tract infection(10.9%),abdominal pain(6.3%),and increased serum creatinine levels(6.3%),rates of adverse events were similar between the two groups(P>0.05). Conclusions:Fenofibric acid can significantly reduce triglycerides and elevate HDL-C levels safely in Chinese patients with severe to moderate HTG without statin or MD patients on top of statin therapy.

Abstract OBJECTIVE To explore the material basis and mechanism of Crataegi Fructus in improving metabolic hypertension(MH) by using network pharmacology and molecular docking technique.METHODS The components of Crataegi Fructus were collected by HERB, ETCM database and literature survey; screening all ingredients of Crataegi Fructus to improve MH targets through databases such as SwissTargetPrediction and GeneCards; build "active ingredient-target-disease" network of Crataegi Fructus with Cytoscape software; DAVID was used to analyze GO enrichment and KEGG pathway. The core components and core targets were verified by molecular docking with Autodock software. RESULTS The total of 89 active components were screened from Crataegi Fructus and acted on 84 targets. Among them, the core active components of Crataegi Fructus to improve MH were maslinic acid, fomefficinic acid B, linolenic acid, linoleic acid, methyl-n-nonylketone, apigenin, ursolic acid, etc. The core targets were CYP19A1, PPARA, ESR1, PTGS2, PPARG, NR3C1, MMP9, TNF, etc. The mechanism of action mainly involved multiple signaling pathways such as inflammation, glycolipid metabolism, and vascular endothelial function. Molecular docking showed that the core active ingredients of Crataegi Fructus had high affinity with core targets. CONCLUSION Crataegi Fructus may regulate multiple signaling pathways such as TNF, IL-17, AGE-RAGE, HIF-1, cGMP-PKG through multi-component regulation, thereby inhibiting inflammatory response, improving glucose and lipid metabolism abnormalities, and improving vascular endothelial function, so as to comprehensively exert the role of improving MH in various aspects.