To analysis the differences between Tripterygium wilfordii and T. hypoglaucum, specimens of their leaves were collected from five production regions and analyzed by ultra performance liquid chromatography coupled with quadrupole time of flight mass spectrometry (UPLC-Q-TOF-MS). The data were analyzed by multivariate statistical method, such as hierarchical cluster analysis (HCA) principal component analysis (PCA) and orthogonal signal correction partial least square discrimination (OPLS-DA). Potential markers with VIP values above 5.0 and corresponding r values above 0.85, were selected and further tested by combining mann-Whitney nonparametric. Those with P < 0.001 and AUC = 1 were confirmed as metabolite markers to discriminate them from each other. Results revealed that the two species were obviously different in their leaf metabolites. Based on their mass spectra, 23 potential metabolite markers were identified to distinguish T. wilfordii from T. hypoglaucum.
Chromatography, High Pressure Liquid ; Drugs, Chinese Herbal ; chemistry ; metabolism ; Mass Spectrometry ; Molecular Structure ; Plant Leaves ; chemistry ; metabolism ; Tripterygium ; chemistry ; classification ; metabolism

OBJECTIVETo make full use of the plant resources of Panax notoginseng, nutritional compositions and mineral elements were analyzed in aerial part of P. notoginseng from different areas in Yunnan.

METHODUsing the national standard method, water, ash, crude fat, crude fiber, crude protein and mineral elements were determined in aerial part of P. notoginseng from different growing areas.

RESULTResults showed that there were higher contents of crude fiber and crude protein, and lower content of crude fat in the stems and flowers of P. notoginseng. Meanwhile, a large number of mineral elements were determined in two locations of P. notoginseng, and the contents of Zn, Fe, Mn, Ca and Mg were obvious higher among these mineral elements.

CONCLUSIONThis study showed that the stems and flowers of P. notoginseng were nutritious and suggested that the aerial part may be utilized as new resources foods.

Flowers ; chemistry ; Nutritive Value ; Panax notoginseng ; chemistry ; Plant Extracts ; analysis ; Plant Leaves ; chemistry ; Plant Stems ; chemistry ; Trace Elements ; analysis

Sanqi (Panax notoginseng) is a valuable unique herb, and is also one of the very fast developed varieties of traditional Chinese medicines in recent years with increasing role in traditional Chinese medicine industry. This paper summarized the main experience, industry development and present situation, pointed out the main problems existing in the industry development. On this basis, we put forward the targets and measures for the development of the Sanqi industry in to provide decision-making reference for the sustainable development of the Sanqi industry in China.
China ; Drug Industry ; economics ; trends ; Drugs, Chinese Herbal ; analysis ; economics ; Medicine, Chinese Traditional ; economics ; trends ; Panax notoginseng ; chemistry ; growth & development

OBJECTIVETo investigate the protective effect of epimedium flavonoids Injection (EFI) on experimental acute myocardial infarction (AMI) rats.

METHODSRats were randomly divided into 6 groups, the acute myocardial infarction model was established by ligating left anterior descending branch of coronary artery (LAD). After operation, the rats in the sham-operation and model group were intravenous injected with 5% glucose injection, those in the positive medicine group were intravenous injected with nitroglycerin 0.3mg/kg, while rats in the low-, middle- and large-dose EFI group were intravenous injected with TFE in a dose of 10, 20, 40 mg/kg respectively. ECG was monitored before and after coronary artery ligation, and after treatment at different time points. At the same time, the millivolt of ST and ST-T segment were measured. The changes of serum creatine phosphokinase (CPK), lactate dehydrogenase (LDH), superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were determined, and the myocardial infarcted area was detected by MTT respectively 3 h after LAD. Results After intravenous injection of EFI in a dose of 10, 20, 40 mg/kg, the myocardial infarcted area of AMI rats could be decreased in different degree, the activity of serum CPK, LDH and the content of MDA decreased (P < 0.05 or P < 0.01), while the activity of serum SOD increased significantly (P < 0.05 or P < 0.01). It could began to lower the elevated ST-T segment 5 min after medication and the action could last for 3 h (P < 0.05 or P < 0.01).

CONCLUSIONEFI has a protective effect against acute myocardial ischemia caused by LAD, and the effect is quickly initiated.

Animals ; Creatine Kinase ; blood ; Epimedium ; chemistry ; Female ; Flavonoids ; isolation & purification ; therapeutic use ; L-Lactate Dehydrogenase ; blood ; Male ; Myocardial Infarction ; drug therapy ; Phytotherapy ; Random Allocation ; Rats ; Rats, Wistar ; Superoxide Dismutase ; blood

Objective To explore if continuous administration of adenosine by peripheral pathway can attenuate myocardial hypertrophy and pulmonary arterial hypertension(PAH)caused by chronic hypoxia and analyze the dose-effect relationships between them.Methods Forty-eight Sprague-Dawley(SD)rats were randomly divided into 8 groups:the hypoxia group(n=6),the hypoxia ade-nosine-treated groups [n=18,adenosine was administrated with different doses 50,100,150 ?g/(kg?min),the hypoxia adenosine-treated group A,B,C],the control group(n=6),the control adenosine-treated control groups [n=18,adenosine was administrated with different doses 50,100,150 ?g/(kg?min),the control adenosine-treated control group A,B,C].On the 21st day of the experiment,the Medlab-U/4CS was used to determined the right ventricular systolic pressure(RVSP)and the mean pulmonary arterial pressure(mPAP)of each rat.The ratio of the weight of right ventricle/left ventricle and septum[RV/(LV+S)] and the ratio of the weight of right ventricle/body weight(RV/BW)were also calculated.The morphological changes in myocardium cells and pulmonary vascular structure were observed.SAS 8.0 software was used to analyze the data.Results Twenty-one days after hypoxia,RVSP,mPAP,RV/(LV+S),RV/BW in hypoxia groups were higher significantly than those in control group and hypoxia adenosine-treated groups(Pa

Objective To study the relationship between peripheral blood hemoglobin (HB) and blood pres- sure.Methods We performed a cross-sectional analysis in 1153 subjects aged 29-83 years.Waist circumfer- ence,HB,blood pressure,high-density lipoprotein cholesterol(HDL-C),low-density lipoprotein cholesterol(LDL- C),triglycerides (TG),total cholesterol (TC) were determined.Results ①With the increasing of blood pres- sure,HB had a clearly increasing trend (HB,normotensive:137.5?14.7 vs prehypertension:143.4?14.4 vs hy- pertension:144.3?13.8 g/L,P

0.05).Conclusions ATP-TCA could be used to individualize chemotherapy by selecting agents for particular patients of cervical cancer.The expression of GST-? and TS protein might be useful biomarkers to predict the resistance to DDP and 5-FU in patients with cervical cancer.

This study was aimed to investigate the effect of berberine on the proliferation and apoptosis of HL-60 cells, and the expression of vascular endothelial growth factor receptor 2 (VEGFR2) in HL-60 cells. Berberine (6 - 96 µg/ml) was added to the HL-60 cell line culture medium, the CCK-8 method was used to reveal the inhibitory effect on cell proliferation, the flow cytometry was used to determine the apoptosis rate and cell cycle in HL-60 cells treated with berberine. The expression of VEGFR2 mRNA and protein were examined by RT-PCR and Western blot respectively. The results showed that the berberine inhibited the proliferation of HL-60 cells and induced their apoptosis in dose- and time-dependent manners. With the increased concentration of berberine, the percentage of HL-60 cells in G(1) phase of cycle increased significantly, and the percentage of HL-60 cells in S phase decreased significantly. The expression of mRNA and protein of VEGFR2 decreased with the increased concentration of berberine. It is concluded that the berberine can inhibit HL-60 cell proliferation and induce HL-60 cell apoptosis. The expression of mRNA and proteins of VEGFR2 decreased after treatment with berberine.
Apoptosis ; drug effects ; Berberine ; pharmacology ; Cell Proliferation ; drug effects ; Flow Cytometry ; Gene Expression Regulation, Leukemic ; HL-60 Cells ; Humans ; Vascular Endothelial Growth Factor Receptor-2 ; metabolism

OBJECTIVERecent studies have shown that cytokines TNF-alpha and IL-6 play important roles in myocardial injury or dysfunction. Transcription nuclear factor (NF-kappa B) have been implicated in the regulation of a variety of cytokines in response to cellular defense. The authors observed the activity of NF-kappa B and cytokines TNF-alpha, IL-6 mRNA expression in myocardium to further investigate the mechanism of myocardial injury caused by infectious pneumonia. The therapeutic effect of exogenous adenosine was also studied by observing the influence on NF-kappa B and cytokines.

METHODSThirty rats were divided into three experimental groups at random, each group had 10 rats. The model of pneumonia was induced by the injection of Staphylococcus aureus into the trachea of rats. Adenosine-treated rats were given daily slow intravenous injection of adenosine at a dose of 150 microg/kg.min for 3 days from the second day. All rats were killed on the fifth day. Myocardial tissues were preserved in liquid nitrogen for examination. Pathological examination of myocardium was done and TNF-alpha and IL-6 mRNA expression was detected by reverse transcription polymerase chain reaction (RT-PCR). NF-kappa B activity was measured by electrophoretic mobility shift assay (EMSA).

RESULTS(1) The myocardium in pneumonia group showed significant pathological lesion when compared with control group (P < 0.01). The pathological lesion of myocardium in adenosine-treated group significantly decreased when compared to pneumonia group (P < 0.05). (2) Significant increase of TNF-alpha and IL-6 mRNA expression was observed in myocardium of pneumonic rats when compared with control group (2.27 +/- 0.27 vs. 1.05 +/- 0.16; 1.89 +/- 0.31 vs. 1.12 +/- 0.25: P < 0.01, respectively). NF-kappa B activity of myocardium in pneumonia group was significantly higher than that in control group (13,033 +/- 1286 vs. 383 +/- 15: P < 0.01). (3) TNF-alpha and IL-6 mRNA expression was significantly decreased in adenosine-treated group when compared with pneumonia group (1.25 +/- 0.18 vs. 2.27; 1.31 +/- 0.25 vs. 1.89 +/- 0.31, P < 0.01, respectively). Comparing to that in pneumonia group, NF-kappa B activity of myocardium in adenosine-treated group was significantly decreased (4 487 +/- 562 vs. 13033 +/- 1286, P < 0.01), but it was still significantly higher than that in control group (4487 +/- 562 vs.383 +/- 15, P < 0.01).

CONCLUSIONSIncreased activity of NF-kappa B and subsequent upregulation of TNF-alpha and IL-6 mRNA expression probably play a pivotal role in the mechanism of myocardial injury in rats with pneumonia. Exogenous adenosine can inhibit inflammatory change by lowering NF-kappa B activity and subsequent down-regulation of TNF-alpha and IL-6 expression. Our findings provide novel therapeutic evidence of adenosine in myocardial injury induced by pneumonia in clinic.

Adenosine ; pharmacology ; Animals ; Anti-Arrhythmia Agents ; pharmacology ; Cytokines ; genetics ; metabolism ; Disease Models, Animal ; Electrophoretic Mobility Shift Assay ; Female ; Gene Expression ; drug effects ; Interleukin-6 ; genetics ; metabolism ; Male ; Myocardium ; metabolism ; NF-kappa B ; genetics ; metabolism ; Pneumonia, Staphylococcal ; drug therapy ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Necrosis Factor-alpha ; genetics ; metabolism

OBJECTIVERecent studies showed that adenosine played important roles in vasodilation. This study aimed to investigate the effects of adenosine, its A1 and A2b receptor agonists on pulmonary artery hypertension (PAH) induced by chronic hypoxia in rats by continuously subcutaneous administration with an osmotic pump for 14 days, and to see if rennin angiotensin system and inducible nitric oxygen synthase (iNOS)/nitric oxide (NO) mediate the effects.

METHODFifty-six male SD rats were randomly assigned to seven groups. Each group included eight rats. They were normoxic group, hypoxic group, adenosine-treated group [adenosine was administered at a dose of 150 µg(kg·min) under the hypoxic condition], adenosine A1 receptor agonist CPA-treated group [CPA was administered at a dose of 20 µg/(kg·min) under the hypoxic condition], CPA plus selective adenosine A1 antagonist DPCPX-treated group [CPA and DPCPX were administered simultaneously under the hypoxic condition, the dose of CPA was the same as the above, and the dose of DPCPX was 25 µg/(kg·min)], adenosine A2b receptor agonist NECA-treated group [NECA was administered at a dose of 30 µg/(kg·min) under the hypoxic condition], NECA plus selective adenosine A2b receptor antagonist MRS-treated group[ NECA and MRS1754 were administered simultaneously under the hypoxic condition, the dose of NECA was the same as the above, and the dose of MRS1754 was 50 µg/(kg·min)]. Osmotic pumps containing adenosine or selective adenosine A1 receptor agonist (CPA), or nonselective but potent adenosine A2b receptor agonist (NECA) were placed subcutaneously 7 days after hypoxia and continuously administered the agents for 14 days.Mean pulmonary artery pressure (mPAP) was detected after administration of the agents. Then blood samples were taken from heart for measurement of renin activity, angiotensin II (AngII) and endothelin-1 (ET-1) concentration by radioimmunoassay, NO by measuring nitrate. Small pulmonary arteries were prepared for immunoreactivity staining of proliferating cell nuclear antigen (PCNA) and iNOS.

RESULT(1) Chronic hypoxia induced PAH [mPAP: (31.38 ± 3.42) mm Hg]. Adenosine or CPA or NECA administered for 14 days by subcutaneous route attenuated the mPAP [(21.17 ± 3.56) mm Hg, (22.88 ± 2.95) mm Hg, (19.81 ± 2.39) mm Hg, respectively], which showed significant difference when compared with hypoxia group (P < 0.05 respectively). (2) Plasma rennin activity and AngII level in hypoxia group [(2.51 ± 0.25) ng/(ml·h), (83.01 ± 9.38) pg/ml] were significantly higher than that in normoxic group (P < 0.05, respectively).(3) Adenosine treatment decreased the rennin activity and AngII level when compared with hypoxic group(P < 0.05, respectively);CPA and NECA attenuated respectively the rennin activity and AngII level of rats induced by chronic hypoxia (P < 0.05, respectively). (4) Adenosine administration for 14 days attenuated the wall thickness induced by chronic hypoxia (P < 0.05). CPA showed no effect on wall thickness, but NECA significantly attenuated the wall thickness (P < 0.05). (5) The number of iNOS staining positive cells in small pulmonary artery was higher in hypoxia group than in that in normoxic rats (23.75 ± 7.91 vs. 8.00 ± 2.20, P < 0.05). Adenosine or CPA, or NECA administration increased respectively the iNOS expression in rats treated with chronic hypoxia. Chronic hypoxia caused significant decrease of nitric oxide level. Adenosine treatment increased the nitric oxide level in rats treated with chronic hypoxia. CPA and NECA also increased respectively the nitric oxide level in rats treated with chronic hypoxia. Chronic hypoxia caused significant increase of ET-1 level. The ET-1 level in rats treated with adenosine, CPA or NCEA respectively were lower than that in chronic hypoxia rats (P < 0.05). (6) Adenosine treatment partially attenuated the number of PCNA-positively stained cells. NECA treatment also attenuated the PCNA expression, but CPA showed no effect.

CONCLUSIONAdenosine and its agonists CPA, NECA administered continually by subcutaneous route attenuate mPAP of rats induced by chronic hypoxia. CPA attenuates mPAP through reduction of RA/AngII activity and balance of NO/ET-1 level. NECA attenuates mPAP by inhibiting PCNA expression and proliferation of mooth muscle of pulmonary artery.

Adenosine ; administration & dosage ; pharmacology ; Angiotensin II ; blood ; Animals ; Disease Models, Animal ; Endothelin-1 ; metabolism ; Hypertension, Pulmonary ; drug therapy ; etiology ; metabolism ; Hypoxia ; complications ; Male ; Nitric Oxide ; blood ; Nitric Oxide Synthase Type II ; metabolism ; Proliferating Cell Nuclear Antigen ; metabolism ; Pulmonary Artery ; drug effects ; physiopathology ; Purinergic P1 Receptor Agonists ; administration & dosage ; pharmacology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Renin ; blood