The combination of medicinal properties refers to expression forms of elements with active properties combined according to a specific sequence. The mode of medicinal property combination refers to the compatible relationship multiple medicinal property combinations. In this paper, based on the mode, safflower, Taohong Siwu decoction, Xuefu Zhuyu decoction and Buyang Huanwu decoction were taken for example to study the characteristics of the compatibility among single herb, herbal pairs and prescriptions. The authors discovered the similarities and differences among them, interpreted the self-similarity in medicinal property combinations of traditional Chinese medicines, and analyzed the compatible relationship among multiple medicinal property combinations, so as to bring forth new ideas in discovering the correlation between the compatibility study mode of traditional Chinese medicines based medicinal property combinations and the efficient compatibility of medicinal property combination.
Drug Combinations ; Drug Prescriptions ; Drug Therapy ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; Humans ; Medicine, Chinese Traditional

ObjectiveTo investigate the number of γδT cells in the peripheral blood from patients with systemic lupus erythematosus(SLE) and their correlation to disease activity.MethodsγδT cells were detected in the peripheral blood from 42 SLE patients and 20 normal controls by flow cytometry.Anniex-V/Pl double-staining flow cytometry was employed to observe the proportion of the apoptotic γδ and CD3+ T cells in 6 SLE patients with active disease and 6 normal controls,respectively.The levels of plasma anti-nuclear antibody and anti-dsDNA antibody were determined by using enzyme-linked immunosorbent assay.Data were analyzed with t test and Pearson's correlation test.ResultsThe percentages of γδT cells were remarkably down-regulated in SLE patients [(3.0±1.8)％ ] with active disease compared with that of those patients with inactive[(5.3±3.0)％] disease and normal controls [(6.8±2.8)％](t=-3.071 and -5.913 respectively,both P＜0.01 ).The absolute number of γδT cells decreased significantly in SLE patients with active disease[ ( 1.7± 1.6)× 107/L ] than those with inactive SLE [ (5.3±3.6)× 107/L ] (t=-3.292,P＜0.01 ),and both were lower than the normal controls [ (10.1±5.0)×l 07/L] (t=-7.247 and -2.905 respectively,both P＜0.01 ).There was a negative correlation between systemic lupus erythematosus disease activity index (SLEDAI) andT cell counts in 30 SLE patients with active disease (r=-0.365,P=0.047).γδT cell percentage (r=-0.336,P=0.030) and counts (r=-0.410,P=0.007) were both inversely correlated with the erythrocyte sedimentation rate,but positive correlation were found between hemoglobulln and γδT cell counts (r=0.409,P=0.007).The apoptosis ofγδT cells in SLE patients was more common than in normal controls(t=2.886,P＜0.05 ).The number of apoptotic γδT cells was higher than that of CD3+ T cells in SLE patients (t=2.952,P＜0.05 ).Conclusion γδT cells of the peripheral blood of SLE patients are down-regulated partially due to excessive apoptosis,which may correlate with the disease activity.

AIM: To investigate the effects of auricularia auricular polysaccharide (AAP) on chronic cerebral ischemia injury in rats. METHODS: The chronic cerebral ischemia mode1 was made by permanent middle cerebral artery occlusion (MCAO) on the right side. AAP at different doses (50 mg/kg and 100 mg/kg) was intragastrically administered at the onset of ischemia and in the following days after operation, once a day for 4 weeks. After 4 weeks of MCAO, Morris water maze test was introduced to examine the learning and memory functions. Nissl staining was performed to detect the survival neurons in hippocampal slices. Level of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in brain tissue were measured. RESULTS: Rats treated with AAP showed a shorter escaping latency in spacial navigation test because the AAP treated rats spent less time to find the platform in spatial probe test. More survival neurons in hippocampal slices were observed from AAP treated rats. Also, the MDA level in brain tissue was reduced and SOD activity in brain tissue was increased in the AAP treated rats with MCAO. CONCLUSION: AAP protects rats from chronic brain ischemic injury, in which its anti-oxidative effect might be involved.

Objective To investigate the effect of TGF-β1/SMAD signaling pathway on K562 cells growth inhibition caused by HMBA. Methods After establishing the in vitro differentiation model with HMBA on K562 cells, the MTT assay was used to detect the proliferation of K562 cells, the cell cycle profile was detected by flow cytometry, and the mRNA expression of TGF-β1, SMAD3, SMAD4 and EVI1 was measured by RT-PCR assay. Results HMBA could inhibit the proliferation and promote the differentiation of K562 cells obviously, which was time and concentration-dependent, and the 72 h corresponding IC50, was about 2 mmol/L. Within 72 h, flow cytometry assay indicated that the ration of G0-G1 phase cells was up-regulated, and the results of RT-PCR showed that relative mRNA expression of TGF-β1, SMAD3 and SMAD4 at mRNA level was increased gradually while that of EVI1 was decreased gradually. Conclusion HMBA can inhibit K562 cells proliferation through TGF-β1/SMAD signaling pathway.

OBJECTIVE Although it is generally believed that nicotine accounts for the beneficial effect of smoking on ulcerative colitis, the underlying mechanisms remain not well- understood. Our previous finding that nicotine inhibits inflammatory responses through inducing miRNA-124 prompted us to ask whether the miRNA is involved in the protective action of nicotine on UC. METHODS MiR-124 expression in colon tissues and cells was determined by q-PCR and in situ hybridization. The effect of miR-124 on protective role of nicotine in ulcerative colitis was evaluated in DSS-treated mice and IL-6-treated Caco-2 colon epithelial cells. Expression of p-STAT3/STAT3 was detected by immuno?histochemistry and Western blot analysis. RESULTS miR- 124 expression is upregulated in colon tissues from patients and DSS- induced colitis. Nicotine treatment further elevated miR- 124 level in colon tissues of the mice, in infiltrated lymphocytes and epithelial cells, and augmented miR- 124 expression in lymphocytes isolated from human ulcerative colon tissues. Administration of nicotine also reduced weight loss, improved DAI and decreased HE score in DSS-induced colitis. Moreover, knock?down of miR-124 in vivo significantly diminished the beneficial effect of nicotine, and in vitro on IL-6-treated Caco-2 colon epithelial cells. Further analysis indicated that nicotine inhibited STAT3 activation in vivo and in IL-6-treated Caco-2 colon epithelial cells and Jurkat human T lymphocytes, in which miR-124 knockdown led to increased activation of STAT3. CONCLUSION These data indicated that nicotine exerts its protective action in UC through inducing miR-124 and its effect on STAT3, suggesting that the miR-124/STAT3 system is a potential target for the therapeutic intervention of UC.

Objective To detect the proliferation inhibition and apoptosis of HL-60 cell induced by APS-1 and APS-2 isolated from Polyporus sp. M05 and to investigate its mechanism. Methods The proliferation inhibition was detected by living cells count method,and chosed proper concentration.Flow cytometry with propidium iodide staining was used to detect cell apoptosis. Semi-quantitative RT-PCR was used to detect the expression of apoptosis related gene. Results APS-1 and APS-2 could significantly inhibit the proliferation of HL-60 cells on a time and dose dependent manner. Apoptosis ratio increased to 47. 9% and 26. 8% after HL-60 cells were exposed to APS-1 and APS-2 respectively for 48 h,and the differences had statistical significance (P <0.01). After being induced by APS-1,mRNA of Bax,Fas,Caspase-3 was upregulated. And after being induced by APS-2,mRNA of Bax,Caspase-3 was upregulated,while Fas mRNA did not change. Conclusion APS-1 and APS-2 can inhibit the proliferation and induce apoptosis of HL-60 cells. Mechanism of HL-60 cell apoptosis induced by APS-1 is related to both mitochondrial pathway and Fas signaling pathway,while apoptosis induced by APS-2 is only related to mitochondrial pathway.

Objective Dendritic cell-associatedC-type lectin-1 ( Dectin-1) is one of the most important receptors in antifungal innate immune response.This study was to construct a recombinant adenovirus vector expressing themurine Dectin-1gene and acquire a high-concentration adenovirus by amplification and purification. Methods The PCR amplification product CLEC7A-pIRES2-EGFP was cloned into the intermediate vector pDONR221, and then recom-bined with the backbone vector pAD/CMV/V5-DEST to produce a re-combinant plasmid pAD-CLEC7A-pIRE2S -EGFP.The recombinant plasmid was linearized with Pac I and transfected into human embryon-ic kidney ( HEK293) cells to produce recombinant adenovirus pAD-CLEC7Ap-IRES 2-EGFP. The adenovirus was propagated in the HEK293 cells and purified by filtering through the cellulose acetate membrane and concentrating column.Fluorescence microscopy and re-al-time PCR were used to determine the expression of the Dectin-1 gene. Results PCR identification, enzyme digestion, and sequen-cing results manifested theDectin-1 gene in the vector, with the final adenovirus titer of 5×1011 IU/mL.Fluorescence microscopy revealed green fluorescence and real-time PCR assay confirmed that the expression of Dectin-1 was improved by 8677.25 times. Conclusion A relatively high-titer adenovirus expressing Dectin-1 was acquired,which may help to further study the high expression of Dectin-1 in anti-fungal innate immunity in vitro and in vivo.

This retrospective analysis compared standard regimen of doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) with the dose-dense ABVD regimen (ABVD-21) in terms of efficacy and toxicity. Patients who had early-stage unfavorable or advanced Hodgkin's lymphoma (HL) according to German Hodgkin Study Group criteria from March 1999 to February 2011 were analyzed for treatment response, long-term survival and hematological toxicity. There were 85 patients in the ABVD-21 group and 118 patients in the ABVD group respectively. The complete remission rates after completion of treatment were 92.9% and 90.7% for ABVD-21 and ABVD, respectively. During a median follow-up period of 62 months, no significant difference was found in projected 10-year progression-free survival (PFS) and overall survival (OS) rates (84.7% and 94.1% respectively for ABVD-21; 81.4% and 91.5% for ABVD). Subgroup analyses showed that ABVD-21 was significantly better than ABVD for patients with IPS≥3 in terms of PFS and OS rates. Grade 3 to 4 leukopenia (51.8% vs. 28.8%, P=0.001) and neutropenia (57.6% vs. 39.0%, P=0.009) were more common with ABVD-21. We were led to conclude that dose-dense ABVD did not result in better tumor control and overall survival than did ABVD for early-stage unfavorable HL. However, patients at high risk, for example, with IPS≥3, may benefit from dose-dense ABVD.

Ectopic ACTH syndrome caused by adrenal pheochromocytoma is very rare.A case was herewith reported and the domestic and foreign literatures were reviewed.The correct diagnosis of the syndrome depends on clinical,biochemical,hormonal,radiographic,pathological investigations,as well as tumor immunohistochemistry for final comprehensive judgments.

Objective To assess the expression pattern of protease-activated receptor 2 (PAR2) in human keratinocytes and to characterize its biological functions in the regulation of skin barrier.Methods Primary human keratinocytes and human N/TERT keratinocytes were used as the subject of this study.The expression and distribution of PAR2 in the keratinocytes were analyzed by using immunoflorescence staining and Western blot.Two different PAR2 agonists,trypsin and a PAR2-activating peptide (AP),as well as a PAR2-antagonistic peptide (H2N-FSLLRY-COOH) and a control peptide were used to induce the activation of PAR2 in the keratinocytes.Then,a fluorescence-based calcium mobilization assay was performed to evaluate the biological function of PAR2.Data were statistically analyzed by one-factor analysis of variance.Results Under normal culture conditions,PAR2 was weakly expressed in keratinocytes,and the expression was unaffected by culture medium composition or culture duration.Calcium mobilization was induced by trypsin of 50-250 nmol/L and the PAR2-activating peptide in a dose-and time-dependent pattern.The maximal activation of PAR2 was observed in keratinocytes treated with the PAR2 agonist HAN-SLIGKV-COOH of 75-250 μmol/L.The PAR2-antagonistic peptide (H2N-FSLLRY-COOH) obviously suppressed the increase in calcium mobilization induced by trypsin,while the control peptide PAR-RAP showed no inductive effect on the PAR2 activation based on the absence of calcium mobilization.The substrate-induced calcium release was complete within 250 seconds,and peaked at 50 seconds after the initial trypsin or PAR-AP stimulation.Moreover,the activation of PAR2 was accompanied by an increase in ERK phosphorylation and elicitation of MAPK signaling pathway in keratinocytes.Conclusions Human keratinocytes positively express PAR2,which can be activated by trypsin and PAR2-activating peptides,and the activation of PAR2 may influence the physiological function of keratinocytes by inducing intracellular calcium release.