Objective To establish RP-HPLC method for determination of Ginsenosides in effective parts of Naomaitong Granules. Methods Using BDS C18 column (200 mm?4.6 mm, 5 ?m) of Dalian Elite, the mobile phase was a mixture of Acetonitrile-water gradient elution. The flow rate was 1.0 mL/min, the wavelength was 203 nm. Results The average recovery rate of Ginsenoside Rg1, Re and Rb1 was 100.71%, 100.14% and 100.94%, respectively, and RSD was 2.27%, 1.88% and 1.95%, respectively. Conclusion The method is simple, accurate and can be used to control the quality of Naomaitong Granules.

AIM:To establish the HPLC fingerprint of Compound Naomaitong effective parts,and to study the correlation analysis between fingerprint peaks and the effective fraction and its relevant herbs. METHODS:The chromatographic fingerprints of the effective fraction and the relevant fractions of its herbs were configured by HPLC/PDAD analysis. The relative deviation of retention time was utilized as indices to evaluate the correlation, the wavelength was set at 203 nm. RESULTS:The fingerprint of Compound Naomaitong effective parts was established and 36 copossessing fingerprint peaks were indicated. The assignment results of 14 peaks effective parts of fraction were indicated. CONCLUSION:The quality of Compound Naomaitong effective parts can be controlled by the HPLC fingerprint.

AIM: To study the pharmacokinetics of ligustilide in the volatile oil from Angelica Sinensis(Oliv.) Diels in the rabbit. METHODS: HPLC method for ligustilide determination in the blood was developed.The HPLC system consisted of C_(18) column using MeOH-H_2O(65∶35,v/v) as mobile phase at a flow rate of 1.0 mL/min and UV detection at 236 nm. RESULTS: Linear calibration curves were obtained over the concentration range of 0.40 ?g?mL~(-1)～10.00 ?g?mL~(-1) for ligustilide.The minimum limit detection was 0.40 ?g?mL~(-1).The recovery of ligusitilide in blood was 90.90% with RSD 2.74%. CONCLUSION: After oral administration of volatile oil,intracorporal process of ligustilide in rabbit accords with 2-compartment model with 1 st order absorption,(2.6638) h and 108.88 h are obtained as t_(1/2?) and t_(1/2?) respectively.

This article was aimed to study the molecular network and bio-function ofBu-Fei-Yi-Shen (BFYS) decoction for chronic obstructive pulmonary disease (COPD) by bioinformatics analysis, in order to provide new ideas for research on pharmacological mechanism of Chinese medicine compound prescription. Components of herbs in BFYS decoction were searched in the databases. Targeted proteins of each component were found from PubChem. Comparison analyses were performed on molecular network, bio-function and canonical pathways by Ingenuity Pathway Analysis (IPA). The results showed that there were 239 target proteins of BFYS decoction. There were 9 molecular networks of BFYS decoction. The top 3 networks' functions were Cellular Development, Energy Production, and Cancer. The top 3 bio-function of BFYS decoction were Cellular Growth and Proliferation, Cell Death and Survival, and Inflammatory Response. The top 3 canonical pathways of BFYS decoction were Cell Cycle:G1/S Checkpoint Regulation, Chronic Myeloid Leukemia Signaling, and Cyclins and Cell Cycle Regulation. It was concluded that the search of target proteins for herbal compounds and bioinformatics analysis by IPA can be used to reveal the molecular network and bio-function of BFYS decoction.

AIM: To compare the contents variation of anthraquinones by 2 kinds of extractive process of Naomaitong extract (Radix et Rhizoma rhei, Rhizoma chuanxiong, Radix et Rhizoma qinseng, Radix puerariae lobatae, etc). METHODS: In application to RP-HPLC, Hypersil ODS2 C_ 18 column, the mobile phase was a mixture of methanol- 0.1% phosphate water (75 ∶25), the wavelength of detecting five aglycons in R. officinale was at 254 nm. RESULTS: The extraction rate of anthraquinones contents extracted by alcoholic extraction was higher than water extraction, the chrysophanol content in separated decoction was higher than that in the mixed decoction. CONCLUSION: There are dynamic variations in the extraction of Chinese medicine mixture. It is necessary to handle samples appropriately according to physichemical attributes of chemical contents.

Objective To compare the variation of ferulic acid contents in Naomaitong by different extraction processes.Methods With ethanol or water as extracting solvent,the four herbal medicines of Rhizoma Chuanxiong,Radix Ginseng,Radix Puerariae,Radix et Rhizoma Rhei,which consisted of Naomaitong prescription,were decocted together or decocted separately firstly then mixed together were evaluated.With ferulic acid extraction rate as the index,the above extraction processes were evaluated.Results The extraction rate of ferulic acid extracted by alcohol was higher than that by water,but the ferulic acid content showed no obvious difference by decocting together or decocted separately firstly then mixed together.Conclusion It is suggested that proper extraction solvents and extraction methods should be adopted according to the different physicochemical characteristics of chemical contents in herbal medicine during extraction.

ObjectiveBased on ultra-high performance liquid chromatography-quadrupole-electrostatic field orbital trap-linear ion-trap mass spectrometry（UPLC-Orbitrap Fusion Lumos Tribrid-MS）， the plasma concentration of ziyuglycoside Ⅰ was determined at different time points after oral administration， and its pharmacokinetic characteristics in normal rats and rats with acute kidney injury were compared. MethodsRats were randomly divided into normal group and model group， the model group received intraperitoneal cisplatin（10 mg·kg^-1） to establish the acute kidney injury model， the normal group was given the same volume of saline. After successful modeling， rats in the normal and model groups were randomly divided into the normal low， medium and high dose groups（2.5， 5， 7.5 mg·kg^-1） and the model low， medium and high dose groups（2.5， 5， 7.5 mg·kg^-1）， 6 rats in each group， and the plasma was collected at different time points after receiving the corresponding dose of ziyuglycoside Ⅰ. Then， the concentration of ziyuglycoside Ⅰ in rat plasma was determined by UPLC-Orbitrap Fusion Lumos Tribrid-MS， and the drug-time curve was poltted. The pharmacokinetic parameters were calculated by Kinetica 5.1 software， and the differences in pharmacokinetic parameters between different administration groups were compared by independent sample t-test with SPSS 22.0. ResultsThe pharmacokinetic results showed that after receiving the different doses of ziyuglycoside Ⅰ， its concentration increased first and then decreased， and all of them reached the maximum plasma concentration at about 0.5 h. The area under the curve（AUC_0-t） and mean retention time（MRT_0-t） of normal and model rats increased with the increased dose， and the clearance（CL） decreased with the increasing dose. Compared with the normal group， the AUC_0-t was significantly increased（P<0.01）， peak concentration（C_max） and CL decreased in model rats at different doses， indicating that the physiological state of the rats could affect the absorption and elimination of ziyuglycoside Ⅰ in vivo. ConclusionThe pharmacokinetic characteristics of ziyuglycoside Ⅰ are quite different in normal rats and acute kidney injury model rats， which may be due to the change of the body environment in the pathological state， then lead to changes in absorption and metabolic processes.

ObjectiveTo explore the possible mechanism of action of Lifei Xiaoji Pill （理肺消积丸， LXP） in the treatment of non small cell lung cancer based on the Warburg effect and the USP47/BACH1 pathway. MethodsFifty C57BL/6 mice were randomly divided into five groups， model group， LXP group， inhibitor group， LXP + inhibitor group， and cisplatin group， with 10 mice in each group. A lung cancer mouse model was established by subcutaneously injecting Lewis cells. On the next day， the model group mice were given 0.2 ml of saline by gavage daily， the LXP group given 240 mg/（kg·d） of LXP solution once a day by gavage， the inhibitor group intraperitoneally injected with P22077 at a dose of 10 mg/（kg·d） every day， the LXP + inhibitor group given both LXP by gavage and P22077 by intraperitoneal injection once a day， and the cisplatin group received 0.5 mg/（kg·d） cisplatin intraperitoneally every other day. All treatments lasted for 14 days. On the day after the last dose， tumor weight and volume were measured， tumor histopathology was examined by HE staining， apoptosis in tumor tissues was detected by TUNEL staining， and proliferation cell nuclear antigen （PCNA） protein levels were detected by immunohistochemistry. Warburg effect indicators， including glucose concentration， lactate content， and adenosine triphosphate （ATP） production in tumor tissues， were measured. Western Blot and qRT-PCR were used to detect the protein and mRNA expression levels of USP47， BACH1， hexokinase 2 （HK2）， and glyceraldehyde 3-phosphate dehydrogenase （GAPDH）. ResultsCompared with the model group， all drug intervention groups showed reduced tumor weight and volume， improved tumor pathology， decreased PCNA positive rate， increased apoptosis rate， and reduced expression levels of USP47， BACH1， and HK2 proteins and mRNA （P＜0.05 or P＜0.01）. Except for lactate content in the cisplatin group， the glucose concentration in tumor tissues of other drug intervention groups increased， while lactate content and ATP production decreased （P＜0.05 or P＜0.01）. Compared with the LXP group， the LXP + inhibitor group showed more significant improvements in these indicators （P＜0.05 or P＜0.01）. Compared with the cisplatin group， the LXP + inhibitor group had lower mRNA expression of HK2 and GAPDH， and lower protein levels of USP47 and HK2 （P＜0.05 or P＜0.01）. Compared with the inhibitor group， the cisplatin group had higher HK2 protein levels， while the LXP + inhibitor group showed lower mRNA expression of BACH1， HK2， and GAPDH （P＜0.05 or P＜0.01）. ConclusionLXP significantly inhibits tumor growth in lung cancer mice， and its mechanism of action may be related to inhibiting the Warburg effect via the USP47/BACH1 pathway.