Licochalcone A induces cell cycle arrest in human lung squamous carcinoma cells via the PI3K/Akt signaling pathway / 南方医科大学学报

OBJECTIVE@#To investigate the effect of licochalcone A (LCA) on the proliferation and cell cycle of human lung squamous carcinoma cells and explore its possible molecular mechanism.@*METHODS@#MTT assay was used to detect the changes in proliferation of H226 cells after treatment with different concentrations of LCA for 48 h, and the IC50 of LCA was calculated. Flow cytometry was used to analyze cell cycle changes in H226 cells treated with 10, 20, and 40 μmol/L LCA, and the expressions of cyclin D1, cyclin-dependent kinase CDK2 and CDK4, and p-PI3K, PI3K, p-Akt, and Akt in the treated cells were detected using Western blotting. The effect of intraperitoneal injection of LCA for 24 days on tumor volume and weight was assessed in a BALB/c-nu mouse model bearing lung squamous carcinoma xenografts.@*RESULTS@#MTT assay showed that LCA significantly decreased the viability of H226 cells with an IC50 of 28.3 μmol/L at 48 h. Flow cytometry suggested that LCA treatment induced obvious cell cycle arrest at the G1 phase. LCA treatment also significantly decreased the expressions of cyclin D1, CDK2, and CDK4, and inhibited the phosphorylation of PI3K and Akt in H226 cells. In the tumor-bearing mice, LCA treatment for 24 days significantly reduced the tumor volume and weight.@*CONCLUSION@#LCA is capable of inhibiting the proliferation and inducing cell cycle arrest in lung squamous carcinoma cells possibility by regulating the PI3K/Akt singling pathway.

Effect of Licochalcone A on Apoptosis in Human Breast Cancer MDA-MB-231 Cells / 中国实验方剂学杂志

Objective:To investigate the effect of licochalcone A （LCA） on apoptosis in human breast cancer MDA-MB-231 cells， and to explore its possible mechanism. Method:MDA-MB-231 cells were treated with LCA of different concentrations， and<italic> </italic>cell counting kit-8 （CCK-8） assay was used to detect the cell viability. The cells were treated with LCA （10， 20， and 40 μmol·L^-1） for 24 h， and apoptosis was detected by Annexin V staining with fluorescein isothiocyanate （FITC） and propidium iodide （PI） （Annexin V-FITC/PI）. The level of intracellular reactive oxygen species （ROS） was detected by 2′，7′-dichlorodihydrofluorescein diacetate （DCFA-DA） fluorescent probe. Mitochondrial membrane potential （MMP） was detected by 5， 5′， 6， 6′-tetrachloro-1， 1′， 3， 3′-tetraethyl-imidacarbocyanine （JC-1） fluorescence probe. Western blot was used to detect the expression of cell apoptosis-related proteins， such as B-cell lymphoma-2 （Bcl-2） and Bcl-2-associated X protein （Bax）， and endoplasmic reticulum （ER） stress-related proteins， such as C/EBP homologous protein （CHOP）， activating transcription factor 4 （ATF4）， protein kinase R-like ER kinase （PERK）， p-PERK， eukaryotic translation initiation factor 2 alpha （eIF2<italic>α</italic>）， and p-eIF2<italic>α</italic>. Result:With the increase in the drug concentration （starting from 5 μmol·L^-1）， the cell viability decreased （<italic>P<</italic>0.05） with IC₅₀of 19.05 μmol·L^-1 as compared with the normal group. Additionally， the apoptosis rates of the LCA groups （10， 20， 40 μmol·L^-1） significantly increased （<italic>P</italic><0.05）， which reached 30.2% （<italic>P</italic><0.05） at LCA concentration of 40 μmol·L^-1. LCA （10， 20， and 40 μmol·L^-1） decreased the expression of Bcl-2 （<italic>P<</italic>0.05） and increased Bax expression （<italic>P<</italic>0.05） in a dose-dependent manner. Besides， the intracellular ROS level was elevated （<italic>P<</italic>0.05） and mitochondrial MMP was reduced （<italic>P<</italic>0.05） after LCA （10， 20， and 40 μmol·L^-1） treatment in a dose-dependent manner， leading to mitochondrial dysfunction. LCA （10， 20， and 40 μmol·L^-1） induced ER stress to up-regulate the expression of CHOP， ATF4， p-PERK， and p-eIF2<italic>α</italic> （<italic>P<</italic>0.05） in a dose-dependent manner. Conclusion:LCA can induce MDA-MB-231 cell apoptosis by increasing intracellular ROS level and reducing MMP to trigger mitochondrial dysfunction and ER stress.

A Comparative Study of Licochalcone A Moisturiser versus Topical Hydrocortisone in Treating Mild-to-Moderate Atopic Dermatitis

Background@#Topical corticosteroids are the mainstay of treatment for patients with atopic dermatitis. However, adverse effects associated with long-term steroid use often limit its use. This interventional study compared the efficacy of a proprietary moisturiser containing licochalcone A, omega-6 fatty acids, and ceramide 3 against 1% hydrocortisone cream in treating patients with mild-to-moderate atopic dermatitis.@*Methods@#Patients with mild-to-moderate atopic dermatitis affecting either the cubital fossa or popliteal fossa symmetrically were given twice-daily applications of the moisturiser and hydrocortisone on opposite sides of the body and monitored for a total of three weeks in a non-randomised half body, doubleblind study. Hydrocortisone was switched to aqueous cream after two weeks, whereas the application of the moisturiser continued until study completion. The assessment of SCORing Atopic Dermatitis (SCORAD) index and Dermatology Life Quality index was performed at baseline and every subsequent follow-up visit to measure patients’ response to treatment. @*Results@#The licochalcone A (LA) moisturiser and 1% hydrocortisone (HC) cream both demonstrated significant reduction in sign and symptom scores after only 1 week of treatment (percentage of reduction in sign and symptom scores: 52.8% [LA] vs 58.5% [HC]). Further reduction in mean sign and symptom scores for both treatments was observed at week 2 (61.3% [LA] vs 56.8% [HC]) and also at week 3 when HC was switched to aqueous cream (70.5% [LA] vs 63.5% [HC→aqueous cream]) (p<0.001 vs baseline within the same treatment arm at weeks 1, 2 and 3). When comparing the mean difference in SCORAD index for both individual as well as total skin signs and symptoms between LA and HC (i.e. inter-arm comparison), there was no significant difference between the two treatments for all the assessed parameters. Patients reported improvements in itching, sleeplessness, and overall quality of life over the course of treatment.@*Conclusion@#The licochalcone A moisturiser can be considered as an effective steroid-sparing alternative to topical corticosteroids in managing mild-to-moderate atopic dermatitis.

Optimization of best processing technology of Glycyrrhizae Radix et Rhizoma Praeparata cum Melle by multi-index QAMS-response surface methodology / 中草药

Objective: Based on response surface methodology, HPLC was applied to quantitatively determine the optimal processing technology of Glycyrrhizae Radix et Rhizoma Praeparata cum Melle (GRRPM) from the perspective of multi-index and comprehensive evaluation. Methods: HPLC was used for quantitative analysis, and the content of liquiritin, liquiritigenin, licochalcone A and glycyrrhetinic acid was used as inspection indexes. Response surface methodology was used to investigate the effects of the adding amount of honey, steaming and soaking time, frying temperature and frying time on the processing technology of GRRPM, and to optimize the optimal processing technology of GRRPM. Results: The chromatographic column was Diamonsil C18 (2) (4.6 mm × 200 mm, 5 μm); mobile phase was acetonitrile-0.1% phosphate aqueous solution, gradient eluting: 0-20 min, 12%-32% acetonitrile; 20-45 min, 32%-70% acetonitrile; 45-75 min, 70%-97% acetonitrile, with detection wavelength of 260 nm, column temperature of 20 ℃, and flow rate of 1 mL/min; Using liquiritin as internal standard, the relative correction factors of glycyrrhizin, licochalcone A, glycyrrhizinic acid and their relative correction factors were determined and calculated to be 0.56, 0.64 and 1.42, respectively. The optimum processing process of GRRPM was as follows: the amount of honey was 1/4, the soaking time was 15 min, frying pan bottom temperature was 160 ℃, and frying time was 13 min. Conclusion: The results of systematic adaptability investigation of the experimental content determination method meet the requirements. The best processing scheme of GRRPM optimized by response surface methodology is feasible and provides scientific basis for formulating quality standards and modern research of GRRPM.

Licochalcone A Inhibits Proliferation and Induces Apoptosis of MH7A Cells by Regulating MAPK Signaling Pathway / 中国实验方剂学杂志

Objective:To study the effects of licochalcone A （LCA） on the proliferation and apoptosis of rheumatoid arthritis fibroblast-like synoviocytes （MH7A） as well as the related inflammatory factors， also to reveal the relevance between mitogen activated protein kinase （MAPK） signaling pathway and LCA regulation of MH7A cell proliferation and apoptosis. Method:MH7A cells were cultured and divided into blank group， LCA groups （10，20，40 μmol·L-1）. The proliferation of MH7A cells was detected by methylthiazolyldiphenyl-tetrazolium bromide（MTT）and immunofluorescence staining. The cell cycle of MH7A cells was determined by flow cytometry after PI staining and apoptosis was detected by flow cytometry after Annexin V/PI staining. The effect of LCA on interleukin-1β（IL-1β） mRNA was detected by Real-time fluorescence quantitative polymerase chain reaction（Real-time PCR）. Western blot was used to detect the effect of LCA on the key proteins of MAPK signaling pathway， meanwhile， PD98059， a specific ERK inhibitor， was used to observe the expression levels of p-ERK and IL-1β. Result:Compared with blank group， LCA could inhibit the proliferation of MH7A cells in a dose-dependent manner， and the number of living cells decreased significantly（P<0.01）， while the number of early apoptotic cells increased significantly（P<0.01）. Compared with the tumor necrosis factor-α （TNF-α，10 μg·L-1）group， LCA could reverse the expression of IL-1β mRNA induced by TNF-α（P<0.01）. and compared with the blank group， LCA also promoted the phosphorylation of ERK， JNK and p38 in a dose-dependent manner（P<0.01）. After ERK inhibitor PD98059 inhibited ERK phosphorylation， the inhibitory effect of LCA 10， 20 μmol·L-1 on IL-1β disappeared. Conclusion:LCA can inhibit the proliferation and induce apoptosis of MH7A cells， which may be related to the phosphorylation of MAPK pathway related proteins， and then inhibit the expression of inflammatory factors.

Licochalcone A in Inhibiting Bleomycin-induced Pulmonary Fibrosis Through TGF-β/Smad Pathway / 中国实验方剂学杂志

Objective: To explore the therapeutic effect of licochalcone A (Lico A) on pulmonary fibrosis (PF). Method: Thirty mice were divided into five group, namely sham, model, Lico A (15, 30 mg·kg-1) and pirfenidone (300 mg·kg-1) groups. All of the groups except for sham group were intratracheally given bleomycin (BLM, 5 mg·kg-1). The sham group was given normal saline. On day 2, the mice were treated with Lico A and pirfenidone, respectively. On day 28, all of the mice were put to death. Then, lung tissues were collected and weighted. Pathological changes in lung tissue were measured by htoxylin eosin(HE) and Masson staining. The α-smooth muscle actin(α-SMA), Collagen I, fibronectin p-Smad2/3 and Smad2/3 were analyzed by Western blot. Then, transforming growth factor-β1 (TGF-β1)-induced MRC-5 cells were employed for evaluating the inhibitory activity of Lico A in vitro. Result: Compared with normal group, several pathological changes, including alveolar space collapse, emphysema, infiltration of inflammatory cells, and collagen deposition were observed in the BLM-treated mice, and these pathological changes were markedly attenuated by subsequent treatment with Lico A. Lico A could significantly inhibit BLM-induced up-regulation of α-SMA and Collagen I and phosphorylation of Smad2/3 in lung tissues of mice(PPβ-induced α-SMA and fibronectin expression in MRC-5 cells(PPConclusion: The preliminary mechanisms of the anti-fibrosis effect of Lico A may inhibit TGF-β/Smad pathway.

Effects of Chinese herb ingredients with different properties on OAT4, URAT1 and serum uric acid level in acute hyperuricemia mice / 中草药

Objective To study the effects of Chinese herb ingredients with different properties on transporters (URAT1 and OAT4) involved in renal urate reabsorption and serum uric acid level in acute hyperuricemia mice. Methods The OAT4, URAT1- overexpressed monoclonal cell line (MDCK-hOAT4, HEK293-hURAT1) was constructed. The inhibition effect and the half maximal inhibitory concentration (IC50) of different ingredients to transport activity of OAT4 and URAT1 mediating 14C-uric acid were determined. The effects of protocatechuic, liquiritigenin and isoliquiritigenin on serum uric acid levels in acute hyperuricemia mice were studied by the acute hyperuricemia mice induced by potassium oxonate and xanthine. Results The results indicated that nobiletin,liquiritigenin, isoliquiritigenin, licochalcone A with bitter flavor showed strong inhibition to OAT4. The IC50 of nobiletin, liquiritigenin, isoliquiritigenin, and licochalcone A on OAT4 were 0.556 μmol/L, 18.40 μmol/L, 6.831 μmol/L, and 6.825 μmol/L, respectively. Protocatechuic acid and liquiritigenin showed strong inhibition to URAT1 with IC50 of 7.709 μmol/L and 14.54 μmol/L, respectively. Liquiritigenin can significantly reduce the level of serum uric acid of acute hyperuricemia mice, increase the excretion of uric acid, and reduce the level of serum creatinine and blood urea nitrogen. Conclusion Nobiletin, liquiritigenin, isoliquiritigenin and licochalcone A can inhibit the transport activity of OAT4, while protocatechuic acid and liquiritigenin can inhibit the transport activity of URAT1. Liquiritigenin can significantly reduce the level of serum uric acid in acute hyperuricemia mice and protect kidney, the mechanism of which may be associated with the decreasing reabsorption of uric acid by inhibiting the activity of URAT1 and OAT4.

Inhibitory effect and mechanism of licochalcone A on NLRP3 inflammasome / 药学学报

Lipopolysaccharide (LPS)-induced bone marrow-derived macrophages (BMDMs), treated with licochalcone A (LCA) and retreated with inflammasome inducers respectively (ATP and nigericin), were used to construct the inflammasome model of NLRP3 (NOD-like receptor family, pyrin domain containing 3), to investigate the inhibitory effect and the molecular mechanism of LCA on the activity of NLRP3 inflammasome. The secretion of mature interleukin (IL)-1β, tumor necrosis factor-α (TNF-α) and caspase-1 in the supernatants were analyzed by ELISA and the Caspase-Glo® 1 Inflammasome Assay. Supernatants and cell lysates were analyzed for the expression of pro-caspase-1, pro-IL-1β, ASC, NLRP3, IL-1β, caspase-1 by immunoblotting. The study shows that LCA inhibited the activity of caspase-1 and the secretion of IL-1β, and suppressed the activity of NLRP3 inflammasome. There was also slight inhibition of NLRC4 inflammasome induced by Lfn-Flic, but no effect on poly(dA:dT)-induced the absent in melanoma 2 (AIM2) inflammasome. Western blot showed that LCA had no effect on the protein expression of NLRP3 and pro-IL-1β, which was mediated by NF-κB pathway. In summary, LCA can inhibit the cleavage of pro-caspase-1 and suppress the secretion of IL-1β to reduce the inflammation response. The study was carried out under the approval of the Scientific Investigation Board of 302 Hospital of PLA.

Effect of licochalcone A on autophagy in renal cell carcinoma via PI3K/Akt/mTOR signaling pathway / 中国中药杂志

To investigate the effect of licochalcone (LCA) on autophagy in renal cell carcinoma (RCC), and further determine whether the mechanism is correlated with the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of mTOR pathway, RCC 786-O and 769-P were used as study subjects. MTT assay was used to examine cell proliferation. The abilities of migration and invasion were detected by Transwell. The autophagy was observed under the fluorescence microscope through acridine orange staining. Green fluorescence spots were observed in Ad-GFP-LC3 transfection experiment. The protein expression was detected by Western blot. MTT assay results showed a dose and time-dependent cytotoxicity in the two cell lines treated with LCA. LCA inhibited migration and invasion in 786-O and 769-P cells. LCA increased the expression levels of LC3-Ⅱ, beclin 1, Atg5, and down-regulated the expression of p62. In addition, LCA inhibited the PI3K/Akt/mTOR pathway. Furthermore, the inhibition of PI3K/Akt by LY294002 or that of mTOR by rapamycin augmented LCA-induced autophagy. The findings demonstrated that LCA inhibited the proliferation, migration, invasion, and induced autophagy by inactivating PI3K/Akt/mTOR signaling pathway in 786-O and 769-P cells.

Anti-inflammatory and Anti-oxidant Effects of Licorice Flavonoids on Ulcerative Colitis in Mouse Model / 中草药·英文版

Objective Licorice (Glycyrrhizae Radix or Liquiritiae Radix) is traditionally used to treat various diseases including inflammation and gastric ulcers. Licorice is rich in flavonoid compounds and possesses anti-inflammatory activities. To investigate the protective effects of licorice flavonoids (LFs) in both acetic acid-induced and dextran sulphate sodium (DSS)-induced ulcerative colitis (UC) mouse model and its underlying mechanism. Acute UC was induced by intra-rectal acetic acid (4% v/v) after pretreatment with LFs (100, 200, and 400 mg/kg, p.o.), 0.9% saline (20 mL/kg, p.o.) or Sulfasalazine (SASP) (600 mg/kg, p.o.) for 10 d. Quantitative analysis of chemical components of LFs was also conducted by HPLC. Our results showed that pre-treatment with LFs significantly reduced the wet weight/length ratio of colon, percentage of affected area, macroscopic and histological damage scores in acid-induced UC mice. LFs also significantly decreased the oxidative stress and pro-inflammatory cytokines, upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) pathway and downregulated nuclear transcription factor kappa B (NF-κB) pathway. At last, LFs also showed obvious antiulcer effect on the DSS-induced UC model. The major components of LFs were licochalcone A, glabrone, licoflavone, and licoflavone B. This study demonstrates that the protective effect of LFs may at least in part be due to its anti-oxidant activity through Nrf2 pathway and anti-inflammatory activity through NF-κB pathway.

Licochalcone A protects against cigarette smoke-mediated acute lung injury in mice by suppressing ERK1/2/NF-κB pathways / 中国药理学通报

Aim To explore the protective roles of lic-ochalcone A ( LA) on mice with cigarette smoke-medi-ated acute lung injury and the related mechanisms. Methods In vivo: Mice were exposed to cigarette smoke ( CS) to establish acute lung injury model. The bronchoalveolar lavage fluid ( BALF ) was conducted for cell counting. The mRNA and protein expression of keratinocyte-derived chemokine ( KC ) , tumor necrosis factor alpha ( TNF-α) , interleukin 1β ( IL-1β) and matrix metalloproteinases ( MMP)-9 in lungs were de-termined. The myeloperoxidase ( MPO ) , superoxide dismutase ( SOD ) activities and glutathione ( GSH ) levels in lungs were quantified. The paraffin sections of lungs were prepared and stained with HE. In vitro:Human lung epithelial cells (BEAS-2B) were exposed to cigarette smoke extract ( CSE ) , which induced cell injury. The releases of interleukin 8 (IL-8) and MMP-9 were assessed. The phosphorylation of mitogen-acti-vated protein kinases ( MAPKs, including ERK1/2, p38 and JNK ) and nuclear factor-κB ( NF-κB ) p65 protein were analyzed by Western blot. Results In vi-vo: The accumulation of inflammatory cells was lower in LA groups than that in model group. In comparison with normal control group, the mRNA and protein lev-els of KC, TNF-α, IL-1βand MMP-9 were significant-ly increased in model group. Following treatment with LA, the above indicators were significantly decreased as compared to model group. In the CS-exposed mice, the MPO activity in lungs was significantly increased, meanwhile the SOD activity and GSH level were signif-icantly decreased compared with the air-exposed ani-mals. CS-induced activity of MPO was significantly in-hibited, which were accompanied by increases in SOD and GSH levels by LA. In vitro: CSE-induced mRNA levels of IL-8 and MMP-9 were significantly inhibited by LA at 2 . 5 and 5 μmol · L-1 . The CSE-induced phosphorylation of ERK1/2 and nucleus NF-κB p65 protein expression were prevented by pretreatment with LA. Conclusions LA has protective effects on CS-ex-posed acute lung injury in mice by preventing CS-in-duced pulmonary inflammation, oxidative stress and protease rise. The exploration of the mechanisms sug-gests that LA exerts protective effects via suppressing ERK1/2/NF-κB pathways.

Inhibitory effects of Licochalcone A on proliferation of melanoma B16 F10 cells / 中国药理学通报

Aim To investigate the mechanism of the melanoma B16 F10 cells proliferation induced by Lico-chalcone A in vitro. Methods The proliferation of B16 F10 cells induced by Licochalcone A was deter-mined by SRB method. The morphological changes were observed using Giemsa staining under the phase contrast microscope equipped with a digital camera. The melanin level was assessed by colorimetric meth-od. The apoptotic rate was determined by Annexin V-FITC/PI assay. Cell cycle distribution was determined by flow cytometry. The mRNA expression levels of B cell lymphoma/lewkmia-2 ( Bcl-2 ) , Bcl-2 associated X protein ( Bax) , the cell cycle protein CyclinE2 and cyclin-dependent kinase-2 ( CDK2 ) CDK2 were detec-ted using Q-PCR analysis. Results The proliferation of B16 F10 cells treated with Licochalcone A was effec-tively inhibited in a concentration and time-dependent manner. A clear morphological change was observed with the increasing concentration of Licochalcone A in B16F10 cells, the dendrite-like projections changed to the narrowing ball shape, which was associated with the increasing melanin level. The low concentration of Licochalcone A could induce B16F10 differentiation, and the high concentration of Licochalcone A could in-duce B16F10 apoptosis, which was accompanied with the increasing G1 phase in cell cycle. The mRNA ex-pression levels of Bcl-2 /Bax, CyclinE2 and CDK2 were markedly reduced. Conclusion Licochalcone A can effectively inhibit the proliferation of B16 F10 cells, induced cell cycle arrest at G1 phase, and fur-ther induced differentiation and apoptosis.

Quality Standard for Anweiyang Capsules / 中国药师

Objective:To improve the quality standard for Anweiyang capsules. Methods: TLC was used to identify Glycyrrhiza inflata Bat. Licochalcone A was determined by RP-HPLC. Using a C18 Column, the mobile phase consisted of acetonitrile-0. 1% phos-phoric acid(40:60), and the detection wavelength was at 376 nm. Results:The herb could be identified by TLC. For licochalcone A, the linear range was from 25. 563 to 1 533. 798 ng, and the average recovery was 99. 8%(n=9). Conclusion:The method is simple and accurate, which can be used to improve and control the quality of Anweiyang capsules.

Anti-carcinogenic effects of non-polar components containing licochalcone A in roasted licorice root

BACKGROUND/OBJECTIVE: Licorice has been shown to possess cancer chemopreventive effects. However, glycyrrhizin, a major component in licorice, was found to interfere with steroid metabolism and cause edema and hypertension. The roasting process of licorice modifies the chemical composition and converts glycyrrhizin to glycyrrhetinic acid. The purpose of this study was to examine the anti-carcinogenic effects of the ethanol extract of roasted licorice (EERL) and to identify the active compound in EERL. MATERIALS/METHODS: Ethanol and aqueous extracts of roasted and un-roasted licorice were prepared. The active fraction was separated from the methylene chloride (MC)-soluble fraction of EERL and the structure of the purified compound was determined by nuclear magnetic resonance spectroscopy. The anti-carcinogenic effects of licorice extracts and licochalcone A was evaluated using a MTT assay, Western blot, flow cytometry, and two-stage skin carcinogenesis model. RESULTS: EERL was determined to be more potent and efficacious than the ethanol extract of un-roasted licorice in inhibiting the growth of DU145 and MLL prostate cancer cells, as well as HT-29 colon cancer cells. The aqueous extracts of un-roasted and roasted licorice showed minimal effects on cell growth. EERL potently inhibited growth of MCF-7 and MDA-MB-231 breast, B16-F10 melanoma, and A375 and A2058 skin cancer cells, whereas EERL slightly stimulated the growth of normal IEC-6 intestinal epithelial cells and CCD118SK fibroblasts. The MC-soluble fraction was more efficacious than EERL in inhibiting DU145 cell growth. Licochalcone A was isolated from the MC fraction and identified as the active compound of EERL. Both EERL and licochalcone A induced apoptosis of DU145 cells. EERL potently inhibited chemically-induced skin papilloma formation in mice. CONCLUSIONS: Non-polar compounds in EERL exert potent anti-carcinogenic effects, and that roasted rather than un-roasted licorice should be favored as a cancer preventive agent, whether being used as an additive to food or medicine preparations.

The chemical component dynamic changes in compatibility of Carthamus tinctorius L. with Glycyrrhiza uralensis Fisch / 中成药

AIM: To study the dynamic change of chemical components in the compatibility of Carthamus tinctorius L.with Glycyrrhiza uralensis Fisch during decoction together. METHODS: By means of HPLC analysis and phytochemical isolation technique,focusing on the differences between chemical components in co-decoction and individual decoction.Two chemical substances which showed quantitative changes during co-decoction had been isolated and identified as Licochalcone A and Licochalcone B,respectively. CONCLUSION: From the method described in this article,it could be concluded that the chemical profiles of TCM drug-pairs prepared by co-decoction are different from that of extract mixture combined by the individual extract of Carthamus tinctorius L.and Clycyrrhiza uralensis Fisch,respectively.