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OBJECTIVE To preliminarily investigate the impacts of galangin （Gal） on fracture healing in osteoporosis （OP） model rats by regulating hypoxia-inducible factor-1α （HIF-1α）/vascular endothelial growth factor （VEGF） signaling pathway. METHODS The OP rat model was constructed by using bilateral ovariectomy surgery. The model rats were randomly divided into sham operation group （normal saline）， model group （normal saline）， Gal low-dose， medium-dose and high-dose groups （2.5， 5， 10 mg/kg）， inhibitor group （10 mg/kg Gal+100 mg/kg HIF-1α/VEGF signaling pathway inhibitor PX-478）， with 12 rats in each group. They were given relevant medicine intraperitoneally， once a day， for 90 consecutive days. The microstructure of rat bones was observed， the biomechanical status of rat femurs was evaluated， and the pathological damage and neovascularization of rat callus tissue were observed. The expression of platelet endothelial cell adhesion molecule-1 （PECAM-1） in the femur was detected. The contents of osteocalcin （OCN）， C-terminal telopeptides of type Ⅰ collagen （CTX-Ⅰ） and bone morphogenetic protein 2 （BMP-2） in serum were detected as well as the expressions of alkaline phosphatase （ALP） and HIF-1α/VEGF signaling pathway- related proteins in callus tissue. RESULTS Compared with the sham operation group， the BMD， BV/TV， Tb.N， Tb.Th， maximum load， the number and area of blood vessels， the average fluorescence intensity of PECAM-1， the contents of OCN and BMP-2， and the expression levels of ALP， HIF-1α and VEGF proteins in the model group were reduced significantly （P＜0.05）， while the content of CTX-Ⅰ increased significantly （P＜0.05）. Compared with the model group， the above indexes of rats were reversed significantly in Gal low-dose， medium-dose and high-dose groups （P＜0.05）， in a dose-dependent manner. Compared with the Gal high-dose group， the above indexes of rats were reversed significantly in the inhibitor group （P＜0.05）. CONCLUSIONS Gal can regulate bone metabolism， improve bone density of OP model rats and promote fracture healing， the mechanism of which may be associated with activating the HIF-1α/VEGF signaling pathway and promoting angiogenesis.
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This study aimed to explore the effects of galangin on energy metabolism and autophagy in gastric cancer MGC803 cells and the underlying mechanism. Cell counting kit-8(CCK-8) was used to detect the effects of galangin at different concentrations on via-bility of MGC803 cells after 48 h intervention. Western blot was carried out to measure the effects of galangin on expression of proteins related to autophagy, nuclear factor-κB(NF-κB) pathway and energy metabolism, followed by the determination of its effects on mRNA expression of energy metabolism-related proteins by Real-time quantitative PCR(qPCR). The impact of galangin on autophagy was explored using AutophagyGreen dye reagent, with autophagosomes and lysosomes observed under the transmission electron microscope(TEM). Nude mice transplanted with gastric cancer MGC803 cells via subcutaneous injection were randomly divided into the following three groups: control(0.5% sodium carboxymethyl cellulose, once a day), 5-fluorouracil(5-FU, 50 mg·kg~(-1), twice a week), and galangin(120 mg·kg~(-1), once a day) groups. The body weight and tumor volume were measured once every three days with a vernier caliper at the same time point by the same person. After 21-d treatment, the tumor tissue was isolated and weighed for the calculation of the tumor-suppressing rate. The comparison with the control group revealed that galangin inhibited the viability of MGC803 cells, up-regulated the protein expression of microtuble-associated protein 1 light chain 3 B(LC3 B) Ⅱ, inhibited the phosphorylation of NF-κB pathway-related proteins, and promoted the formation of autophagosomes in MGC803 cells. However, it did not obviously affect the expression of energy metabolism-related proteins. Furthermore, galangin at 120 mg·kg~(-1) significantly reduced the tumor weight and volume in mice, enhanced LC3 BⅡ protein expression, and inhibited the phosphorylation of NF-κB pathway-related proteins. All these have suggested that galangin inhibited the growth of gastric cancer MGC803 cells both in vivo and in vitro, possibly by inhibiting the NF-κB pathway and enhancing autophagy.
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Animals , Mice , Autophagy , Flavonoids , Mice, Nude , NF-kappa B/genetics , Signal Transduction , Stomach Neoplasms/geneticsABSTRACT
The mortality rate of hepatocellular carcinoma (HCC) remains high, and although there have been several treatment methods, HCC patients still have poor treatment outcome and prognosis in clinical practice. Therefore, it is necessary to find a new drug for the treatment of HCC to improve patients’ survival rate. This article introduces a new antitumor drug, galangin, which can exert an antitumor effect by inhibiting cell proliferation, promoting apoptosis, inducing autophagy, and inhibiting metastasis. In addition, galangin can also inhibit angiogenesis in liver cancer, reverse multidrug resistance, and enhance the synergistic effect between drugs. Therefore, galangin is believed to have a promising future in clinical practice, and it is expected that more studies will focus on the anti-hepatoma cell mechanism of galangin to provide a scientific basis for the clinical translation of galangin.
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Objective: To screen and evaluate PXR/CYP3A4-induced lipid-regulating quality marker in propolis with precise and quantitative method. Methods: The LS174T cell was given certain amount of midazolam injection, along with different dosage of known components found in propolis, after incubation and extraction, the samples were determined for 1’-OH-midazolam, and each compound was evaluated to discover the PXR/CYP3A4 pathway regulatory activity according to the results; Then, compounds selected were used as indexes for UHPLC-MS-MS content determination, and their own values were regarded as a preliminary step of confirming PXR/CYP3A4-induced lipid-regulating quality markers of propolis. Results: In all components tested, chrysin, galangin, heterochlorogenic acid A, quercetin, and caffeic acid phenethylester significantly affected the 1’-OH-midazolam yield compared with blank and positive control, indicating their obvious influence on PXR/CYP3A4 expression; The UHPLC-MS-MS determination showed that except galangin, heterochlorogenic acid A, and quercetin, all the other compounds had adequate content in propolis to take effect. Conclusion: Chrysin, galangin, caffeic acid phenethylester, and quercetin were probably defined as PXR/CYP3A4-induced lipid-regulating quality marker in propolis, which inhibited the expression of such targets to down-regulate blood lipid level; Additionally, the method used for quality marker screening and evaluation in this study was fast, effective and quantitative, and capable of carrying out high throughput active component screening for PXR/CYP3A4 regulatory activities.
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ABSTRACT To evaluate the anti-Helicobacter pylori activity of the major polyphenol compounds of propolis and their cellular damage, both as single molecule or in combination. Honey bees propolis were fractionated by using CPC and preparative HPLC. Four major polyphenols (chrysin, pinocembrin, galangin and caffeic acid phenethyl ester) were identified by thin layer chromatography-mass spectroscopy and liquid chromatography-mass spectroscopy. These compounds inhibited both ATCC and clinical H. pylori strains, with caffeic acid phenethyl ester being the most active. The four compounds presented minimum inhibitory concentration in the range 256-1024 µg ml−1 and a fractional inhibitory concentration of 64-512 µg ml−1. In mixtures all compounds showed an indifference effect (FIC < 0.15) but chrysin + galangin which was synergistic (FIC = 2.0). Killing curves show a similar behavior as the antibiotic amoxycillin. On the other hand, analyses by transmission electron microscopy at sub inhibitory concentration show vesicle formation and cell lysis after exposition to both individual polyphenol compounds and in mixture. The major compounds of propolis show anti-H. pylori activity both as individual compounds and in mixture. When combined they present mainly indifference but exert a lytic activity upon H. pylori, suggesting a potential bactericidal activity of propolis.
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OBJECTIVE：To optimize the hot sand processing technology of Alpinia officinarum，and to provide scientific evidence for the standardized processing of A. officinarum. METHODS：The contents of galangin and curcumin in processed A. officinarum were determined by HPLC. Based on single factor test，using processing temperature and processing time as factors，comprehensive score of galangin and curcumin contents as index，central composite design-response surface method was used to optimize hot sand processing technology of A. officinarum，and the processing technology was validated. RESULTS：The optimal processing technology included processing temperature of 200 ℃ and processing time of 5.5 min. In validation tests，average comprehensive score was 94.38 （RSD＝1.02％），relative deviation of which to predicted value 93.74 was 0.68％. CONCLUSIONS：The optimized processing technology is simple and predictable. It can be used for hot sand processing technology of A. officinarum.
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Objective: To assess the protective effect of galangin on membrane bound enzymes in rats with streptozotocin-induced diabetes. Methods: A single low dose of streptozotocin was injected to adult male albino rats to induce hyperglycemia. Galangin (8 mg/kg) or glibenclamide 600 μg/kg as a standard drug was given orally once daily for 45 days by gavage. Membrane-bound adenosine triphosphatases were determined including total ATPase, sodium-potassium-ATPase, calcium-ATPase and magnesium-ATPase in erythrocytes and tissues (kidney, liver, and heart). Results: The levels of total ATPases, sodium-potassium-ATPase, calcium-ATPase and magnesium-ATPase in erythrocytes and tissues were significantly altered in diabetic rats as compared to that in normal rats. After 45 days of treatment with galangin or glibenclamide, the levels of these enzymes were similar to that of normal control rats. Conclusions: Oral administration of galangin or glibenclamide can improve activities of these membrane-bound ATPases towards normal levels. Mechanism of galangin needs to be further explored in future.
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Objective: To assess the protective effect of galangin on membrane bound enzymes in rats with streptozotocin-induced diabetes. Methods: A single low dose of streptozotocin was injected to adult male albino rats to induce hyperglycemia. Galangin (8 mg/kg) or glibenclamide 600 μg/kg as a standard drug was given orally once daily for 45 days by gavage. Membrane-bound adenosine triphosphatases were determined including total ATPase, sodium-potassium-ATPase, calcium-ATPase and magnesium-ATPase in erythrocytes and tissues (kidney, liver, and heart). Results: The levels of total ATPases, sodium-potassium-ATPase, calcium-ATPase and magnesium-ATPase in erythrocytes and tissues were significantly altered in diabetic rats as compared to that in normal rats. After 45 days of treatment with galangin or glibenclamide, the levels of these enzymes were similar to that of normal control rats. Conclusions: Oral administration of galangin or glibenclamide can improve activities of these membrane-bound ATPases towards normal levels. Mechanism of galangin needs to be further explored in future.
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Objective To study the changes of flavonoid components in honey before and after refining. Methods Six batches of honey from different sources were collected and refined based on Chinese Drugs Pharmacy. Solid phase extraction was used to enrich flavonoids from samples. HPLC-TQ-MS was established to determine the contents of 15 flavonoids in crude and refined honey, the separation was performed on a Thermo Accucore RP-MS (100 mm × 2.1 mm, 2.6 μm) column with the gradient elution of methanol-0.1% formic acid water, the flow rate was 0.3 mL/min, and the column temperature was 30 ℃. MS condition: Electrospray ionization (ESI) source was applied and operated in the positive multiple reaction monitoring (MRM) modes. Results Twelve kinds of flavonoids in three species, flavonoids, dihydroflavonoids, and isoflavones, were detected in honey, which including quercetin, morin, xanthophyllin, kaempferol, apigenin, wogonin, galangin, chrysin in flavonoids; pinobanksin, naringin, and pinocembrin in dihydroflavonoids; genistein in isoflavones. There was significant difference in the species and contents of flavonoids between crude honey and refined honey. After refining, rutin and narirutin were detected which have not been reported in references, and the contents of 12 kinds of flavonoids have increased at different degrees. The contents of quercetin, morin, xanthophyllin, kaempferol, apigenin, wogonin, pinocembrin, and chrysin in linden honey have increased, but the contents of pinobanksin, naringin, and galangin have decreased; all the contents of the components in acacia honey have increased except apigenin, especially the quercetin and morin; The content of 12 kinds of flavonoids in the honey of various flowers and Chinese date honey all have increased. Conclusion Refining can change the species and contents of flavonoids in honey.
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Objective To prepare surface molecular imprinted polymers (MIP) of galangin by using surface molecular imprinting technique. Methods Galangin MIP was prepared by surface polymerization method at the surface of silica gel, which was modified with (3-aminopropyl) trimethoxysilane, by using galangin as the template molecule, methacrylic acid (MAA) as the functional monomer, and N,N′-methylenebisacrylamide (MBA) as crosslinking agent. The polymer was characterized by infrared spectroscopy and scanning electron microscopy. And its adsorption properties were studied by static and competitive adsorption method. Results The experimental research showed that the optimal preparation condition was that the molar ration of galangin to MAA was 1∶4, with molar ration of MAA to MBA 1∶7, reaction temperature 40 ℃ and reaction time 12 h. Infrared spectrum and scanning electron microscopy showed that MIP was successfully grafted on the surface of silica gel, and recognition holes and sites selectively appeared for galangin molecules. Adsorption experiments exhibited that MIP had specific recognition and good affinity for galangin molecules. Compared to the controls of breviscapine and luteolin, the selectivity coefficients of MIP to galangin were 11.2 and 5.3, respectively. Conclusion MIP has good recognition and high selectivity for galangin, which provides a new method for the separation and extraction of flavonoids from Chinese medicine.
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Previously, we demonstrated that galangin (3,5,7-trihydroxyflavone) protects human keratinocytes against ultraviolet B (UVB)-induced oxidative damage. In this study, we investigated the effect of galangin on induction of antioxidant enzymes involved in synthesis of reduced glutathione (GSH), and investigated the associated upstream signaling cascades. By activating nuclear factor-erythroid 2-related factor (Nrf2), galangin treatment significantly increased expression of glutamate-cysteine ligase catalytic subunit (GCLC) and glutathione synthetase (GSS). This activation of Nrf2 depended on extracellular signal-regulated kinases (ERKs) and protein kinase B (AKT) signaling. Inhibition of GSH in galangin-treated cells attenuated the protective effect of galangin against the deleterious effects of UVB. Our results reveal that galangin protects human keratinocytes by activating ERK/AKT-Nrf2, leading to elevated expression of GSH-synthesizing enzymes.
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Humans , Catalytic Domain , Extracellular Signal-Regulated MAP Kinases , Glutamate-Cysteine Ligase , Glutathione Synthase , Glutathione , Keratinocytes , Proto-Oncogene Proteins c-aktABSTRACT
Galangin (3,5,7-trihydroxyflavone) is a polyphenolic compound abundant in honey and medicinal herbs, such as Alpinia officinarum. In this study, we investigated the anti-inflammatory effects of galangin under in vitro and in vivo neuroinflammatory conditions caused by polyinosinic-polycytidylic acid (poly(I:C)), a viral mimic dsRNA analog. Galangin suppressed the production of nitric oxide, reactive oxygen species, and pro-inflammatory cytokines in poly(I:C)-stimulated BV2 microglia. On the other hand, galangin enhanced anti-inflammatory interleukin (IL)-10 production. Galangin also suppressed the expression of pro-inflammatory markers in poly(I:C)-injected mouse brains. Further mechanistic studies showed that galangin inhibited poly(I:C)-induced nuclear factor (NF)-κB activity and phosphorylation of Akt without affecting MAP kinases. Interestingly, galangin increased the expression and transcriptional activity of peroxisome proliferator-activated receptor (PPAR)-γ, known to play an anti-inflammatory role. To investigate whether PPAR-γ is involved in the anti-inflammatory function of galangin, BV2 cells were pre-treated with PPAR-γ antagonist before treatment of galangin. We found that PPAR-γ antagonist significantly blocked galangin-mediated upregulation of IL-10 and attenuated the inhibition of tumor necrosis factor (TNF)-α and IL-6 in poly(I:C)-stimulated microglia. In conclusion, our data suggest that PI3K/Akt, NF-κB, and PPAR-γ play a pivotal role in mediating the anti-inflammatory effects of galangin in poly(I:C)-stimulated microglia.
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Animals , Mice , Alpinia , Brain , Cytokines , Gene Expression , Hand , Honey , In Vitro Techniques , Interleukin-10 , Interleukin-6 , Interleukins , Microglia , Negotiating , Nitric Oxide , Peroxisomes , Phosphorylation , Phosphotransferases , Plants, Medicinal , Poly I-C , Reactive Oxygen Species , Tumor Necrosis Factor-alpha , Up-RegulationABSTRACT
Galangin (3,5,7-trihydroxyflavone) is a polyphenolic compound abundant in honey and medicinal herbs, such as Alpinia officinarum. In this study, we investigated the anti-inflammatory effects of galangin under in vitro and in vivo neuroinflammatory conditions caused by polyinosinic-polycytidylic acid (poly(I:C)), a viral mimic dsRNA analog. Galangin suppressed the production of nitric oxide, reactive oxygen species, and pro-inflammatory cytokines in poly(I:C)-stimulated BV2 microglia. On the other hand, galangin enhanced anti-inflammatory interleukin (IL)-10 production. Galangin also suppressed the expression of pro-inflammatory markers in poly(I:C)-injected mouse brains. Further mechanistic studies showed that galangin inhibited poly(I:C)-induced nuclear factor (NF)-κB activity and phosphorylation of Akt without affecting MAP kinases. Interestingly, galangin increased the expression and transcriptional activity of peroxisome proliferator-activated receptor (PPAR)-γ, known to play an anti-inflammatory role. To investigate whether PPAR-γ is involved in the anti-inflammatory function of galangin, BV2 cells were pre-treated with PPAR-γ antagonist before treatment of galangin. We found that PPAR-γ antagonist significantly blocked galangin-mediated upregulation of IL-10 and attenuated the inhibition of tumor necrosis factor (TNF)-α and IL-6 in poly(I:C)-stimulated microglia. In conclusion, our data suggest that PI3K/Akt, NF-κB, and PPAR-γ play a pivotal role in mediating the anti-inflammatory effects of galangin in poly(I:C)-stimulated microglia.
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Animals , Mice , Alpinia , Brain , Cytokines , Gene Expression , Hand , Honey , In Vitro Techniques , Interleukin-10 , Interleukin-6 , Interleukins , Microglia , Negotiating , Nitric Oxide , Peroxisomes , Phosphorylation , Phosphotransferases , Plants, Medicinal , Poly I-C , Reactive Oxygen Species , Tumor Necrosis Factor-alpha , Up-RegulationABSTRACT
Objective: To explore the inductive effect of galangin on HPV-positive human cervical cancer cells and the possible mechanism. Methods: Two HPV-positive human cervical cancer cell lines (SiHa cell and HeLa cell) and one HPV-negative human cervical cancer cell line (C-33-A cell) were given different concentration of galangin (20, 40, and 80 μmol/L) for 24, 48, and 72 h. Three human cervical cancer cell lines and relative cell viabilities were determined by the MTT method. Apoptosis and cell cycle were analyzed by flow cytometry. Western blotting analysis was used to determine the protein expression levels of Bcl-2 family proteins. Results: Cell proliferation of two HPV-positive human cervical cancer cells was significantly inhibited by galangin in a dose- and time-dependent manner, and galangin had no effect on cell proliferation of HPV-negative human cervical cancer cells. Cell cycle detection results showed that galangin could reversibly arrest the two HPV-positive cell lines, either in G1 or in G2/M phases. Flow cytometry results showed that beyond certain galangin concentration or/and over 24 h exposure, the cells underwent apoptosis. The data of Western blotting showed that 40 μmol/L galangin up-regulated the expression levels of Bad, Bid, and Bax, but down-regulated Bcl-2 and Bcl-w. Conclusion: Galangin can inhibit the proliferation of HPV-positive cervical cancer cells and promote apoptosis, which may be associated with the regulation of Bcl-2 family proteins expression.
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Objective To investigate the antiangiogenic effect of galangin in vitro and in vivo.Methods The inhibitory ef?fect of galangin on human umbilical vein endothelial cells(EaHy926)was tested by sulphorhodamine(SRB)method,the EaHy926 endothelial cell migration was assessed using in vitro model system,and the in vivo antiangiogenic effect of galangin at 1,5 and 10 μg was evaluated using the chorioallantoic membrane(CAM)model.The H22 tumor-bearing model was established using BALB/c nude mice,which were divided into five groups:The model group,positive control group〔ip cyclophosphamide 20 mg/(kg·d)〕and the galangin 10,20 and 40 mg/(kg·d)groups,respectively.After the daily administration for 15 consecutive days,the tumors grown in the nude mice were examined and the microvessel density(MVD)was tested via examining the expression of CD31 in the tumor tissues by immunohistochemistry in order to evaluate the effect of galangin to the tumor growth and the angiogenesis of the tumors. Result Galangin inhibited both the growth,migration and Matrigal tubule of EaHy926 cells in a dose-dependent manner in the in vitro test. Further in the in vivo test,galangin could also obviously inhibit the angiogenesis of CAM at the 5 and 10 μg concentration.The tumor mass and the relative tumor volume in the 20 and 40 mg/(kg·d)galangin groups and the positive control cyclophosphamide group were significantly lower(P<0.05)than those in the model group in the in vivo nude mice test. The tumor inhibitory rates of those three groups were 34.17%,79.73% and 55.75%,respectively.The MVD was also significantly lower in the high dosage galangin groups than that in the model group. Conclusion Galangin showed the obvious anti-angiogenenic effect both in vitro and in vivo in the present study.
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Objective Galangin is a natural flavonoid with antineoplastic activity .SIRT1 is an important member of Sirtuin family which parcitipate in many physiological process .The aim of this study was to investigate the effect of SIRT 1 on HepG2 cell apop-tosis induced by galangin . Methods HepG2 cells were pre-treated with SIRT1 inhibitor EX-527 for 2 hours, and then galangin for 24 hours.DMSO solvent control group, EX-527 treatment group, galangin treatment group and EX-527 and galangin co-treatment group were established.Hoechst 33342 staining, flow cytometry and western blot were performed to detect the apoptosis of HepG2 cells.After regu-lating the expression of SIRT1 in HepG2 cells with RNA interference and transfection of exogenous genes , these cells were treated with ga-langin for 24 hours.Negative control group , vector control group , SIRT1 knock down group , blank control group , blank vector group ,and SIRT1 upregulation group were established .Western blot and Flow cytometry were performed to detect the apoptosis of HepG 2 cells. Results The apoptosis rate and the gray level ratio of shear band of PARP 1 and GAPDH that of galangin group [(11.62± 0.55) %, 0.89±0.01]and EX-527+galangin group[(25.75±0.61) %, 1.15±0.06] were all increased(P<0.01),when these were compared with DMSO solvent control group [(2.49±0.22) %, 0.06±0.00];and those in EX-527+galangin group were also markedly increased compared with galangin group (P<0.01).The result of western bolt was that the gray level ratio of PARP 1 and GAPDH of SIRT1 knocked down group(0.06±0.01) was markedly decreased compared with vector control group (1.11±0.05)and without adenovi-rus infection group (1.10±0.04)(P<0.01).The apoptosis rate and the gray level ratio of shear band of PARP 1 and GAPDH that of SIRT1 knocked down group were markedly increased compared with vector control group and without adenovirus infection group ( P<0.01).The gray level ratio of PARP1 and GAPDH of SIRT1 up-regulated group (1.63±0.04) was markedly increased compared with blank control group (0.89±0.02) and without plasmid transfection group (0.87±0.03) (P<0.01).The apoptosis rate and the gray lev-el ratio of shear band of PARP 1 and GAPDH that of SIRT1 up-regulated group were markedly decreased compared with blank control group and without plasmid transfection group (P<0.01). Conclusion SIRT1 inhibited galangin-induced apoptosis in HepG2 cells.
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OBJECTIVE:To investigate the in vitro transdermal absorption properties of galangin and effects of different pene-tration enhancers on its transdermal behaviors,and provide reference for developing skin preparations using galangin as APIs in the treatment of vitiligo. METHODS:HPLC was used to determine the galangin content. Using cumulative permeation rate (Q) and the transdermal rate(J)of galangin as indexes,the effect of absorption of receiving solution [20%,40% polyethylene glycol 400 (PEG400)solution and 30% ethanol solution] and rotating rate(200,300,400 r/min)on galangin in complete skin of mice were investigated,as well as the azone(1%,3%,5%)and propylene glycol(10%,20%,40%)alone or combination on its penetra-tion promotion. And the transdermal properties of galangin in complete skin,exfoliating skin,dermis skin of rats and mice were de-tected. RESULTS:The best permeability of complete skin of mice showed in 40% PEG400 solution at rotating speed of 300 r/min with 5% azone alone,J was 3.2570 μg/(cm2·h). Js of complete skin,exfoliating skin,dermis skin of mice were 2.7199,34.016, 33.874 μg/(cm2·h),respectively;and those of rats were 0.4996,9.5124,17.406 μg/(cm2·h). CONCLUSIONS:Galangin can penetrate the complete skin of mice and rats,however,the penetration quantity is far lower than exfoliating skin and dermis skin.
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Objective:To investigated the activity inhibition and inhibitory type of polyphenol oxidase (PPO) induced by galangin and the interaction mechanism of galangin with polyphenol oxidase was preliminarily indicated,and prove the related mechanism of galangin on proliferation of on human melanoma A375 cells.Methods: The activity inhibition and inhibitory type of PPO induced by galangin were investigated by spectrophotometric method,and interation mechanism of galangin with PPO was preliminarily indicated by fluorescence quenching and molecular docking,and chelating copper ions with the inhibitory mechanism of galangin on polyphenol oxidase was measured.Results: Galangin was a competitive inhibitor,the IC50 and Ki on PPO were obtained to be (47.86±3.33) and (24.83±1.45)μmol/L,respectively.Fluorescence spectrum indicated the fluorescence of PPO was quenched effectively by galangin and the binding constant Ka was obtained to be (4.67±0.43)×104 L/mol.Chelating copper ions and molecular simulation further showed that galangin was combined with active center of copper ions,and formed hydrogen bonds with catalytic site His259.Luteolin could induce the apoptosis of A375 cells significantly,and the tyrosinase activity and melanin synthesis were decreased.Conclusion: Galangin as a competitive polyphenol oxidase inhibitor and reduced the activity of polyphenol oxidase.which provides the theoretical basis for the clinical anti skin cancer.
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Objective To explore the effect of galangin on the inhibition of proliferation and invasion in human lung cancer A549 cell lines and its mechanism thereof. Methods MTS assay was employed to detect the ability of cell proliferation with different concentrations (0, 5, 10, 20, 40, 60 and 100μmol/L) of galangin after A549 cells were cultured in 96 well-plate. Transwell assay was employed to detect the ability of cell invasion. Western blot assay was employed to detect the protein expression levels of Survivin, p27, CD44, ICAM, MMP-2/9 and the phosphorylation of PI3K and AKT. Results The cell proliferation rate of A549 cell line was suppressed with increased concentration of galangin treatment, and IC50 was 44.7μmol/L. The concentrations of 10μmol/L and 20μmol/L were used for the following study. The ability of cell invasion was decreased with 0, 10 and 20μmol/L concentrations of galangin treatment (P<0.05). The protein expression of p27 was increased and the expressions of other proteins were decreased with 0, 10 and 20μmol/L galangin treatmenmt (P<0.05). Conclusion Galangin can significantly inhibit the cell proliferation and invasion of human lung cancer A549 cell line, and which is a potential anti-lung cancer drug. The mechanisms may be related with the regulated related gene expression and the inhibited phosphorylation of PI3K and AKT.
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Objective: To study the chemical constituents from the aerial parts of Glycyrrhiza uralensis. Methods: The compounds were isolated and purified by silica gel, Sephadex LH-20 column chromatography, and HPLC. The structures of the compounds were identified on the basis of chemical and spectral methods. Results: Twelve compounds were isolated from the ethanol extract of the the the aerial parts of G. uralensis and identified as (2S)-3'-(2-hydroxy-3-methylbut-3-enyl)-4',5,7-trihydroxy-dihydroflavanone (1), pinocembrin (2), sigmoidin B (3), licoflavanone (4), 6-prenylnaringenin (5), pinobanksin (6), galangin (7), genistein (8), pratensein (9), kaempferol-3-O-β-D-rutinoside (10), rutin (11), and α,α'-dihydro-3,5,3'-trihydroxy-4'-methoxy-5'-isopentenyl-stilbene (12). Conclusion: Compound 1 is a new compound named hydroxylicoflavanone, and compounds 3, 6, 7, and 9 are isolated from this plant for the first time.