Galangin improves cardiac remodeling and dysfunction after myocardial infarction via inhibiting cardiomyocyte apoptosis and inflammation / 中华老年心脑血管病杂志

Objective To investigate the effect of galangin on cardiac remodeling and cardiac func-tion after myocardial infarction(MI).Methods A total of 32 male C57/BL6 mice(8-10 weeks old)were subjected for MI modeling,and finally 24 mice were assigned into control group[sham operation+hydroxycellulose sodium(CMC-Na)],model group(MI+CMC-Na),and experimental group(MI+galangin),with 8 mice in each group.After MI modeling,the mice of the experimen-tal group were given 40 mg/kg galangin by gavage for 4 weeks,and those of the control group and the model group were given the same volume(0.4 ml)of CMC-Na solution.HE staining was used to observe the size of the infarct area.The mRNA levels of inflammatory factors in the heart were detected by qRT-PCR,and protein levels of related signaling pathway proteins were measured with Western blotting.Immunofluorescence(IF)assay was applied to detect the infiltration of in-flammatory cells in the infarct border zone.TUNEL staining was employed to detect cell apoptosis in the infarct border zone.Results At 4 weeks after modeling,larger infarct size,enhanced expression levels of IL-1β,IL-6,TNF-α,p-P65,p-IκBα and Bax,elevated apoptotic rate,decreased cardiac function indicators such as FS and LVEF,and reduced Bcl-2 expression level were observed in the model group than the control group(P＜0.05).The experimental group had sig-nificant smaller myocardial infarct size[(11.64±0.64)％vs(21.84±1.94)％],less CD3 positive T cells[(3.10±0.46)％vs(6.28±0.24)％],F4-80 positive macrophages[(1.98±0.50)％vs(5.35±0.62)％]and LY6G positive neutrophils[(6.33±0.67)％vs(11.33±1.77)％],decreased expression levels of IL-1β,IL-6,TNF-α,p-P65,p-IκBα and Bax,reduced apoptotic rate[(21.45± 1.62)％vs(35.68±0.88)％],and increased FS and LVEF values and Bcl-2 expression level when compared with the model group(P＜0.05).Conclusion Galangin improves myocardial remode-ling and cardiac dysfunction after MI by inhibiting inflammatory response and cell apoptosis.

Study on the mechanism of galangin promoting fracture in osteoporosis model rats / 中国药房

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.

Effect of galangin on hypoxia-inducible factor-1α-mediated epithelial mesenchymal transformation in gastric cancer cells / 中国药理学通报

Aim To investigate the effect of galangin(GLA) on gastric cancer in hypoxic microenvironment. Methods The gastric cancer SGC-7901 cell line was induced with CoCl

Therapeutic evaluation of galangin on cartilage protection and analgesic activity in a rat model of osteoarthritis

BACKGROUND Osteoarthritis (OA) is a form of arthritis due to degradation of articular cartilage. OA is asso ciated with stiffness, joint pain, and dysfunction, affecting adults worldwide. Galangin is a bioactive fla vonoid that exerts several therapeutic and biological activities. Anti-hyperglycemic, anti-inflammatory, anti-cancer, and anti-apoptotic activities of galangin have been reported in several studies. In the present study, rats were divided into normal control, OA (control), galangin 10 mg/kg (low-dose), galangin 100 mg/kg (high-dose), and celecoxib 30 mg/kg (positive control) groups. All doses were administered orally for 14 consecutive days. The urinary type II collagen (mCTX-II) level as well as reactive oxygen spe cies, tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, superoxide dismutase, catalase, lipid peroxidation, reduced glutathione, and glutathione peroxidase levels were measured. In addition, the CTX-II mRNA and protein expression levels were measured. RESULTS Galangin supplementation significantly reduced the mCTX-II level compared with controls. Galangin treatment significantly reduced reactive oxygen species, lipid peroxidation, interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha levels, but increased catalase, superoxide dismutase, glu tathione peroxidase, and reduced glutathione levels. Galangin treatment significantly reduced the CTX-II mRNA and protein expression levels. The low CTX-II level in tissue indicated the inhibition of cartilage degradation. CONCLUSIONS In summary, supplementation with galangin was effective against OA. The identification of potential therapeutic agents that inhibit inflammation may be useful for the management and prevention of OA

Galangin enhances autophagy by inhibiting NF-κB pathway in gastric cancer MGC-803 cells / 中国中药杂志

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.

Mechanism of the inhibitory effect of galangin on hepatoma cells / 临床肝胆病杂志

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.

UHPLC-MS-MS high throughput analysis-based screening and evaluation of PXR/CYP3A4-induced lipid-regulating quality marker in propolis / 中草药

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.

Propolis polyphenolic compounds affect the viability and structure of Helicobacter pylori in vitro

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.

Optimization of the Hot Sand Processing Technology for Alpinia officinarum by Central Composite Design-response Surface Method / 中国药房

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.

Galangin ameliorates changes of membrane-bound enzymes in rats with streptozotocin-induced hyperglycemia

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.

Galangin ameliorates changes of membrane-bound enzymes in rats with streptozotocin-induced hyperglycemia

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.

Preparation of galangin molecular imprinted polymers on silica gel surface and its adsorption properties / 中草药

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.

Comparative analysis of species and contents of flavonoids before and after honey refining / 中草药

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.

Galangin Activates the ERK/AKT-Driven Nrf2 Signaling Pathway to Increase the Level of Reduced Glutathione in Human Keratinocytes

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.

The study of the inhibition effects of SIRT1 on the apoptosis induced by Galangin in HepG2 cells / 医学研究生学报

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.

Inductive effects of galangin on apotosis of human papilloma virus positive cervical cancer cells / 中草药

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.

Galangin induces apoptosis of glioma cells through Wnt/β-Catenin signal pathway / 中华神经医学杂志

Objective To investigate the effect of galangin on proliferation and apoptosis of glioma cells in vitro.Methods (1) The glioma cells U87 and U25 1were divided into blank control group,DMSO group,100,200,300 and 400 μmol/L galangin treatment groups.MTT was used to study the effects of drugs on the proliferation of U251 and U87 cells.(2) Hoechest staining was used to observe cell apoptosis in the presence of different concentrations of galangin (0,100 and 200 μmol/L).(3) Flow cytometry was employed to detect the apoptosis of U251 and U87 cells in the presence of different concentrations of galangin (1 00 and 200 μmol/L).(4) Western blotting was employed to detect the expressions of apoptosis-related protein 3-Catenin,B-cell lymphoma-2 (Bcl-2),Bcl-2 related protein gene (Bax),cleaved-caspase-3,cleaved-caspase-9 and poly (ADP-ribose) polymerase (PARP) in the presence of different concentrations of galangin.Results (1) The proliferation of U251 and U87 cells was obviously inhibited atter 100,200,300 and 400 μmol/L galangin treatments,and dose-effect relation was noted.The concentrations of galangin at half rate of inhibition (IC50) were 281,321,276 and 229 μmol/L in U251 cells,and 289.4,261.1,247.4 and 225.3 μ mol/L in the U87 cells after 100,200,300 and 400μmol/L galangin treatments for 24 h.(2) Under the action of galangin,corresponding increase in apoptosis rates of U251 and U87 cells was noted following the increase of galangin concentrations (0,100 and 200 μmol/L),with significant differences (P＜0.05).(3) The detection of cell apoptosis by flow cytometry found similar changes.(4) Western blotting results indicated that galangin at the concentration of 0,100 and 200 μmol/L could significantly decrease the expressions of apoptosis-related protein 3-Catenin and Bcl-2,and increase the Bax,cleaved-caspase-3 and cleaved-caspase-9,and cleaved-PARP expressions;significant differences were noted between each two concentrations (P＜0.05).Conclusion Galangin can inhibit proliferation of glioma cells U251 and U87,and induce mitochondrial pathway of apoptosis via Wnt/β-Catenin signaling.

Galangin Suppresses Pro-Inflammatory Gene Expression in Polyinosinic-Polycytidylic Acid-Stimulated Microglial Cells

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.

Galangin Suppresses Pro-Inflammatory Gene Expression in Polyinosinic-Polycytidylic Acid-Stimulated Microglial Cells

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.

The effect of galangin on the inhibition of proliferation and invasion of human lung cancer cells and its mechanism / 天津医药

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.