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PubMed2005

The effects of apigenin-7-O-beta-D-glucuronopyranoside on reflux oesophagitis and gastritis in rats.

1. This study evaluated the inhibitory action of apigenin-7-O-beta-D-glucuronopyranoside (AGC), apigenin, and omeprazole on reflux oesophagitis and gastritis in rats. AGC was isolated from Clerodendron trichotomum leaves. 2. Oesophagitis and gastritis were induced by surgical procedure and the administration of indomethacin, respectively. The intraduodenal (i.d.) administration of AGC decreased the volume of gastric juice and increased the gastric pH compared with apigenin and omeprazole. The acid output was more inhibited by AGC in a dose-dependent manner than by apigenin and omeprazole. Compared with apigenin and omeprazole, AGC significantly decreased the size of gastric lesions, which were induced by exposure of the gastric mucosa to indomethacin. 3. Malondialdehyde (MDA) content, which is the end product of lipid peroxidation, was increased significantly after the induction of reflux oesophagitis. The MDA content was decreased by AGC (i.d. 3 mg kg(-1)), but not by either apigenin or omeprazole. This suggests that AGC has an antioxidative effect. In the oesophagitis group, the mucosal levels of glutathione (GSH) were significantly lower than that in the normal group. However, the GSH levels were preserved after administering the AGC, suggesting that AGC possesses scavenging activity. 4. In summary, AGC is more potent than apigenin and omeprazole at inhibiting reflux oesophagitis and gastritis and may therefore be a promising drug for their treatment.

Animals↗
PubMed2006

Apigenin inhibits immunostimulatory function of dendritic cells: Implication of immunotherapeutic adjuvant.

Apigenin, one of the most common flavonoids, has been shown to possess anti-inflammatory, anticarcinogenic, and free radical-scavenging properties. However, the influence of apigenin on the immunostimulatory effects and maturation of dendritic cells (DC) remains, for the most part, unknown. In this study, we have attempted to ascertain whether apigenin influences the expression of surface molecules, dextran uptake, cytokine production, and T-cell differentiation as well as the signaling pathways underlying these phenomena in murine bone marrow-derived DC. In the presence of apigenin, CD80, CD86, and major histocompatibility complex class I and II molecules, expressions on DC were significantly suppressed, and lipopolysaccharide (LPS)-induced interleukin (IL)-12 expression was impaired. The DC proved highly efficient at antigen capture, as evidenced by the observation of mannose receptor-mediated endocytosis in the presence of apigenin. The LPS-induced activation of mitogen-activated protein kinase, the nuclear translocation of its nuclear factor-kappaB p65 subunit, and the induction of the T-helper 1 response were all impaired in the presence of apigenin, whereas the cell-mediated immune response remained normal. These findings provide new insight into the immunopharmacological functions of apigenin and its effects on DC, and they may also prove useful in the development of adjuvant therapies for individuals suffering from acute or chronic DC-associated diseases.

Active Transport, Cell Nucleus↗
PubMed2004

Suppression of constitutive and tumor necrosis factor alpha-induced nuclear factor (NF)-kappaB activation and induction of apoptosis by apigenin in human prostate carcinoma PC-3 cells: correlation with down-regulation of NF-kappaB-responsive genes.

PURPOSE: Development of androgen independence and resistance to apoptosis in prostate cancer are often correlated with high levels of serum tumor necrosis factor (TNF)-alpha in these patients. The loss of sensitivity to TNF-alpha-induced apoptosis in androgen-insensitive prostate carcinoma cells is due in part to constitutive activation of Rel/nuclear factor (NF)-kappaB transcription factors that regulate several cell survival and antiapoptotic genes. Our previous studies have demonstrated growth inhibitory and apoptotic effects of apigenin, a common plant flavonoid, in a variety of human prostate carcinoma cells. Here we examined whether apigenin is effective in inhibiting NF-kappaB expression in androgen-insensitive human prostate carcinoma cells exhibiting high constitutive levels of NF-kappaB. EXPERIMENTAL DESIGN: Using androgen-insensitive human prostate carcinoma PC-3 cells, the effect of apigenin was assessed on NF-kappaB activation by electrophoretic mobility shift assay and reporter gene assay. Expression of NF-kappaB subunits p65 and p50, IkappaBalpha, p-IkappaBalpha, in-beads kinase assay and NF-kappaB-regulated genes were determined by Western blot analysis. Apoptosis was determined by annexin V/propidium iodide staining after fluorescence-activated cell-sorting analysis. RESULTS: Treatment of cells with 10-40- micro M doses of apigenin inhibited DNA binding and reduced nuclear levels of the p65 and p50 subunits of NF-kappaB. Apigenin inhibited IkappaBalpha degradation and IkappaBalpha phosphorylation and significantly decreased IKKalpha kinase activity. Apigenin also inhibited TNF-alpha-induced activation of NF-kappaB via the IkappaBalpha pathway, thereby sensitizing the cells to TNF-alpha-induced apoptosis. The inhibition of NF-kappaB activation correlated with a decreased expression of NF-kappaB-dependent reporter gene and suppressed expression of NF-kappaB-regulated genes [specifically, Bcl2, cyclin D1, cyclooxygenase-2, matrix metalloproteinase 9, nitric oxide synthase-2 (NOS-2), and vascular endothelial growth factor]. CONCLUSIONS: Our results indicate that inhibition of NF-kappaB by apigenin may lead to prostate cancer suppression by transcriptional repression of NF-kappaB-responsive genes as well as selective sensitization of prostate carcinoma cells to TNF-alpha-induced apoptosis.

Apigenin↗
PubMed2006

The dietary flavonoid apigenin sensitizes malignant tumor cells to tumor necrosis factor-related apoptosis-inducing ligand.

Dietary flavonoid apigenin is expected to have preventive and therapeutic potential against malignant tumors. In this report, we show for the first time that apigenin markedly induces the expression of death receptor 5 (DR5) and synergistically acts with exogenous soluble recombinant human tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) to induce apoptosis in malignant tumor cells. TRAIL is a promising candidate for cancer therapeutics due to its ability to selectively induce apoptosis in cancer cells. The combined use of apigenin and TRAIL at suboptimal concentrations induces Bcl-2-interacting domain cleavage and the activation of caspases-8, -10, -9, and -3. Furthermore, human recombinant DR5/Fc chimera protein and caspase inhibitors dramatically inhibit apoptosis induced by the combination of apigenin and TRAIL. On the other hand, apigenin-mediated induction of DR5 expression is not observed in normal human peripheral blood mononuclear cells. Moreover, apigenin does not sensitize normal human peripheral blood mononuclear cells to TRAIL-induced apoptosis. These results suggest that this combined treatment with apigenin and TRAIL might be promising as a new therapy against malignant tumors.

Apigenin↗
PubMed1990

On the accumulation of apigenin in chamomile flowers.

By preparing and analysing extracts of fresh chamomile flowers from outdoor and greenhouse cultures, it was possible to show that apigenin does not actually occur in living chamomile flowers. Apigenin is the result of post-harvest processes converting apigenin 7-glycoside and its derivatives into the aglycone. The different apigenin/apigenin 7-glycoside ratios reported in the literature for various chamomile samples can easily be explained as the result of different post-harvest conditions. The accumulation of free apigenin in chamomile flowers must be ascribed to the enzymatic degradation of apigenin 7-glycoside and other glycosidic derivatives of apigenin. Thus, the selection of chamomile types yielding large amounts of apigenin seems to be based on a degradation product.

Journal Article↗
PubMed1986

Anti-mutagenesis and anti-promotion by apigenin, robinetin and indole-3-carbinol.

We assessed the anti-mutagenic and anti-promotion properties of two flavones, apigenin and robinetin, and of indole-3-carbinol, because these compounds have been reported in vegetables, the consumption of which has been associated with reduced rates of cancer. However, the active components of these foods and their effects on carcinogenesis have not been established. Anti-mutagenicity was determined in the Salmonella typhimurium assay by measuring the effects of the test compounds on bacterial mutagenesis induced by methyl-nitrosourea (MNU), methyl-n-nitro-N-nitrosoguanidine (MNNG), benzo[a]pyrene (BaP) or 2-aminoanthracene (2-AA). Inclusion of apigenin resulted in a 62% and a 43% inhibition of mutagenicity with 13 nmol of 2-AA and 30 nmol BaP respectively. Robinetin caused an 87% inhibition of mutagenicity by 2-AA, but indole-3-carbinol had little or no effect on the mutagenicity of any of the compounds. None of the three compounds inhibited mutagenesis by MNU or MNNG and none were mutagenic or toxic when tested in the absence of mutagenic compounds at doses up to 20 micrograms/plate. Anti-promotion properties were assessed by measuring the effects of apigenin, robinetin and indole-3-carbinol on induction of ornithine decarboxylase activity (ODC) in mouse epidermis by 17 nmol 12-O-tetradecanoyl phorbol-13-acetate (TPA). Pretreatment of the skin half an hour before TPA with apigenin, robinetin, butylated hydroxyanisole, 13-cis-retinoic acid (all at 50 mumol) or di-fluoromethylornithine (1.6 mumol) inhibited ODC induction at 6 h after TPA by 67-80%. Pretreatment with 50 mumol indole-3-carbinol caused a 78% elevation in the TPA induction at this time. Dose response measurements were conducted with apigenin, indole-3-carbinol and robinetin. Inhibition by 30-90% of TPA-induced ODC was observed at 6 h after TPA in mice pretreated with 12.5-100 mumol apigenin. Pretreatment with 37.5 or 50 mumol indole-3-carbinol or 0.5, 12.5 or 25 mumol robinetin resulted in elevated induction of epidermal ODC by TPA at 6 h after TPA. However, treatment with 50 or 100 mumol robinetin diminished ODC induction at 6 h after TPA. Treatment with 100 mumol apigenin or 50 or 100 mumol indole-3-carbinol in non-TPA-treated mouse skin caused elevations in epidermal ODC. In comparing the time course of ODC induction, indole-3-carbinol (50 mumol) pretreatment shifted the induction of epidermal ODC to earlier times, in addition to elevating ODC induction by TPA.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Acetylaminofluorene↗
PubMedDate not supplied

Inhibition of ultraviolet light induced skin carcinogenesis in SKH-1 mice by apigenin, a plant flavonoid.

Apigenin, a widely distributed plant flavonoid, was previously found to inhibit chemically induced ornithine decarboxylase (ODC) activity and skin tumor promotion. The purpose of the present research was to determine if apigenin is effective in the prevention of ultraviolet-B light (UVB) induced skin carcinogenesis. Further studies ascertained if apigenin would be expected to absorb UVB light in a manner to prevent DNA damage in a cell free system. ODC activity was induced with 0.45 J/cm2 ultraviolet A and B (UVA/B) light. Apigenin (5 mumoles/200 microliters DMSO:acetone, 1:9) treatment from 12 hours before until 1 hour following UVA/B exposure was effective in inhibition (25-45% inhibition) of ODC activity measured at 28 hours following UVA/B exposure. Mouse skin carcinogenesis was induced by exposure to a total dose of 40 J/cm2 UVB over 11 weeks. Treatment with 10 mumoles apigenin in 200 microliters DMSO:acetone (1:9) prior to each UVB exposure resulted in reduction in cancer incidence (52% inhibition) and an increase in tumor free survival in comparison with control mice (P < 0.01). Apigenin (0-100 microM) did not prevent the in vitro production of photoproducts in salmon sperm DNA suggesting that apigenin did not inhibit UVA/B induced ODC activity or UVB induced skin carcinogenesis by simply absorbing ultraviolet light or decreasing DNA damage.

Animals↗
PubMed2000

Apigenin inhibits endothelial-cell proliferation in G(2)/M phase whereas it stimulates smooth-muscle cells by inhibiting P21 and P27 expression.

Apigenin is a plant flavonoid that is thought to play a role in the prevention of carcinogenesis. However, its mechanism of action has not yet been elucidated. Because of the importance of angiogenesis in tumor growth, we investigated the effect of apigenin on endothelial and smooth-muscle cells in an in vitro model. Apigenin markedly inhibited the proliferation, and, to a lesser degree, the migration of endothelial cells, and capillary formation in vitro, independently of its inhibition of hyaluronidase activity. In contrast, it strongly stimulated vascular smooth-muscle-cell proliferation. The molecular mechanisms of apigenin activity were analyzed in these 2 types of cells. Our results show that apigenin inhibits endothelial-cell proliferation by blocking the cells in the G(2)/M phase as a result of the accumulation of the hyperphosphorylated form of the retinoblastoma protein. Apigenin stimulation of smooth-muscle cells was attributed to the reduced expression of 2 cyclin-dependent kinase inhibitors, p21 and p27, which negatively regulate the G(1)-phase cyclin-dependent kinase.

Animals↗
PubMed2006

A simple HPLC method for the determination of apigenin in mouse tissues.

The flavone apigenin occurs in many leafy vegetables and fruits. It has been reported to have cancer chemopreventive efficacy in rodents. An HPLC method described previously for the determination of tricin, the dimethoxy cogener of apigenin, was modified and validated for measurement of apigenin in mouse tissues. Separation was carried out on a Hypersil-BDS C(18) column (4.6 x 250 mm) with an isocratic mobile phase of 55% methanol in 0.1 m ammonium acetate, pH 5.10, containing 0.27 mm disodium ethylenediamine tetraacetic acid. UV detection was at 336 nm, without interference from endogenous tissue compounds. The assay was linear in the range 25-400 ng/mL, 0.25-4 microg/mL and 2.5-40 microg/mL, with r(2) > 0.99 in all cases, for mouse plasma, liver and intestinal mucosa, respectively. Apigenin in mouse plasma, liver and intestinal mucosa was efficiently extracted with 0.1 m acetic acid in acetone. The assay recovery at low, medium and high concentrations was between 94.6 and 131.7% for all biomatrices, with a relative standard deviation of <10%. The lower limit of quantification for plasma was 25 ng/mL with a relative standard deviation of <15%. The method was used to measure the steady-phase apigenin levels in tissues of mice receiving apigenin in their diet.

Animals↗
PubMed2005

Apigenin inhibits oxidative stress-induced macromolecular damage in N-nitrosodiethylamine (NDEA)-induced hepatocellular carcinogenesis in Wistar albino rats.

Apigenin (4',5,7-trihydroxyflavone), a flavone subclass of flavonoid widely distributed in many herbs, fruits, and vegetables is a substantial component of the human diet and has been shown to possess a variety of biological activities including tumor growth inhibition and chemoprevention. Recent studies in several biological systems have shown that apigenin induces tumor growth inhibition, cell cycle arrest, and apoptosis. Free radical-induced degradation of polyunsaturated fatty acid results in electrophilic products and causes severe oxidative stress. Oxidative stress induced by free radicals, nonoxidizing species, electrophiles, and associated DNA damages have been frequently coupled with carcinogenesis. In the present study, the protective role of apigenin was examined against the oxidative stress caused by N-nitrosodiethylamine (NDEA) and phenobarbital (PB) in Wistar albino rats. Oxidative stress was measured in terms of lipid peroxidation (LPO) and protein carbonyl formation. Oxidative stress-induced DNA damage was measured by single cell gel electrophoresis (comet assay). Apigenin exhibited its antioxidant defense against NDEA-induced oxidative stress. We have observed minimal levels of LPO and DNA damage in apigenin-treated hepatoma bearing animals. Based on the results, we suggest that apigenin may be developed as a promising chemotherapeutic agent against the development of chemical carcinogenesis.

Albinism↗
PubMed2004

Decreased pro-inflammatory cytokine production by LPS-stimulated PBMC upon in vitro incubation with the flavonoids apigenin, luteolin or chrysin, due to selective elimination of monocytes/macrophages.

Apigenin and its structural analogues chrysin and luteolin were used to evaluate their capacity to inhibit the production of pro-inflammatory cytokines by lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells (PBMC). Furthermore, flowcytometric analysis was performed to compare the effects of apigenin, chrysin, luteolin, quercetin and naringenin on the different cell types present in PBMC. LPS-stimulated PBMC were cultured in the presence of the flavonoids and TNFalpha, IL-1beta and IL-6 were measured in the supernatants. In parallel, metabolic activity of the PBMC was determined by measuring succinate dehydrogenase activity. Apigenin, chrysin and luteolin dose-dependently inhibited both pro-inflammatory cytokine production and metabolic activity of LPS-stimulated PBMC. With increasing concentration of apigenin, chrysin or luteolin the monocytes/macrophages disappeared as measured by flowcytometry. This also appeared to occur in the non-LPS-stimulated PBMC. At the same time there was an increase in dead cells. T- and B-lymphocytes were not affected. Quercetin and naringenin had virtually no effects on cytokines, metabolic activity or on the number of cells in the studied cell populations. In conclusion, monocytes were specifically eliminated in PBMC by apigenin, chrysin or luteolin treatment in vitro at low concentrations (around 8 microM), in which apigenin appeared to be the most potent.

Adult↗
PubMed2004

Simultaneous determination of luteolin and apigenin in dog plasma by RP-HPLC.

A specific and accurate high-performance liquid chromatographic method has been developed and validated for the simultaneous determination of luteolin and apigenin in the plasma of dog. The sample was treated with 6.0% perchloric acid to precipitate the protein. Luteolin and apigenin were extracted with ethyl acetate. The organic layer separated was dried and reconstituted in the mobile phase. The HPLC separation was performed on C18 column and the UV detector was set at 350 nm. The standard curve for luteolin and apigenin in plasma were linear over the range of 38.5-4350 and 16.5-1860 ng/ml, with the correlation coefficients 0.9996 and 0.9999, respectively. The assay recoveries for luteolin and apigenin ranged from 102.7 to 104.5% and 93.8-101.8%, respectively. The intra- and inter-day precisions (R.S.D.) for luteolin and apigenin were all less than 7.9%. The sample was stable within 24 h at 4 degrees C storage, 30 days at -20 degrees C storage, and undergoing four freeze-thaw-assay cycles. The limits of detection (LOD) of luteolin and apigenin were 1.82 and 1.94 ng/ml, while the limits of quantification (LOQ) were 7.84 and 6.29 ng/ml, respectively. The method developed was applied successfully to study pharmacokinetics of the effective composition (luteolin) of Chrysanthemum morifolium extract in dogs after single dose of oral administration.

Administration, Oral↗
PubMed2005

Apigenin induces apoptosis in Hep G2 cells: possible role of TNF-alpha and IFN-gamma.

Flavonoids are one of the biologically active plant food constituents, possessing potential chemopreventive properties against a wide variety of chronic diseases. Apigenin, a common dietary flavonoid abundantly present in fruits and vegetables is believed to possess preventive and therapeutic potential against various cancers. In the present study, we have evaluated regulation of apoptotic cell death by apigenin (25 and 50 microM) in human hepatoblastoma derived cell line Hep G2. Apigenin-induced programme cell death in terms of TNF-alpha, IFN-gamma release and induction of caspases activity. TNF-alpha and IFN-gamma levels in apigenin-pretreated groups were significantly and dose dependently elevated as compared to the control values (28-39% and 66-85%), (208-336% and 579-1088%), respectively. Treatment of apigenin significantly induced caspase-3, -7, -10 and caspase-9 activity (160-209% and 203-270%) in a dose-dependent manner. The effects on caspases, TNF-alpha, and IFN-gamma processes mediate the plausible mechanism of apoptosis induction of apigenin.

Apigenin↗
PubMed2001

Apigenin decreases expression of the myofibroblast phenotype.

We investigated the effect of the dietary flavonoid apigenin on myofibroblast function. We report that in myofibroblasts treated with apigenin, proliferation and basal levels of alpha1(I) collagen and alpha-smooth muscle actin mRNAs were markedly reduced. Apigenin also attenuated the transforming growth factor-beta-stimulated increases of alpha1(I) collagen and alpha-smooth muscle actin mRNAs. Characterization of the apigenin effects indicates that apigenin reduces both the stability of the alpha1(I) collagen mRNA and the rate of transcription of the alpha1(I) collagen gene through a cycloheximide-sensitive pathway. Western blot analyses indicate that Akt activity is reduced in apigenin-treated myofibroblasts.

Actins↗
PubMed2000

Suppression by apigenin of peritoneal metastasis of intestinal adenocarcinomas induced by azoxymethane in Wistar rats.

The effect of a naturally occurring flavonoid apigenin on the development of bombesin-enhanced peritoneal metastasis from intestinal adenocarcinomas induced by azoxymethane was investigated in male Wistar rats. From the start of the experiment, rats were given weekly s.c. injections of azoxymethane (7.4 mg/kg body weight) for 10 weeks and s.c. injection of bombesin (40 microg/kg body weight) every other day, and from week 16, s.c. injections of apigenin (0.75 or 1.5 mg/kg body weight) every other day until the end of the experiment in week 45. Bombesin significantly increased the incidence of intestinal tumors and cancer metastasis to the peritoneum in week 45. It also significantly increased the labeling index of intestinal cancers. Although administration of apigenin at either dose with bombesin had little or no effect on the enhancement of intestinal carcinogenesis by bombesin, the location, histologic type, depth of involvement, infiltrating growth patterns and labeling index, it was found to decrease significantly the incidence of cancer metastasis. Apigenin significantly decreased the incidence of lymphatic vessel invasion of adenocarcinomas, which was enhanced by bombesin. In vitro experiments revealed that apigenin inhibited bombesin-enhanced phosphorylation of mitogen-activated protein kinase (MAPK), but not matrix metalloprotease (MMP)-9 expression. Our findings indicate that apigenin inhibits cancer metastasis through inhibition of phosphorylation of MAPK.

Adenocarcinoma↗
PubMed2006

Apigenin inhibits tumor angiogenesis through decreasing HIF-1alpha and VEGF expression.

Apigenin is a non-toxic dietary flavonoid with anti-tumor properties. We recently showed that apigenin-inhibited hypoxia-inducible factor-1 (HIF-1) and vascular endothelial growth factor (VEGF) expression in human ovarian cancer cells under normoxic condition. However, the effect of apigenin in angiogenesis remains to be elucidated. Angiogenesis is the formation of new blood vessels and is required for tumor growth and metastasis. In this study, we showed that apigenin-inhibited expression of HIF-1 and VEGF in different cancer cells under both normoxic and hypoxic conditions. We demonstrated that apigenin significantly inhibited tumor angiogenesis in vivo, by using both the chicken chorioallantoic membrane and Matrigel plug assays. The inhibition of tumor angiogenesis was associated with the decrease of HIF-1 and VEGF in tumor tissues. Taken together, our results show that apigenin suppresses tumor angiogenesis through HIF-1 and VEGF expression.

Animals↗
PubMed2005

Apigenin inhibits VEGF and HIF-1 expression via PI3K/AKT/p70S6K1 and HDM2/p53 pathways.

Apigenin is a nontoxic dietary flavonoid that has been shown to possess anti-tumor properties and therefore poses special interest for the development of a novel chemopreventive and/or chemotherapeutic agent for cancer. Ovarian cancer is one of the most common causes of cancer death among women. Here we demonstrate that apigenin inhibits expression of vascular endothelial growth factor (VEGF) in human ovarian cancer cells. VEGF plays an important role in tumor angiogenesis and growth. We found that apigenin inhibited VEGF expression at the transcriptional level through expression of hypoxia-inducible factor 1alpha (HIF-1alpha). Apigenin inhibited expression of HIF-1alpha and VEGF via the PI3K/AKT/p70S6K1 and HDM2/p53 pathways. Apigenin inhibited tube formation in vitro by endothelial cells. These findings reveal a novel role of apigenin in inhibiting HIF-1 and VEGF expression that is important for tumor angiogenesis and growth, identifying new signaling molecules that mediate this regulation.

Apigenin↗
PubMed2006

Influence of apigenin on gtf gene expression in Streptococcus mutans UA159.

Apigenin, a potent inhibitor of glucosyltransferase activity, affects the accumulation of Streptococcus mutans biofilms in vitro by reducing the formation of insoluble glucans and enhancing the soluble glucan content of the polysaccharide matrix. In the present study, we investigated the influence of apigenin on gtfB, gtfC, and gtfD expression in S. mutans UA159. Apigenin (0.1 mM) significantly decreased the expression of gtfB and gtfC mRNA (P < 0.05); in contrast, it increased the expression of gtfD in S. mutans growing in the planktonic state. The protein levels of GTF B, GTF C, and GTF D in culture supernatants were also affected; less GTF B and C were detected, whereas the level of GTF D was significantly elevated (P < 0.05). A similar profile of gtf expression was obtained with biofilms, although an elevated concentration (1 mM) of apigenin was required to elicit the effects. The influence of apigenin on gtf gene expression was independent of any effect on GTF activity, did not involve inhibition of growth or effects on pH, and was not affected by addition of sucrose. The data show that apigenin modulates the genetic expression of virulence factors in S. mutans.

Apigenin↗