Trihydroxyflavone Research Articles

Effects of Antimicrobial Flavonoids Against Representative Bacteria and Fungi: A Review of the Literature.

Effective medications are becoming more necessary to combat the global rise in antimicrobial resistance. The findings that some flavonoids have antibacterial properties have urged interest in flavonoid research. The aim of this work was to investigate the inhibitory properties of fisetin, fisetinidin, 7,3`,4`-trihydroxyflavone (THF), and 7,3`,4`-trihydroxyflavonol (THF-) against selected pathogenic bacteria and fungi and to review the literature on relevant compounds. An in vitro experiment was performed on 19 organisms (gram-positive, gram-negative, and yeast fungi) using varying concentrations (100-1000 ug/mL) of fisetin, fisetinidin, THF, and THF-. Using the agar well diffusion method. The in vitro activity of flavonoid compounds against gram-positive, gram-negative, and yeasts was assessed using a serial dilution of the four compounds against organism suspensions (50 µL of 0.5 McFarland). Inoculated agar plates were incubated aerobically at 37oC. The results of inhibition were recorded after 24, 48, and 72 hours. Various classes of flavonoids from different sources have been reviewed for their antimicrobial effects. They showed various inhibitory reactions against a plethora of gram-positive, gram-negative, and yeast organisms. In the present study, the selected four compounds have shown varying antibacterial effects, as have the reviewed flavonoids from the literature. With minimum inhibitory concentrations (MICs) ranging from 100ug/mL to 1000 ug/mL, the substances fisetin, fisetinidin, THF, and THF- demonstrated inhibitory action against the examined species. The main activity was against Staphylococcus,Bacillus,Acinetobacter,Proteus, andPseudomonasspecies. Fisetin and fisetinidin did not inhibitEscherichia coli, whereas THF and THF- exhibited inhibitory action. Flavonoids, a readily accessible dietary ingredient, remain a viable treatment option for infectious diseases. This study suggests that THF, THF-, fisetin, and fisetinidin may be helpful in stopping the growth of some pathogens, especially staphylococci. Improvements to flavonoids' pharmacokinetics and diffusion may encourage their use in therapy as an adjuvant to conventional medications.

BDNF mimetics recover palmitic acid-induced injury in cardiomyocytes by ameliorating Akt-dependent mitochondrial impairments

Cardiac lipotoxicity is a prevalent consequence of lipid metabolism disorders occurring in cardiomyocytes, which in turn precipitates the onset of heart failure. Mimetics of brain-derived neurotrophic factor (BDNF), such as 7,8-dihydroxyflavone (DHF) and 7,8,3′-trihydroxyflavone (THF), have demonstrated significant cardioprotective effects. However, it remains unclear whether these mimetics can protect cardiomyocytes against lipotoxicity. The aim of this study was to examine the impact of DHF and THF on the lipotoxic effects induced by palmitic acid (PA), as well as the concurrent mitochondrial dysfunction. H9c2 cells were subjected to treatment with PA alone or in conjunction with DHF or THF. Various factors such as cell viability, lactate dehydrogenase (LDH) release, death ratio, and mitochondrial function including mitochondrial membrane potential (MMP), mitochondrial-derived reactive oxygen species (mito-SOX) production, and mitochondrial respiration were assessed. PA dose-dependently reduced cell viability, which was restored by DHF or THF. Additionally, both DHF and THF decreased LDH content, death ratio, and mito-SOX production, while increasing MMP and regulating mitochondrial oxidative phosphorylation in cardiomyocytes. Moreover, DHF and THF specifically activated Akt signaling. The protective effects of DHF and THF were abolished when an Akt inhibitor was used. In conclusion, BDNF mimetics attenuate PA-induced injury in cardiomyocytes by alleviating mitochondrial impairments through the activation of Akt signaling.

Primary Determination of the Composition of Secondary Metabolites in the Wild and Introduced Artemisia martjanovii Krasch: Samples from Yakutia

Artemisia martjanovii Krasch is a rare representative of the genus Artemisia in Siberia and the Far East. The phytochemical composition of this endangered species is essential for its potential use in medicine. We used tandem mass spectrometry and HPLC-MS/MS methods to describe the metabolome from the stem and leaf extracts of A. martjanovii from Yakutia. The metabolome profile analysis of A. martjanovii grown in the Botanical Garden of the North-Eastern Federal University, Yakutsk, Russia, and the wild A. martjanovii from Khangalassky district, Republic of Sakha (Yakutia) differed significantly both in the polyphenol composition and other compound classes. In total, we identified 104 bioactive constituents from stem and leaf extracts, 56 compounds from the polyphenol group, and 48 from other compound classes. Twenty-seven compounds classified as polyphenol groups, i.e., flavones apigenin, trihydroxy(iso)flavone, salvigenin, cirsiliol, cirsilineol, nevadensin, syringetin, gardenin B, thymonin, and chrysoeriol C-hexoside; flavonols: taxifolin, tetrahydroxy-dimethoxyflavone-hexoside, etc.; and 26 compounds from other classes are being reported for the first time in the genus Artemisia L.

7,8,3′-Trihydroxyflavone prevents doxorubicin-induced cardiotoxicity and mitochondrial dysfunction via activating Akt signaling pathway in H9c2 cells

Clinical application of the widely used chemotherapeutic agent, doxorubicin (DOX), is limited by its cardiotoxicity. Mitochondrial dysfunction has been revealed as a crucial factor in DOX-induced cardiotoxicity. 7,8,3′-Trihydroxyflavone (THF) is a mimetic brain-derived neurotrophic factor with neuroprotective effects. However, the potential effects of THF on DOX-induced cardiomyocyte damage and mitochondrial disorders remain unclear. H9c2 cardiomyoblasts were exposed to DOX and/or THF at different concentrations. Cardiomyocyte injury was evaluated using lactate dehydrogenase (LDH) assay and Live/Dead cytotoxicity kit. Meanwhile, mitochondrial membrane potential (MMP), morphology, mitochondrial reactive oxygen species (mito-ROS) production, and the oxygen consumption rate of cardiomyocytes were measured. The protein levels of key mitochondria-related factors such as adenosine monophosphate-activated protein kinase (AMPK), mitofusin 2 (Mfn2), dynamin-related protein 1 (Drp1), and optic atrophy protein 1 (OPA1) were examined. We found that THF reduced LDH content and death ratio of DOX-treated cardiomyocytes in a concentration-dependent manner, while increasing MMP without significantly affecting the routine and maximum capacity of mitochondrial respiration. Mechanistically, THF increased the activity of Akt and protein levels of Mfn2 and heme oxygenase 1 (HO-1). Moreover, inhibition of Akt reversed the protective role of THF, increased mito-ROS levels, and repressed Mfn2 and HO-1 expression. Therefore, we conclude, THF relieves DOX-induced cardiotoxicity and improves mitochondrial function by activating Akt-mediated Mfn2 and HO-1 pathways. This finding provides promising therapeutic insights for DOX-induced cardiac dysfunction.

Galangin attenuates adenine-induced chronic renal failure by inhibiting transforming growth factor beta (TGF-β) expression

Introduction: Galangin (3,5,7 tri-hydroxy flavone), naturally active flavonoid is derived from the rhizomes of Alpinia officinarum is proven to be effective antioxidant, anti-inflammatory, anti-cancer. However, protective effects of galangin in chronic renal failure (CRF) is not explored. Objectives: This study is aimed to investigate the nephroprotective activity of galangin in adenine-induced CRF rats. Materials and Methods: Adenine induced rats were administered galangin 20 mg/kg and 40 mg/kg body weight (BW) serum renal and hepatic parameters, and renal antioxidant-lipid peroxidation parameters, histological studies were carried out. The mechanism of action was investigated by flow cytometry. Results: Galangin has normalized serum renal and hepatic parameters, reduced oxidative stress and lipid peroxidation. Histopathology confirms nephroprotection. The percentage number of cells expressing transforming growth factor beta (TGF-β) was reduced with galangin treatment. Conclusion: Galangin exerts nephroprotection in adenine induced CRF by inhibiting TGF-β expression.

Retraction to “Aluminium(iii), Fe(ii) Complexes and Dyeing Properties of Apigenin(5,7,4′-trihydroxy flavone)”

Retraction to “Aluminium(iii), Fe(ii) Complexes and Dyeing Properties of Apigenin(5,7,4′-trihydroxy flavone)”

5,6,7 trihydroxy flavone armoured neurodegeneration caused by Quinolinic acid induced huntington’s like disease in rat striatum - reinstating the level of brain neurotrophins with special reference to cognitive-socio behaviour, biochemical and histopathological aspects

Huntington Disease (HD), a predominant Neurodegenerative Disorder which might be induced by endogenous neurotoxin called Quinolinic Acid (QA), an N-methyl-D aspartate receptor (NMDAR) agonist, the bilaterally intrastriatal administration (200 nm/2 μL of saline) offers rise to the toxic events like neuronal death, neuroinflammation by inflicting excitotoxicity and oxidative stress in the striatum of male Wistar rats by exhibiting the behavioural changes which was accessed by rotarod, open field analysis. In this study, the neuropharmacological effect of Baicalein (BC) against QA induced HD was evaluated. Baicalein (BC), scientifically 5,6,7 trihydroxy flavone present naturally in the edible plants like Scutellaria baicalensis and Oroxylum indicum possess a better neuroprotective effect in the dosage of 10 mg/kg and 30 mg/kg intraperitoneally in the striatum of HD induced rats. This study proved that BC is efficient to revive the level of enzymatic & non-enzymatic antioxidants and mitochondrial complexes by decreasing the number of inflammatory mediators such as MDA, protein carbonyls and Nitric Oxide at the significance of P < 0.01 and restores the amount of BDNF and GDNF thereby preventing the neurophysiological changes which were analysed by haematoxylin & eosin staining. Thus finally, the protective effect of Baicalein displays the up-gradation of psychological and behavioural changes induced by QA.

The subgroup of 2′-hydroxy-flavonoids: Molecular diversity, mechanism of action, and anticancer properties

Flavonoids are abundant in nature, structurally very diversified and largely investigated. However, the subgroup of 2′-hydroxyflavonoids is much less known and not frequently studied. The present review identifies the major naturally-occurring and synthetic 2′-hydroxyflavonoid derivatives and discusses their structural characteristics and biological properties, with a focus on anticancer activities. The pharmacological properties of 2′-hydroxyflavone (2′-HF) and 2′-hydroxyflavanone (2′-HFa) are detailed. Upon binding to the Ral-interacting protein Rlip implicated in the transport of glutathione conjugates, 2′-HFa inhibits tumor cell proliferation and restrict tumor growth, in particular in breast cancer models. Among the synthetic derivatives, the characteristics of the anticancer product 2D08 (2′,3′,4′-trihydroxy flavone) are detailed to shed light on the molecular mechanism of action of this compound, as a regulator of protein SUMOylation. Inhibition of protein SUMOylation by 2D08 blocks cancer cell migration and invasion, and the compound greatly enhances the anticancer effects of conventional cytotoxic drugs like etoposide. The structural role of the 2′-hydroxyl group on the phenyl C-ring of the flavonoid is discussed, notably the capacity to engage intramolecular H-bonding interactions with the O1 atom on the B-ring of the chromone unit (or the oxygen of a 3-OH group when it is presents). The 2′-hydroxyl group of flavonoid appears as a regulator of the conformational freedom between the bicyclic A-B unit and the appended phenyl C-ring, favoring the planarity of the molecule. It is an essential group accounting for the biological properties of 2′-HF, 2′-HFa and structurally related compounds. This review shed light on 2′-hydroxyflavonoids to encourage their use and chemical development.

BDNF Outperforms TrkB Agonist 7,8,3'-THF in Preserving the Auditory Nerve in Deafened Guinea Pigs.

In deaf subjects using a cochlear implant (CI) for hearing restoration, the auditory nerve is subject to degeneration, which may negatively impact CI effectiveness. This nerve degeneration can be reduced by neurotrophic treatment. Here, we compare the preservative effects of the naturally occurring tyrosine receptor kinase B (TrkB) agonist brain-derived neurotrophic factor (BDNF) and the small-molecule TrkB agonist 7,8,3′-trihydroxyflavone (THF) on the auditory nerve in deafened guinea pigs. THF may be more effective than BDNF throughout the cochlea because of better pharmacokinetic properties. The neurotrophic compounds were delivered by placement of a gelatin sponge on the perforated round window membrane. To complement the histology of spiral ganglion cells (SGCs), electrically evoked compound action potential (eCAP) recordings were performed four weeks after treatment initiation. We analyzed the eCAP inter-phase gap (IPG) effect and measures derived from pulse-train evoked eCAPs, both indicative of SGC healthiness. BDNF but not THF yielded a significantly higher survival of SGCs in the basal cochlear turn than untreated controls. Regarding IPG effect and pulse-train responses, the BDNF-treated animals exhibited more normal responses than both untreated and THF-treated animals. We have thus confirmed the protective effect of BDNF, but we have not confirmed previously reported protective effects of THF with our clinically applicable delivery method.

Isothymusin, a Potential Inhibitor of Cancer Cell Proliferation: An In Silico and In Vitro Investigation.

Since centuries plant-based compounds are known for the treatment of cancer in both traditional and contemporary medicine. The problems like target non-specificity and toxicity are well-known regarding anticancer drugs. Therefore, target specific search of novel entities is constant. Isothymusin is a dimethoxy, trihydroxy flavone present in plants like Ocimum sanctum, and Limnophilla geoffrayi. There are limited reports available on the anticancer potential of isothymusin. The effects of isothymusin on redox status, cell cytotoxicity, and targets involved in the promotion and progression of the cancer cells have been investigated. Antiproliferative efficacy was evaluated by MTT, Neutral Red Uptake, and Sulforhodamine-B assays. The spectrophotometric methods were adopted to study the effect against selected targets. Redox activity was assessed by in vitro antioxidant assays and the interaction study, ADMET profiling, and toxicity assessments were done in silico. Isothymusin scavenges the radicals, i.e., DPPH and nitric oxide with moderate ferric reducing potential. It affected the proliferation of leukemia, colon, skin, and breast cancer cell lines by more than 50% but moderately affected prostate, kidney, lung, hepatic, and breast adenocarcinoma (up to 48%). Isothymusin inhibited the enzymes associated with the promotion stage of cancer, including cycloxygenase- 2 and lipoxygenase-5. Additionally, it also inhibited the activity of proliferation markers like cathepsin- D, dihydrofolate reductase, hyaluronidase, and ornithine-decarboxylase. Besides, in silico studies supported the in vitro enzyme inhibition assays outcome. Toxicity studies showed promising results of chemical descriptors and non-skin-irritant, moderate ocular-irritancy, and in vitro Ames test confirmed non-mutagenic nature. Isothymusin showed radical scavenging and anti-proliferative activities, which may be taken up as a phytochemical lead for the synthesis of analogues possessing enhanced anticancer potential.

Age-Dependency of Neurite Outgrowth in Postnatal Mouse Cochlear Spiral Ganglion Explants.

Background: The spatial gap between cochlear implants (CIs) and the auditory nerve limits frequency selectivity as large populations of spiral ganglion neurons (SGNs) are electrically stimulated synchronously. To improve CI performance, a possible strategy is to promote neurite outgrowth toward the CI, thereby allowing a discrete stimulation of small SGN subpopulations. Brain-derived neurotrophic factor (BDNF) is effective to stimulate neurite outgrowth from SGNs. Method: TrkB (tropomyosin receptor kinase B) agonists, BDNF, and five known small-molecule BDNF mimetics were tested for their efficacy in stimulating neurite outgrowth in postnatal SGN explants. To modulate Trk receptor-mediated effects, TrkB and TrkC ligands were scavenged by an excess of recombinant receptor proteins. The pan-Trk inhibitor K252a was used to block Trk receptor actions. Results: THF (7,8,3′-trihydroxyflavone) partly reproduced the BDNF effect in postnatal day 7 (P7) mouse cochlear spiral ganglion explants (SGEs), but failed to show effectiveness in P4 SGEs. During the same postnatal period, spontaneous and BDNF-stimulated neurite outgrowth increased. The increased neurite outgrowth in P7 SGEs was not caused by the TrkB/TrkC ligands, BDNF and neurotrophin-3 (NT-3). Conclusions: The age-dependency of induction of neurite outgrowth in SGEs was very likely dependent on presently unidentified factors and/or molecular mechanisms which may also be decisive for the age-dependent efficacy of the small-molecule TrkB receptor agonist THF.

6,7,4'-Trihydroxyflavone inhibits osteoclast formation and bone resorption in vitro and in vivo.

The balance between the osteoblasts and the osteoclasts is important for the maintenance of the skeleton of the human body. The osteoclasts absorb bone after differentiated into polymorphonuclear cells by the fusion of monocytes/macrophages. We have found that 6,7,4'-Trihydroxyflavone (THF), a compound from the heartwood of Dalbergia Odorifera inhibits receptor activator of NF-κB ligand (RANKL)-induced osteoclast differentiation, actin ring formation, and bone resorption in RAW 264.7 cells and bone marrow macrophage. THF significantly inhibited the c-Jun-N-terminal kinase signaling pathway without affecting extracellular signal-regulated kinase, p38, and AKT signaling. Moreover, THF inhibited the expression of c-Fos, nuclear factor-activated T cells cytoplasm 1, cathepsin K, and c-src by RANKL. We used a lipopolysaccharide (LPS)-induced bone loss model in mice. Consequently, bone volume per tissue volume, trabecular number's reduction was recovered in THF-treated mice, and trabecular separation's augmentation was also attenuated by THF administration. In summary, THF inhibits RANKL-induced osteoclast differentiation by MAPK signaling pathway and inhibits bone resorption by destroying the actin ring in mature osteoclasts. THF also prevented LPS-induced bone loss in a mice model. Thus, THF may be useful in the treatment of bone diseases associated with excessive osteoclast differentiation and bone resorption.

7, 8, 3'-Trihydroxyflavone protects H/R-induced apoptosis and induces in vivo growth of human embryonic stem cell-derived cardiomyocytes.

Cellular therapy of human embryonic stem cell-derived cardiomyocytes (hES-CMs) holds great promise for regenerating infarcted cardiac tissues. Yet, the major challenge remains as little cells survived after grafting. In this study, we examined whether treating hES-CMs with 7, 8, 3'-Trihydroxyflavone (THF) may improve hES-CMs developments both in vitro and in vivo. HES-CMs were differentiated in vitro, and treated with 5 μ59M THF for 24 h. The control hES-CMs were treated with PBS. Possible effect of THF on hES-CM differentiation was assessed by viability and western blot assays. HES-CMs were also treated with hypoxia/reoxygenation (H/R)-condition to induce apoptosis. The effect of THF on rescuing H/R-induced hES-CM apoptosis was assessed by TUNEL and western blot assays. HES-CMs were then grafted into infarcted rat hearts. The effect of THF on promoting in vivo growth of hES-CMs was examined by immunohistochemistry. THF pretreatment did not alter the differentiation process of hES-CMs. Under H/R condition, THF rescued hES-CM apoptosis, activated TrkA and TrkB signaling pathways through phosphorylation and induced VEGF production. In in vivo rat model of myocardial infarction, THF induced the growth of transplanted hES-CMs by promoting Cardiac Troponin I and CD31. THF has pro-cardiac effect on hES-CMs by protecting cells from H/R induced apoptosis and promoting in vivo growth of cell transplantation in infarcted hearts. These results may help optimizing the cellular therapy of using human embryonic stem cells to benefiting patients suffered from heart attack. This article is protected by copyright. All rights reserved.

7,8,3′-Trihydroxyflavone ameliorate oxidative stress in vivo and promotes neurite regeneration in vitro in rat retinal ganglion cells

In this study, we investigate the mechanism of 7,8,3′-Trihydroxyflavone (THF) on retinal oxidative stress and retinal ganglion cell (RGC) growth. Oxidative stress was induced by ocular hypertension (O.H.) in rat retina in vivo. Rats were then systemically injected with THF. We found THF ameliorated O.H.-induced oxidative stress in retina by reducing caspase-3 activity, downregulating MDA level and augmenting glutathione peroxidase expression. In addition, neonatal RGCs were cultured in vitro, and treated with THF. It was demonstrated that THF promoted neurite regeneration in RGC explant, and activated receptor kinase B (TrkB) signaling pathway through phosphorylation. In THF-treated RGC explant, application of TrkB antagonist, ANA12, effectively reversed the pro-neuronal effect of THF on promoting RGC neurite outgrowth, and inhibited TrkB signaling pathway through dephosphorylation. Thus, we concluded that THF could inhibit retinal oxidative stress and promote RGC growth through TrkB-dependent signaling pathway, thus providing a novel pharmaceutical candidate for glaucoma.

Chemical constituents from fresh tubers of Dioscorea bulbifera

Eighteen compounds were isolated from the 95% ethanol extract of fresh tubers of Dioscorea bulbifera by column chromatography over silica gel,Sephadex LH-20, and ODS. Their structures were elucidated by spectroscopic data analysis as 6-hydroxy-2,10,10-trimethoxy-anthracen-9-one(1), diosgenin (2), stigmasterol(3), 3, 7-dimethoxy-5, 3', 4'-trihydroxyflavone(4), 2, 7-dihydroxy-3, 4-dimethoxyphenanthrene(5), 3, 7-dihydroxy-2, 4-dimethoxy phenanthrene(6), 2, 7-dihydroxy-4-methoxyphenanthrene (7), 2, 7-dihydroxy-3, 4-dimethoxy-9, 10-dihydroxy phenanthrene(8), azelaic acid (9), 8-epidiosbulbin E acetate (10), 1, 7-bis-(4-hydroxyphenyl)-4E, 6E-heptadien-3-one(11), diosbulbin B(12), pentacosanoic acid 2', 3'-dihydroxypropyl ester(13), 2, 7-dihydroxy-4-methoxy-9, 10-dihydroxy-phenanthrene (14), 1, 7-bis-(4-hydroxyphenyl)-1E, 4E, 6E-heptatrien-3-one (15), 6-ethoxy-1H-pyrimidine-2, 4-dione (16), 3, 5, 4'-trihydroxy-bibenzyl (17), and diosbulbin F (18). Compound 1 is a new compound, and compounds 7, 9, 13, and 16 were isolated from this plant for the first time.

7, 8, 3'-Trihydroxyflavone Promotes Neurite Outgrowth and Protects Against Bupivacaine-Induced Neurotoxicity in Mouse Dorsal Root Ganglion Neurons.

Background7, 8, 3′-trihydroxyflavone (THF) is a novel pro-neuronal small molecule that acts as a TrkB agonist. In this study, we examined the effect of THF on promoting neuronal growth and protecting anesthetics-induced neurotoxicity in dorsal root ganglion (DRG) neurons in vitro.Material/MethodsNeonatal mouse DRG neurons were cultured in vitro and treated with various concentrations of THF. The effect of THF on neuronal growth was investigated by neurite outgrowth assay and Western blot. In addition, the protective effects of THF on bupivacaine-induced neurotoxicity were investigated by apoptosis TUNEL assay, neurite outgrowth assay, and Western blot, respectively.ResultsTHF promoted neurite outgrowth of DRG neurons in dose-dependent manner, with an EC50 concentration of 67.4 nM. Western blot analysis showed THF activated TrkB signaling pathway by inducing TrkB phosphorylation. THF also rescued bupivacaine-induced neurotoxicity by reducing apoptosis and protecting neurite retraction in DRG neurons. Furthermore, the protection of THF in bupivacaine-injured neurotoxicity was directly associated with TrkB phosphorylation in a concentration-dependent manner in DRG neurons.ConclusionsTHF has pro-neuronal effect on DRG neurons by promoting neurite growth and protecting against bupivacaine-induced neurotoxicity, likely through TrkB activation.

A flavonoid compound from Chrysosplenium nudicaule inhibits growth and induces apoptosis of the human stomach cancer cell line SGC-7901

Context: Gastric cancer remains highly prevalent, but treatment options are limited. Natural products have proved to be a rich source of anticancer drugs. Chrysosplenium nudicaule Ledeb. (Saxifragaceae) is a perennial herb that grows in the highlands of China. It has been used as a traditional Chinese medicine to treat digestive diseases for hundreds of years. Recent studies revealed that this herb had anticancer activity, and the flavonoids were speculated to be the effective components. 6,7,3′-Trimethoxy-3,5,4′-trihydroxy flavone (TTF) and 5,4′-dihydroxy-3,6,3′trimethoxy-flavone-7-O-β-d-glucoside (DTFG) are flavonoid compounds isolated from Chrysosplenium nudicaule.Objective: This study examined the effect of TTF and DTFG on SGC-7901 human stomach cancer cell in vitro to determine the anticancer and induction of apoptosis properties of TTF.Materials and methods: The proliferation of cells treated with 32, 16, 8, 4, and 2 μg/mL of TTF or DTFG for 24, 48, and 72 h was assessed by the MTT assay. After being treated with TTF, the apoptosis of SGC-7901 cells was assessed by acridine orange staining, ultrastructure, electrophoresis of DNA fragmentation, and flow cytometry.Results: Results indicated that TTF inhibited the growth of cancer cells with an IC50 value of 8.33 μg/mL after 72 h incubation. However, DTFG showed no inhibitory effect on the growth of the cancer cell. Further studies on TTF also confirmed that it was able to induce apoptosis of SGC-7901 cells at a concentration as low as 4 μg/mL.Discussion and conclusion: The apoptotic effect of TTF makes it a promising candidate for future chemotherapeutic application in treating stomach cancer.

Apigenin-induced apoptosis in A375 and A549 cells through selective action and dysfunction of mitochondria

We isolated apigenin (5,7,4'-trihydroxy flavone) from ethanolic extract of Lycopodium clavatum (LC) used as a homeopathic mother tincture for treatment of various diseases. We assessed the anticancer potentials of the compound using human malignant melanoma cell line A375 and a lung carcinoma cell line A549 and focussed on its putative molecular mechanism of action on apoptosis induction. We examined the cytotoxicity of apigenin in both cancer cells and normal peripheral blood mononuclear cells (PBMC). A375 cells were more prone to apigenin-induced apoptosis, as compared with A549 cells after 24 h of treatment, while PBMC showed little or no cytotoxicity to apigenin. We also evaluated the effects of apigenin on interaction with DNA by comparative analysis of circular dichroism spectral data and melting temperature profiles (Tm) of calf thymus DNA (CT-DNA) treated with or without apigenin. Reactive oxygen species (ROS) accumulation in mitochondria, super-oxide dismutase and total thiol group (GSH) activities were also analyzed. The apoptotic process involved mitochondrial pathway associated with apigenin-DNA interaction, DNA fragmentation, ROS accumulation, cytochrome c (cyt c) release and mitochondrial transmembrane potential depolarization, Bax, caspase 3, 9, PARP, up-regulation, Bcl-2 down-regulation and down-regulation of cyt c in the mitochondrial fraction. Results of mitochondrial inner membrane swelling measurements, intracellular ADP/ATP ratio and ATPase activity showed that in A549 cells, apigenin did not appear to directly target the mitochondrial oxidative phosphorylation system but rather acted at an upstream step to activate the mitochondrial apoptotic pathway. However, apigenin could directly target and impair mitochondrial function in A375 cells by breaking down their oxidative phosphorylation system. Collectively, these results suggest that apigenin exhibits anticancer potential in A375 and A549 cells that may be mediated through DNA interaction, damage and mitochondrial dysfunction either by direct or indirect action on mitochondrial oxidative phosphorylation system.

Extraction of natural color component from the bark of Belleric myrobalan (Terminalia bellerica): Kinetic and adsorption studies

Baicalein, a trihydroxy flavone from the bark of Terminalia bellerica was identified as a natural colorant. The potential of the natural color component on silk yarn was tested. Its properties of color fastness with regard to light, washing and crocking were investigated and found to be satisfactory. Thermodynamic parameters were evaluated. The positive value of enthalpy of dyeing suggests the endothermic nature of dyeing and the negative entropy implies that the dye molecules are orderly arranged on silk. The positive value of free energy confirms the affinity between the dye molecules and the protein content of silk. Further, adsorption studies were carried out to determine the best fit isotherm model for the present dyeing system. The Langmuir isotherm model fitted the experimental data very well with a relatively high regression coefficient compared to the Freundlich and Tempkin-Pyzhev isotherm models. In conclusion, the Terminalia bellerica bark can be used as a potential source of natural dye for silk.

Aluminium(III), Fe(II) Complexes and Dyeing Properties of Apigenin (5,7,4'-trihydroxy flavone)

Aluminium(III), Fe(II) Complexes and Dyeing Properties of Apigenin (5,7,4'-trihydroxy flavone)