Luteolin

1 Achyrocline sp. 2 Anagallis sp. 3 Antennaria sp. 4 Asphodelus sp. 5 Baptisia sp. 6 Chaerophyllum sp. 7 Chamaemelum sp. 8 Chamomilla sp. 9 Cirsium sp. 10 Crataegus sp. 11 Cuminum sp. 12 Cymbopogon sp. 13 Cynara sp. 14 Daphne sp. 15 Dendranthema sp. 16 Drimys sp. 17 Eclipta sp. 18 Equisetum sp. 19 Eriodictyon sp. 20 Euphrasia sp. 21 Galium sp. 22 Genista sp. 23 Ginkgo sp. 24 Hydnocarpus sp. 25 Hypericum sp. 26 Ilex sp. 27 Inula sp. 28 Lavandula sp. 29 Leucanthemum sp. 30 Linum sp. 31 Lippia sp. 32 Lycopodium sp. 33 Marchantia sp. 34 Mentha sp. 35 Meum sp. 36 Olea sp. 37 Ononis sp. 38 Perilla sp. 39 Persicaria sp. 40 Pimpinella sp. 41 Pinguicula sp. 42 Polygonum sp. 43 Rehmannia sp. 44 Reseda sp. 45 Rosmarinus sp. 46 Salix sp. 47 Salvia sp. 48 Tanacetum sp. 49 Tecoma sp. 50 Teucrium sp. 51 Thymus sp. 52 Trifolium sp. 53 Trigonella sp. 54 Verbascum sp. 55 Veronica sp.

Luteolin from Flos Chrysanthemi and its derivatives: New small molecule Bcl-2 protein inhibitors.[Pubmed:25193233]

Bioorg Med Chem Lett. 2014 Oct 1;24(19):4672-4677.

Over-expression of the Bcl-2 anti-apoptotic proteins is closely related to tumorigenesis and associated with drug resistance. Here we report that Luteolin, a main substance found in Flos Chrysanthemi, directly binds to and shows inhibitory activity against the Bcl-2 protein. We studied the binding mode of Luteolin and its derivatives with target proteins, their structure-activity relationship, and their effect on the human leukemia cell line HL-60. The results suggest that Luteolin and its derivatives with a benzyl group introduced to the B ring, are new small molecule Bcl-2 protein inhibitors, and their anti-tumor activity is likely related to their effect on the Bcl-2 protein.

Luteolin, a flavonoid with potential for cancer prevention and therapy.[Pubmed:18991571]

Curr Cancer Drug Targets. 2008 Nov;8(7):634-46.

Luteolin, 3',4',5,7-tetrahydroxyflavone, is a common flavonoid that exists in many types of plants including fruits, vegetables, and medicinal herbs. Plants rich in Luteolin have been used in Chinese traditional medicine for treating various diseases such as hypertension, inflammatory disorders, and cancer. Having multiple biological effects such as anti-inflammation, anti-allergy and anticancer, Luteolin functions as either an antioxidant or a pro-oxidant biochemically. The biological effects of Luteolin could be functionally related to each other. For instance, the anti-inflammatory activity may be linked to its anticancer property. Luteolin's anticancer property is associated with the induction of apoptosis, and inhibition of cell proliferation, metastasis and angiogenesis. Furthermore, Luteolin sensitizes cancer cells to therapeutic-induced cytotoxicity through suppressing cell survival pathways such as phosphatidylinositol 3'-kinase (PI3K)/Akt, nuclear factor kappa B (NF-kappaB), and X-linked inhibitor of apoptosis protein (XIAP), and stimulating apoptosis pathways including those that induce the tumor suppressor p53. These observations suggest that Luteolin could be an anticancer agent for various cancers. Furthermore, recent epidemiological studies have attributed a cancer prevention property to Luteolin. In this review, we summarize the progress of recent research on Luteolin, with a particular focus on its anticancer role and molecular mechanisms underlying this property of Luteolin.

Luteolin inhibits hyperglycemia-induced proinflammatory cytokine production and its epigenetic mechanism in human monocytes.[Pubmed:24623679]

Phytother Res. 2014 Sep;28(9):1383-91.

Hyperglycemia is a key feature in diabetes. Hyperglycemia has been implicated as a major contributor to several complications of diabetes. High glucose levels induce the release of proinflammatory cytokines. Luteolin is a flavone isolated from celery, green pepper, perilla leaf, and chamomile tea. Luteolin has been reported to possess antimutagenic, antitumorigenic, antioxidant, and anti-inflammatory properties. In this study, we investigated the effects of Luteolin on proinflammatory cytokine secretion and its underlying epigenetic regulation in high-glucose-induced human monocytes. Human monocytic (THP-1) cells were cultured under controlled (14.5 mM mannitol), normoglycemic (NG, 5.5 mM glucose), or hyperglycemic (HG, 20 mM glucose) conditions, in the absence or presence of Luteolin. Luteolin (3-10 muM) was added for 48 h. While hyperglycemic conditions significantly induced histone acetylation, NF-kappaB activation, and proinflammatory cytokine (IL-6 and TNF-alpha) release from THP-1 cells, Luteolin suppressed NF-kappaB activity and cytokine release. Luteolin also significantly reduced CREB-binding protein/p300 (CBP/p300) gene expression, as well as the levels of acetylation and histone acetyltransferase (HAT) activity of the CBP/p300 protein, which is a known NF-kappaB coactivator. These results suggest that Luteolin inhibits HG-induced cytokine production in monocytes, through epigenetic changes involving NF-kappaB. We therefore suggest that Luteolin may be a potential candidate for the treatment and prevention of diabetes and its complications.

Luteolin inhibits Cr(VI)-induced malignant cell transformation of human lung epithelial cells by targeting ROS mediated multiple cell signaling pathways.[Pubmed:25448439]

Toxicol Appl Pharmacol. 2014 Dec 1;281(2):230-41.

Hexavalent chromium [Cr(VI)] is a well-known human carcinogen associated with the incidence of lung cancer. Inhibition of metal induced carcinogenesis by a dietary antioxidant is a novel approach. Luteolin, a natural dietary flavonoid found in fruits and vegetables, possesses potent antioxidant and anti-inflammatory activity. We found that short term exposure of human bronchial epithelial cells (BEAS-2B) to Cr(VI) (5muM) showed a drastic increase in ROS generation, NADPH oxidase (NOX) activation, lipid peroxidation, and glutathione depletion, which were significantly inhibited by the treatment with Luteolin in a dose dependent manner. Treatment with Luteolin decreased AP-1, HIF-1alpha, COX-2, and iNOS promoter activity induced by Cr(VI) in BEAS-2B cells. In addition, Luteolin protected BEAS-2B cells from malignant transformation induced by chronic Cr(VI) exposure. Moreover, Luteolin also inhibited the production of pro-inflammatory cytokines (IL-1beta, IL-6, IL-8, TNF-alpha) and VEGF in chronic Cr(VI) exposed BEAS-2B cells. Western blot analysis showed that Luteolin inhibited multiple gene products linked to survival (Akt, Fak, Bcl-2, Bcl-xL), inflammation (MAPK, NF-kappaB, COX-2, STAT-3, iNOS, TNF-alpha) and angiogenesis (HIF-1alpha, VEGF, MMP-9) in chronic Cr(VI) exposed BEAS-2B cells. Nude mice injected with BEAS-2B cells chronically exposed to Cr(VI) in the presence of Luteolin showed reduced tumor incidence compared to Cr(VI) alone treated group. Overexpression of catalase (CAT) or SOD2, eliminated Cr(VI)-induced malignant transformation. Overall, our results indicate that Luteolin protects BEAS-2B cells from Cr(VI)-induced carcinogenesis by scavenging ROS and modulating multiple cell signaling mechanisms that are linked to ROS. Luteolin, therefore, serves as a potential chemopreventive agent against Cr(VI)-induced carcinogenesis.

Luteolin inhibits ROS-activated MAPK pathway in myocardial ischemia/reperfusion injury.[Pubmed:25476833]

Life Sci. 2015 Feb 1;122:15-25.

AIMS: Luteolin is a falconoid compound that has an antioxidant effect, but its contribution to ROS-activated MAPK pathways in ischemia/reperfusion injury is seldom reported. Here, we have confirmed that it exhibits an antioxidant effect in myocardial ischemia/reperfusion injury (MIRI) by inhibiting ROS-activated MAPK pathways. MAIN METHODS: We exposed rat hearts into the left anterior descending coronary artery (LAD) ligation for 30min followed by 1h of reperfusion. Observations were carried out using electrocardiography; detection of hemodynamic parameters; and testing levels of lactate dehydrogenase (LDH), creatine kinase (CK), total superoxide dismutase (T-SOD), and malondialdehyde (MDA). Mitogen-activated protein kinase (MAPK) pathway was measured by western blot and transmission electron microscopy was applied to observe the myocardial ultrastructure. Rat H9c2 cell in 95% N2 and 5% CO2 stimulated the MIRI. Oxidation system mRNA levels were measured by real-time PCR; mitochondrial membrane potential and apoptosis were measured by confocal microscopy and flow cytometry; western blot analysis was used to assay caspase-3, -8, and -9 and MAPK pathway protein expression; the MAPK pathway was inhibited using SB203580 (p38 MAPK inhibitor) and SP600125 (c-Jun NH2-terminal kinase inhibitor) before H9c2 cells were exposed to hypoxia/reoxygenation injury to show the modulation of the changes in ROS generation, cell viability and apoptosis. KEY FINDINGS: In vivo, Luteolin can ameliorate the impaired mitochondrial morphology, regulating the MAPK pathway to protect MIRI. In vitro, Luteolin can affect the oxidation system, mitochondrial membrane potential and MAPK pathway to anti-apoptosis. SIGNIFICANCE: These results reveal a ROS-MAPK mediated mechanism and mitochondrial pathway through which Luteolin can protect myocardial ischemia/reperfusion injury.

Biphasic effects of luteolin on interleukin-1beta-induced cyclooxygenase-2 expression in glioblastoma cells.[Pubmed:25409926]

Biochim Biophys Acta. 2015 Jan;1853(1):126-35.

Success in developing therapeutic approaches to target brain tumor-associated inflammation in patients has been limited. Given that the inflammatory microenvironment is a hallmark signature of solid tumor development, anti-inflammatory targeting strategies have been envisioned as preventing glioblastoma initiation or progression. Consumption of foods from plant origin is associated with reduced risk of developing cancers, a chemopreventive effect that is, in part, attributed to their high content of phytochemicals with potent anti-inflammatory properties. We explored whether Luteolin, a common flavonoid in many types of plants, may inhibit interleukin (IL)-1beta function induction of the inflammation biomarker cyclooxygenase (COX)-2. We found that IL-1beta triggered COX-2 expression in U-87 glioblastoma cells and synergized with Luteolin to potentiate or inhibit that induction in a biphasic manner. Luteolin pretreatment of cells inhibited IL-1beta-mediated phosphorylation of inhibitor of kappaB, nuclear transcription factor-kappaB (NF-kappaB) p65, extracellular signal-regulated kinase-1/2, and c-Jun amino-terminal kinase in a concentration-dependent manner. Luteolin also inhibited AKT phosphorylation and survivin expression, while it triggered both caspase-3 cleavage and expression of glucose-regulated protein 78. These effects were all potentiated by IL-1beta, in part through increased nuclear translocation of NF-kappaB p65. Finally, Luteolin was able to reduce IL-1 receptor gene expression, and treatment with IL-1 receptor antagonist or gene silencing of IL-1 receptor prevented IL-1beta/Luteolin-induced COX-2 expression. Our results document a novel adaptive cellular response to Luteolin, which triggers anti-survival and anti-inflammatory mechanisms that contribute to the chemopreventive properties of this diet-derived molecule.

Luteolin suppresses inflammation-associated gene expression by blocking NF-kappaB and AP-1 activation pathway in mouse alveolar macrophages.[Pubmed:17977562]

Life Sci. 2007 Nov 30;81(23-24):1602-14.

Luteolin, a plant flavonoid, has potent anti-inflammatory properties both in vitro and in vivo. However, the molecular mechanism of Luteolin-mediated immune modulation has not been fully understood. In this study, we examined the effects of Luteolin on the production of nitric oxide (NO) and prostaglandin E(2) (PGE(2)), as well as the expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) in mouse alveolar macrophage MH-S and peripheral macrophage RAW 264.7 cells. Luteolin dose-dependently inhibited the expression and production of these inflammatory genes and mediators in macrophages stimulated with lipopolysaccharide (LPS). Semi-quantitative reverse-transcription polymerase chain reaction (RT-PCR) assay further confirmed the suppression of LPS-induced TNF- alpha, IL-6, iNOS and COX-2 gene expression by Luteolin at a transcriptional level. Luteolin also reduced the DNA binding activity of nuclear factor-kappa B (NF-kappaB) in LPS-activated macrophages. Moreover, Luteolin blocked the degradation of IkappaB-alpha and nuclear translocation of NF-kappaB p65 subunit. In addition, Luteolin significantly inhibited the LPS-induced DNA binding activity of activating protein-1 (AP-1). We also found that Luteolin attenuated the LPS-mediated protein kinase B (Akt) and IKK phosphorylation, as well as reactive oxygen species (ROS) production. In sum, these data suggest that, by blocking NF-kappaB and AP-1 activation, Luteolin acts to suppress the LPS-elicited inflammatory events in mouse alveolar macrophages, and this effect was mediated, at least in part, by inhibiting the generation of reactive oxygen species. Our observations suggest a possible therapeutic application of this agent for treating inflammatory disorders in lung.

A critical role of luteolin-induced reactive oxygen species in blockage of tumor necrosis factor-activated nuclear factor-kappaB pathway and sensitization of apoptosis in lung cancer cells.[Pubmed:17296806]

Mol Pharmacol. 2007 May;71(5):1381-8.

Nuclear factor kappaB (NF-kappaB) activated by tumor necrosis factor (TNF) attenuates the TNF-induced apoptosis pathway. Therefore, blockage of NF-kappaB should improve the anticancer activity of TNF. Luteolin, a naturally occurring polyphenol flavonoid, has been reported to sensitize colorectal cancer cells to TNF-induced apoptosis through suppression of NF-kappaB; however, the mechanisms of this effect have not been well elucidated. In this article, we provide evidence showing a critical role of reactive oxygen species (ROS) accumulation induced by Luteolin in modulating TNF-activated pathways in lung cancer cells. Luteolin effectively suppressed NF-kappaB, whereas it potentiated the c-Jun N-terminal kinase (JNK) to increase apoptosis induced by TNF in lung cancer cells. Our results further demonstrate that Luteolin induced an early phase ROS accumulation via suppression of the cellular superoxide dismutase activity. It is noteworthy that suppression of ROS accumulation by ROS scavengers butylated hydroxyanisole, and N-acetyl-L-cysteine prevented the Luteolin-induced suppression of NF-kappaB and potentiation of JNK and significantly suppressed the synergistic cytotoxicity seen with cotreatment of Luteolin and TNF. Taken together, these results suggest that the accumulation of ROS induced by Luteolin plays a pivotal role in suppression of NF-kappaB and potentiation of JNK to sensitize lung cancer cells to undergo TNF-induced apoptosis.

Luteolin (Luteolol) is a flavanoid with anti-inflammatory, anti-cancer properties, including the induction of apoptosis and cell cycle arrest, and the inhibition of metastasis and angiogenesis, in several cancer cell lines, including human non-small lung cancer cells.

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