Guest guest Posted July 10, 2006 Report Share Posted July 10, 2006 Does anybody take luteolin? My new doc wants me to order it. Expensive. - Kate Eur J Pharmacol. 2006 Jul 10;541(1-2):95-105. Epub 2006 Apr 5. Related Articles, Links Click here to read Luteolin inhibits lipopolysaccharide actions on human gingival fibroblasts. Gutierrez-Venegas G, Kawasaki-Cardenas P, Rita Arroyo-Cruz S, Maldonado-Frias S. Laboratorio de Bioquimica de la Division de Estudios de Posgrado de la Facultad de Odontologia, Universidad Nacional Autonoma de Mexico, Ciudad Universitaria, 04510 Mexico, D.F., Mexico. Periodontal disease comprises a group of infections that lead to inflammation of the gingiva, periodontal tissue destruction, and in severe cases is accompanied by alveolar bone loss with tooth exfoliation. Actinobacillus actinomycetemcomitans is a Gram-negative microorganism, which possesses and produces lipopolysaccharide (LPS) molecules that play a key role in disease development. Human gingival fibroblasts are the major constituents of gingival connective tissue and may interact directly with bacteria and bacterial products including LPS. Flavonoids possess antioxidant and anti-inflammatory properties that reduce inflammatory molecule expression in macrophages and monocytes. In this study, we evaluated the ability of diverse flavonoids to regulate nitric oxide production of LPS- stimulated human gingival fibroblasts, and studied the effect of luteolin on diminish phosphorylation in mitogen-activated protein kinase (MAPK) family members as well as in protein kinase B (Akt), nuclear factor kappa B (NF-kappaB) activation, inducible nitric oxide synthase (NOS) expression, and nitric oxide (NO) synthesis. We also found that pretreatment with three flavonoids, including quercetin, genistein, and luteolin, blocked nitric oxide synthesis in a dose- dependent fashion. Luteolin exerted the strongest blocking action on expression of this inflammatory mediator. Luteolin pretreatment attenuated LPS-induced extracellular signal-regulated kinase, p38, and Akt phosphorylation. LPS treatment of human gingival fibroblasts resulted in NF-kappaB translocation. Cell pretreatment with luteolin abolished LPS effects on NF-kappaB translocation. In addition, luteolin treatment blocked LPS-induced cellular proliferation inhibition without affecting genetic material integrity. We concluded that luteolin interferes with LPS signaling pathways, reducing activation of several mitogen-activated protein kinase family members, and inhibits inflammatory mediator expression. PMID: 16762341 [PubMed - in process] 1: J Pharmacol Exp Ther. 2001 Jan;296(1):181-7.Click here to read Links Luteolin inhibits an endotoxin-stimulated phosphorylation cascade and proinflammatory cytokine production in macrophages. * Xagorari A, * Papapetropoulos A, * Mauromatis A, * Economou M, * Fotsis T, * Roussos C. " P. Livanos " Laboratory, Evangelismos Hospital, Department of Critical Care and Pulmonary Services, University of Athens, Athens, Greece. Flavonoids are naturally occurring polyphenolic compounds with a wide distribution throughout the plant kingdom. In the present study, we compared the ability of several flavonoids to modulate the production of proinflammatory molecules from lipopolysaccharide (LPS)- stimulated macrophages and investigated their mechanism(s) of action. Pretreatment of RAW 264.7 with luteolin, luteolin-7-glucoside, quercetin, and the isoflavonoid genistein inhibited both the LPS- stimulated TNF-alpha and interleukin-6 release, whereas eriodictyol and hesperetin only inhibited TNF-alpha release. From the compounds tested luteolin and quercetin were the most potent in inhibiting cytokine production with an IC(50) of less than 1 and 5 microM for TNF-alpha release, respectively. To determine the mechanisms by which flavonoids inhibit LPS signaling, we used luteolin and determined its ability to interfere with total protein tyrosine phosphorylation as well as Akt phosphorylation and nuclear factor-kappaB activation. Pretreatment of the cells with luteolin attenuated LPS-induced tyrosine phosphorylation of many discrete proteins. Moreover, luteolin inhibited LPS-induced phosphorylation of Akt. Treatment of macrophages with LPS resulted in increased IkappaB-alpha phosphorylation and reduced the levels of IkappaB-alpha. Pretreatment of cells with luteolin abolished the effects of LPS on IkappaB-alpha. To determine the functional relevance of the phosphorylation events observed with IkappaB-alpha, macrophages were transfected either with a control vector or a vector coding for the luciferase reporter gene under the control of kappaB cis-acting elements. Incubation of transfected RAW 264.7 cells with LPS increased luciferase activity in a luteolin-sensitive manner. We conclude that luteolin inhibits protein tyrosine phosphorylation, nuclear factor-kappaB-mediated gene expression and proinflammatory cytokine production in murine macrophages. PMID: 11123379 [PubMed - indexed for MEDLINE] 1: Br J Pharmacol. 2002 Aug;136(7):1058-64.Click here to read Links Inhibition of LPS-stimulated pathways in macrophages by the flavonoid luteolin. * Xagorari A, * Roussos C, * Papapetropoulos A. P. Livanos Laboratory, Evangelismos Hospital, Department of Critical Care and Pulmonary Services, School of Medicine, Ploutarchou 3, 5th floor, University of Athens, Athens, Greece 10675. 1: We have previously shown that the flavonoid luteolin inhibits the expression of pro-inflammatory molecules induced by LPS. In the present study we tested the ability of luteolin to block signalling pathways implicated in LPS-induced inflammatory gene expression in macrophages. 2: Exposure of the murine macrophage cell line RAW 264.7 to LPS increased phosphorylation of the mitogen-activated protein kinase family members ERK1/2, p38 and JNK1/2 in a time-dependent manner. Pretreatment of RAW 264.7 with luteolin inhibited the LPS- induced ERK1/2 and p38, but not JNK1/2, phosphorylation, and blocked the LPS-induced TNF-alpha release. 3: To investigate which of these pathways contribute to the inhibitory effects of luteolin on TNF- alpha release, cells were pretreated with pharmacological inhibitors of these pathways; PD98059 and SB203580 when used alone failed to inhibit TNF-alpha release, whereas pretreatment with both agents attenuated TNF-alpha release. 4: We have previously shown that luteolin blocks Akt phosphorylation in response to LPS in RAW 264.7 macrophages. To determine the role of Akt in TNF-alpha release, cells were transiently transfected with a dominant negative form of Akt (K179M). Overexpression of K179M Akt did not alter LPS-induced TNF- alpha release, suggesting that inhibition of this kinase does not mediate the inhibitory action of luteolin. 5: In addition, DRB (a pharmacological inhibitor of CK2) blocked TNF-alpha release in a concentration-dependent manner, whereas co-treatment of cells with luteolin and DRB did not have an additive effect. 6: We conclude that luteolin interferes with LPS signalling by reducing the activation of several MAPK family members and that its inhibitory action on TNF- alpha release correlates with inhibition of ERK, p38 and CK2 activation. PMID: 12145106 [PubMed - indexed for MEDLINE] Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 10, 2006 Report Share Posted July 10, 2006 I just began taking it about 3 weeks ago. My Dr. has it compounded so it is not quite as expensive. Email me and I will tell you who my Dr. is. I think it is helping me. I am very optimistic. Marie --- Kate <KateDunlay@...> wrote: > Does anybody take luteolin? My new doc wants me to > order it. Expensive. > > - Kate > > Eur J Pharmacol. 2006 Jul 10;541(1-2):95-105. Epub > 2006 Apr 5. > Related Articles, Links > Click here to read > Luteolin inhibits lipopolysaccharide actions on > human gingival > fibroblasts. > > Gutierrez-Venegas G, Kawasaki-Cardenas P, Rita > Arroyo-Cruz S, > Maldonado-Frias S. > > Laboratorio de Bioquimica de la Division de > Estudios de Posgrado > de la Facultad de Odontologia, Universidad Nacional > Autonoma de > Mexico, Ciudad Universitaria, 04510 Mexico, D.F., > Mexico. > > Periodontal disease comprises a group of > infections that lead to > inflammation of the gingiva, periodontal tissue > destruction, and in > severe cases is accompanied by alveolar bone loss > with tooth > exfoliation. Actinobacillus actinomycetemcomitans is > a Gram-negative > microorganism, which possesses and produces > lipopolysaccharide (LPS) > molecules that play a key role in disease > development. Human gingival > fibroblasts are the major constituents of gingival > connective tissue > and may interact directly with bacteria and > bacterial products > including LPS. Flavonoids possess antioxidant and > anti-inflammatory > properties that reduce inflammatory molecule > expression in > macrophages and monocytes. In this study, we > evaluated the ability of > diverse flavonoids to regulate nitric oxide > production of LPS- > stimulated human gingival fibroblasts, and studied > the effect of > luteolin on diminish phosphorylation in > mitogen-activated protein > kinase (MAPK) family members as well as in protein > kinase B (Akt), > nuclear factor kappa B (NF-kappaB) activation, > inducible nitric oxide > synthase (NOS) expression, and nitric oxide (NO) > synthesis. We also > found that pretreatment with three flavonoids, > including quercetin, > genistein, and luteolin, blocked nitric oxide > synthesis in a dose- > dependent fashion. Luteolin exerted the strongest > blocking action on > expression of this inflammatory mediator. Luteolin > pretreatment > attenuated LPS-induced extracellular > signal-regulated kinase, p38, > and Akt phosphorylation. LPS treatment of human > gingival fibroblasts > resulted in NF-kappaB translocation. Cell > pretreatment with luteolin > abolished LPS effects on NF-kappaB translocation. In > addition, > luteolin treatment blocked LPS-induced cellular > proliferation > inhibition without affecting genetic material > integrity. We concluded > that luteolin interferes with LPS signaling > pathways, reducing > activation of several mitogen-activated protein > kinase family > members, and inhibits inflammatory mediator > expression. > > PMID: 16762341 [PubMed - in process] > > 1: J Pharmacol Exp Ther. 2001 Jan;296(1):181-7.Click > here to read Links > Luteolin inhibits an endotoxin-stimulated > phosphorylation > cascade and proinflammatory cytokine production in > macrophages. > > * Xagorari A, > * Papapetropoulos A, > * Mauromatis A, > * Economou M, > * Fotsis T, > * Roussos C. > > " P. Livanos " Laboratory, Evangelismos > Hospital, > Department of Critical Care and Pulmonary Services, > University of > Athens, Athens, Greece. > > Flavonoids are naturally occurring polyphenolic > compounds with a > wide distribution throughout the plant kingdom. In > the present study, > we compared the ability of several flavonoids to > modulate the > production of proinflammatory molecules from > lipopolysaccharide (LPS)- > stimulated macrophages and investigated their > mechanism(s) of action. > Pretreatment of RAW 264.7 with luteolin, > luteolin-7-glucoside, > quercetin, and the isoflavonoid genistein inhibited > both the LPS- > stimulated TNF-alpha and interleukin-6 release, > whereas eriodictyol > and hesperetin only inhibited TNF-alpha release. > From the compounds > tested luteolin and quercetin were the most potent > in inhibiting > cytokine production with an IC(50) of less than 1 > and 5 microM for > TNF-alpha release, respectively. To determine the > mechanisms by which > flavonoids inhibit LPS signaling, we used luteolin > and determined its > ability to interfere with total protein tyrosine > phosphorylation as > well as Akt phosphorylation and nuclear > factor-kappaB activation. > Pretreatment of the cells with luteolin attenuated > LPS-induced > tyrosine phosphorylation of many discrete proteins. > Moreover, > luteolin inhibited LPS-induced phosphorylation of > Akt. Treatment of > macrophages with LPS resulted in increased > IkappaB-alpha > phosphorylation and reduced the levels of > IkappaB-alpha. Pretreatment > of cells with luteolin abolished the effects of LPS > on IkappaB-alpha. > To determine the functional relevance of the > phosphorylation events > observed with IkappaB-alpha, macrophages were > transfected either with > a control vector or a vector coding for the > luciferase reporter gene > under the control of kappaB cis-acting elements. > Incubation of > transfected RAW 264.7 cells with LPS increased > luciferase activity in > a luteolin-sensitive manner. We conclude that > luteolin inhibits > protein tyrosine phosphorylation, nuclear > factor-kappaB-mediated gene > expression and proinflammatory cytokine production > in murine > macrophages. > > PMID: 11123379 [PubMed - indexed for MEDLINE] > > 1: Br J Pharmacol. 2002 Aug;136(7):1058-64.Click > here to read Links > Inhibition of LPS-stimulated pathways in > macrophages by the > flavonoid luteolin. > > * Xagorari A, > * Roussos C, > * Papapetropoulos A. > > P. Livanos Laboratory, Evangelismos > Hospital, Department > of Critical Care and Pulmonary Services, School of > Medicine, > Ploutarchou 3, 5th floor, University of Athens, > Athens, Greece 10675. > > 1: We have previously shown that the flavonoid > luteolin inhibits > the expression of pro-inflammatory molecules induced > by LPS. In the > present study we tested the ability of luteolin to > block signalling > pathways implicated in LPS-induced inflammatory gene > expression in > macrophages. 2: Exposure of the murine macrophage > cell line RAW 264.7 > to LPS increased phosphorylation of the > mitogen-activated protein > kinase family members ERK1/2, p38 and JNK1/2 in a > time-dependent > manner. Pretreatment of RAW 264.7 with luteolin > inhibited === message truncated === __________________________________________________ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 10, 2006 Report Share Posted July 10, 2006 I don't know much about it, but if it does what's claimed, anti-inflammatory, andtioxidant, immunomodulator (calms immune hyperactivity), then it sounds good. I saw it referenced along with Quercetin, which is a supplement that , the vet, is excited about. Quercetin seemed to exacerbate my own symptoms, but seems to really help with some people according to . I don't know if the two substances are closely related or just similar in action. Your doc sounds pretty informed. If you do take it, please report back any results. penny Wikepedia Luteolin classified as a bioflavonoid, and is thought to play an important role in the human body as an antioxidant, a free radical scavenger, an agent in the prevention of inflammation, a promoter of carbohydrate metabolism, and an immune system modulator. These characteristics of luteolin are also believed to play an important part in the prevention of cancer. Multiple research experiments describe luteolin as a biochemical agent that can dramatically reduce inflammation and the symptoms of septic shock. Retrieved from "http://en.wikipedia.org/wiki/Luteolin" 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.Biochem Pharmacol. 2005 Jan 15;69(2):241-8. http://www.raysahelian.com/luteolin.html Kate <KateDunlay@...> wrote: Does anybody take luteolin? My new doc wants me to order it. Expensive.- KateEur J Pharmacol. 2006 Jul 10;541(1-2):95-105. Epub 2006 Apr 5. Related Articles, LinksClick here to readLuteolin inhibits lipopolysaccharide actions on human gingival fibroblasts.Gutierrez-Venegas G, Kawasaki-Cardenas P, Rita Arroyo-Cruz S, Maldonado-Frias S.Laboratorio de Bioquimica de la Division de Estudios de Posgrado de la Facultad de Odontologia, Universidad Nacional Autonoma de Mexico, Ciudad Universitaria, 04510 Mexico, D.F., Mexico.Periodontal disease comprises a group of infections that lead to inflammation of the gingiva, periodontal tissue destruction, and in severe cases is accompanied by alveolar bone loss with tooth exfoliation. Actinobacillus actinomycetemcomitans is a Gram-negative microorganism, which possesses and produces lipopolysaccharide (LPS) molecules that play a key role in disease development. Human gingival fibroblasts are the major constituents of gingival connective tissue and may interact directly with bacteria and bacterial products including LPS. Flavonoids possess antioxidant and anti-inflammatory properties that reduce inflammatory molecule expression in macrophages and monocytes. In this study, we evaluated the ability of diverse flavonoids to regulate nitric oxide production of LPS- stimulated human gingival fibroblasts, and studied the effect of luteolin on diminish phosphorylation in mitogen-activated protein kinase (MAPK) family members as well as in protein kinase B (Akt), nuclear factor kappa B (NF-kappaB) activation, inducible nitric oxide synthase (NOS) expression, and nitric oxide (NO) synthesis. We also found that pretreatment with three flavonoids, including quercetin, genistein, and luteolin, blocked nitric oxide synthesis in a dose- dependent fashion. Luteolin exerted the strongest blocking action on expression of this inflammatory mediator. Luteolin pretreatment attenuated LPS-induced extracellular signal-regulated kinase, p38, and Akt phosphorylation. LPS treatment of human gingival fibroblasts resulted in NF-kappaB translocation. Cell pretreatment with luteolin abolished LPS effects on NF-kappaB translocation. In addition, luteolin treatment blocked LPS-induced cellular proliferation inhibition without affecting genetic material integrity. We concluded that luteolin interferes with LPS signaling pathways, reducing activation of several mitogen-activated protein kinase family members, and inhibits inflammatory mediator expression.PMID: 16762341 [PubMed - in process]1: J Pharmacol Exp Ther. 2001 Jan;296(1):181-7.Click here to read LinksLuteolin inhibits an endotoxin-stimulated phosphorylation cascade and proinflammatory cytokine production in macrophages.* Xagorari A,* Papapetropoulos A,* Mauromatis A,* Economou M,* Fotsis T,* Roussos C." P. Livanos" Laboratory, Evangelismos Hospital, Department of Critical Care and Pulmonary Services, University of Athens, Athens, Greece.Flavonoids are naturally occurring polyphenolic compounds with a wide distribution throughout the plant kingdom. In the present study, we compared the ability of several flavonoids to modulate the production of proinflammatory molecules from lipopolysaccharide (LPS)- stimulated macrophages and investigated their mechanism(s) of action. Pretreatment of RAW 264.7 with luteolin, luteolin-7-glucoside, quercetin, and the isoflavonoid genistein inhibited both the LPS- stimulated TNF-alpha and interleukin-6 release, whereas eriodictyol and hesperetin only inhibited TNF-alpha release. From the compounds tested luteolin and quercetin were the most potent in inhibiting cytokine production with an IC(50) of less than 1 and 5 microM for TNF-alpha release, respectively. To determine the mechanisms by which flavonoids inhibit LPS signaling, we used luteolin and determined its ability to interfere with total protein tyrosine phosphorylation as well as Akt phosphorylation and nuclear factor-kappaB activation. Pretreatment of the cells with luteolin attenuated LPS-induced tyrosine phosphorylation of many discrete proteins. Moreover, luteolin inhibited LPS-induced phosphorylation of Akt. Treatment of macrophages with LPS resulted in increased IkappaB-alpha phosphorylation and reduced the levels of IkappaB-alpha. Pretreatment of cells with luteolin abolished the effects of LPS on IkappaB-alpha. To determine the functional relevance of the phosphorylation events observed with IkappaB-alpha, macrophages were transfected either with a control vector or a vector coding for the luciferase reporter gene under the control of kappaB cis-acting elements. Incubation of transfected RAW 264.7 cells with LPS increased luciferase activity in a luteolin-sensitive manner. We conclude that luteolin inhibits protein tyrosine phosphorylation, nuclear factor-kappaB-mediated gene expression and proinflammatory cytokine production in murine macrophages.PMID: 11123379 [PubMed - indexed for MEDLINE]1: Br J Pharmacol. 2002 Aug;136(7):1058-64.Click here to read LinksInhibition of LPS-stimulated pathways in macrophages by the flavonoid luteolin.* Xagorari A,* Roussos C,* Papapetropoulos A. P. Livanos Laboratory, Evangelismos Hospital, Department of Critical Care and Pulmonary Services, School of Medicine, Ploutarchou 3, 5th floor, University of Athens, Athens, Greece 10675.1: We have previously shown that the flavonoid luteolin inhibits the expression of pro-inflammatory molecules induced by LPS. In the present study we tested the ability of luteolin to block signalling pathways implicated in LPS-induced inflammatory gene expression in macrophages. 2: Exposure of the murine macrophage cell line RAW 264.7 to LPS increased phosphorylation of the mitogen-activated protein kinase family members ERK1/2, p38 and JNK1/2 in a time-dependent manner. Pretreatment of RAW 264.7 with luteolin inhibited the LPS- induced ERK1/2 and p38, but not JNK1/2, phosphorylation, and blocked the LPS-induced TNF-alpha release. 3: To investigate which of these pathways contribute to the inhibitory effects of luteolin on TNF- alpha release, cells were pretreated with pharmacological inhibitors of these pathways; PD98059 and SB203580 when used alone failed to inhibit TNF-alpha release, whereas pretreatment with both agents attenuated TNF-alpha release. 4: We have previously shown that luteolin blocks Akt phosphorylation in response to LPS in RAW 264.7 macrophages. To determine the role of Akt in TNF-alpha release, cells were transiently transfected with a dominant negative form of Akt (K179M). Overexpression of K179M Akt did not alter LPS-induced TNF- alpha release, suggesting that inhibition of this kinase does not mediate the inhibitory action of luteolin. 5: In addition, DRB (a pharmacological inhibitor of CK2) blocked TNF-alpha release in a concentration-dependent manner, whereas co-treatment of cells with luteolin and DRB did not have an additive effect. 6: We conclude that luteolin interferes with LPS signalling by reducing the activation of several MAPK family members and that its inhibitory action on TNF- alpha release correlates with inhibition of ERK, p38 and CK2 activation.PMID: 12145106 [PubMed - indexed for MEDLINE] Quote Link to comment Share on other sites More sharing options...
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