Chemopreventive effect of dietary flavonoid morin on chemically induced rat tongue carcinogenesis

Kawabata, Ken‐ichi; Tanaka, Takuji; Honjo, Satoshi; Kakumoto, Mikio; Hara, Akira; Makita, Hiroki; Tatematsu, Norichika; Ushida, Jun; Tsuda, Hiroyuki; Mori, Hideki

doi:10.1002/(sici)1097-0215(19991029)83:3<381::aid-ijc14>3.0.co;2-x

Cited by 80 publications

(35 citation statements)

References 25 publications

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“…It was reported that morin could modulate the activities of the metabolic enzymes, including cytochrome P450 (Hodek et al, 2002), and it is also an antioxidant that protects various human cells, like myocytes, endothelial cells, hepatocytes and erythrocytes, against oxidative damages (Wu et al, 1993;Kitagawa et al, 2004). Moreover, morin acts as a chemopreventive agent against oral carcinogenesis in vitro and in vivo (Kawabata et al, 1999;Brown et al, 2003). Our study shows that pretreatment with morin, a flavonoid ameliorates adenosine triphosphatases and glycoproteins and exhibits beneficial role on cardiac mitochondrial function during ISO induced myocardial infarction in male Wistar rats (Al-Numair et al, 2012; Al-Numair et al, 2012).…”

Section: Introductionmentioning

confidence: 57%

Morin, A Flavonoid, On Lipid Peroxidation And Antioxidant Status In Experimental Myocardial Ischemic Rats

Al‐Numair¹,

Govindasamy²,

Alsaif³

et al. 2014

Afr. J. Trad. Compl. Alt. Med.

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Background: Myocardial infarction affects a large population in the world. Lipid peroxide metabolism plays an important role in the pathology of myocardial infarction. Objective: The present study was designed to investigate the antioxidant potential of morin, a flavonoid in isoproterenol (ISO)-induced myocardial infarction (MI), in rats. Materials and Methods: Male albino Wistar rats were pre-treated with morin (40 mg/kg), daily for a period of 30 days. After the treatment period, ISO (85 mg/kg), was subcutaneously injected in rats at an interval of 24 h for 2 days. R e s u l t s : ISO-administered rats showed elevated levels of thiobarbituric acid reactive substances (TBARS), and lipid hydro-peroxide (LOOH), in plasma and heart. Pretreatment with morin, the above changes were significantly reduced to near normal level. ISOadministered rats showed decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) in heart. In addition, decrease the levels non enzymatic antioxidants such as reduced glutathione (GSH), vitamin C and vitamin E in plasma and heart while ceruloplasmin in plasma. Conclusion: Pretreatment with morin, reversed these above biochemical changes towards normalcy. These findings revealed that, the morin possess antioxidant activity in experimentally induced cardiac toxicity.

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Section: Introductionmentioning

confidence: 57%

Morin, A Flavonoid, On Lipid Peroxidation And Antioxidant Status In Experimental Myocardial Ischemic Rats

Al‐Numair¹,

Govindasamy²,

Alsaif³

et al. 2014

Afr. J. Trad. Compl. Alt. Med.

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“…Morin (3,5,7,2',4'-pentahydroxyflavone) is a flavonoid originally isolated from members of the Moraceae family. It has been reported to possess certain properties that regulate the inflammatory response which leads to carcinogenesis arrest and cancer progression (6,7).…”

Section: Introductionmentioning

confidence: 99%

The flavonoid morin from Moraceae induces apoptosis by modulation of Bcl-2 family members and Fas receptor in HCT 116 cells

Hwangbo

Lee

et al. 2015

International Journal of Oncology

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Abstract. It is evident based on literature that flavonoids from fruit can safely modulate cancer cell biology and induce apoptosis. Therefore, we investigated the anticancer activity of morin, a flavonoid which is plentiful in twigs of mulberry focusing on apoptosis, and its mechanisms. Morin upregulated the Fas receptor, and activates caspase-8, -9 and -3 in HCT-116 cells. Morin also activates Bid, and induced the loss of mitochondrial membrane potential (MMP, ∆Ψ m ) with Bax protein activation and cytochrome c release. In addition, morin induced ROS generation which was not blocked by N-acetylcysteine. Morin also suppressed Bcl-2 and cIAP-1, anti-apoptotic proteins, which may contribute to augmentation of morin-triggered apoptosis. As an upstream signaling pathway, suppressed Akt activity by morin was associated to apoptosis. This study suggests that morin induces caspase-dependent apoptosis through extrinsic pathway by upregulating Fas receptor as well as through the intrinsic pathway by modulating Bcl-2 and IAP family members, and ROS generation, and that Akt is the critical upstream signaling that regulates the apoptotic effect of morin in human colon cancer HCT-116 cells.

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“…Morin (3,5,7,2 ¶,4 ¶-pentahydroxyflavone; Fig. 1A) is a flavone originally isolated from members of the Moraceae family, such as mulberry figs and others Chinese herbs.…”

mentioning

confidence: 99%

Morin (3,5,7,2′,4′-Pentahydroxyflavone) Abolishes Nuclear Factor-κB Activation Induced by Various Carcinogens and Inflammatory Stimuli, Leading to Suppression of Nuclear Factor-κB–Regulated Gene Expression and Up-regulation of Apoptosis

Manna

Aggarwal

Sethi

et al. 2007

Clinical Cancer Research

121

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Purpose: Morin is a flavone that exhibits antiproliferative, antitumor, and anti-inflammatory effects through a mechanism that is not well understood. Because of the role of transcription factor nuclear factor-nB (NF-nB) in the control of cell survival, proliferation, tumorigenesis, and inflammation, we postulated that morin mediates its effects by modulating NF-nB activation. Experimental Design: We investigated the effect of morin on NF-nB pathway activated by inflammatory agents, carcinogens, and tumor promoters. The effect of this flavone on expression of NF-nB^regulated gene products involved in cell survival, proliferation, and invasion was also examined. Results: We showed by DNA-binding assay that NF-nB activation induced by tumor necrosis factor (TNF), phorbol 12-myristate 13-acetate, lipopolysaccharide, ceramide, interleukin-1, and H 2 O 2 was suppressed by morin; the suppression was not cell type specific. The suppression of NF-nB by morin was mediated through inhibition of InBa (inhibitory subunit of NF-nB) kinase, leading to suppression of phosphorylation and degradation of InBa and consequent p65 nuclear translocation. Morin also inhibited the NF-nB^dependent reporter gene expression activated by TNF, TNF receptor (TNFR) 1, TNFR1-associated death domain, TNFR-associated factor 2, NFnB^inducing kinase, InB kinase, and the p65 subunit of NF-nB. NF-nB^regulated gene products involved in cell survival [inhibitor of apoptosis (IAP) 1, IAP2, X chromosome-linked IAP, Bcl-xL, and survivin], proliferation (cyclin D1and cyclooxygenase-2), and invasion (matrix metalloproteinase-9) were down-regulated by morin. These effects correlated with enhancement of apoptosis induced byTNF and chemotherapeutic agents. Conclusion: Overall, our results indicate that morin suppresses the activation of NF-nB and NF-nB^regulated gene expression, leading to enhancement of apoptosis. This may provide the molecular basis for the ability of morin to act as an anticancer and anti-inflammatory agent.

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Chemopreventive effect of dietary flavonoid morin on chemically induced rat tongue carcinogenesis

Cited by 80 publications

References 25 publications

Morin, A Flavonoid, On Lipid Peroxidation And Antioxidant Status In Experimental Myocardial Ischemic Rats

Morin, A Flavonoid, On Lipid Peroxidation And Antioxidant Status In Experimental Myocardial Ischemic Rats

The flavonoid morin from Moraceae induces apoptosis by modulation of Bcl-2 family members and Fas receptor in HCT 116 cells

Morin (3,5,7,2′,4′-Pentahydroxyflavone) Abolishes Nuclear Factor-κB Activation Induced by Various Carcinogens and Inflammatory Stimuli, Leading to Suppression of Nuclear Factor-κB–Regulated Gene Expression and Up-regulation of Apoptosis

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