Inhibition of chemical carcinogenesis by berberine in rats and mice

Anis, Karim; Rajeshkumar, N.V.; Kuttan, Ramadasan

doi:10.1211/0022357011775901

Cited by 137 publications

(75 citation statements)

References 13 publications

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“…In the experiment presented here, we observed that the administration of NDEA induced an increase in the hepatic GSH concentration in rats. Similar findings have been reported by other authors (Jeena et al 1999;Rajeshkumar & Kuttan 2000;Anis et al 2001;Rajkapoor et al 2005). Marinho et al (1997) reported that chronic exposure to this carcinogen caused an increase in the activities of g-glutamyl transferase and g-glutamylcysteine synthetase that correlated well with the increase in GSH content.…”

Section: Discussionsupporting

confidence: 90%

Protective effect of yellow tea extract on N-nitrosodiethylamine-induced liver carcinogenesis

Kujawska

Ewertowska

Adamska

et al. 2016

Pharmaceutical Biology

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Context Yellow tea containing the same catechins as other types of tea but in different proportions has been suggested to possess potent anticancer activities. Objective This study investigates the chemopreventive effect of yellow tea aqueous extract against N-nitrosodiethylamine (NDEA)-induced liver carcinogenesis in rats by employing histological and biochemical methods. Materials and methods Wistar rats were divided randomly into four groups: control (I), yellow tea (II), NDEA (III), and yellow tea + NDEA (IV). Groups II and IV were exposed via a diet to yellow tea extract in a concentration of 10 g/kg feed; groups III and IV received 0.01% NDEA in drinking water. The experiment lasted for 13 weeks. Results Daily intake of yellow tea in an average dose of 800 mg/kg b.w. alleviated the carcinogenic effect of NDEA as evidenced by reversed histopathological changes towards normal hepatocellular architecture and decreased lipid peroxidation, protein carbonyl formation, and DNA degradation by 64%, 37% and 15%, respectively, as compared with values obtained in NDEA alone-treated rats. Treatment with yellow tea extract caused protection of superoxide dismutase (SOD) and catalase (CAT); their activity was recovered by 47% and 12%, respectively, as compared with the NDEAtreated rats. Moreover, the extract normalized the NDEA-induced activity of paraoxonase 1 (PON1) and glutathione peroxidase (GPx), while a further increase in the level of reduced glutathione (GSH) was noticed. Conclusions On the basis of these findings, it can be concluded that treatment with yellow tea partially protected the livers of rats from NDEA-induced hepatocarcinogenesis and that its antioxidant activity contributed to this effect. ARTICLE HISTORY

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Section: Discussionsupporting

confidence: 90%

Protective effect of yellow tea extract on N-nitrosodiethylamine-induced liver carcinogenesis

Kujawska

Ewertowska

Adamska

et al. 2016

Pharmaceutical Biology

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“…has been reported to possess antineoplastic activities in various cell lines and also in the tumor bearing animals (Jagetia & Baliga, 2004). Studies have also shown that berberine was effective in preventing chemical carcinogenesis in rats and mice (Anis et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Anticancer activity ofBerberis aristatain Ehrlich ascites carcinoma-bearing mice: A preliminary study

Pai¹,

Srilatha²,

Suryakant³

et al. 2011

Pharmaceutical Biology

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“…Animal studies have shown that berberine can suppress chemicalinduced carcinogenesis (10), tumor promotion (11), and tumor invasion (12). It is a radiosensitzer of tumor cells but not of normal cells (13).…”

Section: Introductionmentioning

confidence: 99%

Berberine Modifies Cysteine 179 of IκBα Kinase, Suppresses Nuclear Factor-κB–Regulated Antiapoptotic Gene Products, and Potentiates Apoptosis

et al. 2008

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Berberine, an isoquinoline alkaloid derived from a plant used traditionally in Chinese and Ayurvedic medicine, has been reported to exhibit chemopreventive and anti-inflammatory activities through unknown mechanism. Because of the critical role of the transcription factor nuclear factor-KB (NF-KB) in these processes, we investigated the effect of berberine on this pathway. We found that berberine suppressed NF-KB activation induced by various inflammatory agents and carcinogens. This alkaloid also suppressed constitutive NF-KB activation found in certain tumor cells. Suppression of NF-KB activation occurred through the inhibition of phosphorylation and degradation of IKBA by the inhibition of IKB kinase (IKK) activation, leading to suppression of phosphorylation and nuclear translocation of p65, and finally to inhibition of NF-KB reporter activity. Inhibition of IKK by berbeine was direct and could be reversed by reducing agents. Site-specific mutagenesis suggested the involvement of cysteine residue 179 in IKK.

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Inhibition of chemical carcinogenesis by berberine in rats and mice

Cited by 137 publications

References 13 publications

Protective effect of yellow tea extract on N-nitrosodiethylamine-induced liver carcinogenesis

Protective effect of yellow tea extract on N-nitrosodiethylamine-induced liver carcinogenesis

Anticancer activity ofBerberis aristatain Ehrlich ascites carcinoma-bearing mice: A preliminary study

Berberine Modifies Cysteine 179 of IκBα Kinase, Suppresses Nuclear Factor-κB–Regulated Antiapoptotic Gene Products, and Potentiates Apoptosis

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