Renal carcinogenesis induced by ferric nitrilotriacetate in mice, and protection from it by Brazilian propolis and Artepillin C

Kimoto, Tetsuo; Koya, Satomi; Hino, Keiko; Yamamoto, Yoshiyuki; Nomura, Yutaka; Micallef, Mark; Hanaya, Toshiharu; Arai, Shigeyuki; Ikeda, Masao; Kurimoto, Masashi

doi:10.1046/j.1440-1827.2000.01097.x

Cited by 53 publications

(35 citation statements)

References 18 publications

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“…There are no available in vivo studies investigating the effects of CAPE on MM cells. However, results supporting our study have been reported in various studies investigating the in vivo effects of CAPE on various cancer models (42,43). Among them is the in vivo study by Onori et al in which, after intraperitoneal CAPE at 10 mg/kg was administered to BALB/c mice, tumor growth was found to be reduced within 77 days, the latent period of the tumor was increased 2-fold, and no differences were observed in the fibrosis or inflammation in either the carrier-or CAPE-treated animals with no other tissue/organ damage.…”

Section: Discussionsupporting

confidence: 92%

An in vitro and in vivo investigation of the cytotoxic effects of caffeic acid (3,4-dihydroxycinnamic acid) phenethyl ester and bortezomib in multiple myeloma cells

Altayli¹,

Koru²,

Ongoru³

et al. 2015

Turk J Med Sci

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IntroductionMultiple myeloma (MM) is a hematologic cancer characterized by uncontrolled monoclonal plasma cell proliferation (1). MM is currently an incurable B-cell malignancy that accounts for nearly 10% of human hematopoietic cancers and 1% of all human cancers (2). Presently, the 2 most effective treatment choices for patients with MM are tandem high-dose chemotherapy followed by autologous stem cell infusion, or allogeneic hematopoietic stem cell transplantation after myeloablative therapy or reduced-intensity conditioning (1). The proteasome inhibitor bortezomib is a novel drug with promising efficacy, even for patients with relapsed refractory MM (3,4). Nevertheless, these choices are not appropriate in all patients, and drug resistance often increases over time. Consequently, there is a need for new treatment options that can augment the effectiveness of current treatments (5,6).Background/aim: In this study, the in vitro and in vivo effectiveness of caffeic acid (3,4-dihydroxycinnamic acid) phenethyl ester (CAPE) in combination with bortezomib, a proteasome inhibitor, was explored in multiple myeloma (MM) cells. Materials and methods:The cytotoxic effects of CAPE and bortezomib were determined by XTT cell proliferation assay. Apoptosis levels were analyzed with annexin V-fluorescein isothiocyanate, nuclear factor kappa beta (NF-κB) was analyzed with electrophoretic mobility-shift assay, and interleukin (IL)-6 levels were analyzed with enzyme-linked immunosorbent assay to evaluate CAPE's mechanism of action. To investigate the in vivo effectiveness of CAPE and bortezomib, an experimental plasmacytoma model was induced in BALB/c mice.Results: Increasing concentrations of CAPE and bortezomib decreased the proliferation of ARH-77 cells in a dose-dependent manner. With doses of CAPE IC50, a significant increase in apoptosis and a significant decrease in IL-6 levels were detected. The NF-κB DNAbinding activity decreased compared to the basal ARH-77 level. The administration of CAPE alone or in combination with bortezomib increased the rate of survival compared to the control group. Conclusion:We think that our study, which is the first to demonstrate the in vitro and in vivo effectiveness of the combined use of CAPE and bortezomib, will be a pioneer for future human applications of CAPE in MM.

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Section: Discussionsupporting

confidence: 92%

An in vitro and in vivo investigation of the cytotoxic effects of caffeic acid (3,4-dihydroxycinnamic acid) phenethyl ester and bortezomib in multiple myeloma cells

Altayli¹,

Koru²,

Ongoru³

et al. 2015

Turk J Med Sci

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“…One finding indicated that DHCA exhibited inhibitory effects on renal carcinogenesis as a result of its oxy-radical scavenging property (Kimoto et al, 2000). Matsuno et al (1997) reported that DHCA was one of the effective anti-tumor compounds found in propolis and Kimoto et al (2001) and Kimoto et al (1998) showed that the DHCA is capable of reducing the mass of the tumor.…”

Section: Introductionmentioning

confidence: 99%

Supercritical CO2 extraction of raw propolis and its dry ethanolic extract

Paviani

Saito

Dariva

et al. 2012

Braz. J. Chem. Eng.

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-Three types of propolis extract were prepared and analyzed with respect to their global extraction yields and with respect to the concentration of the following markers: 3,5-diprenyl-4-hydroxycinnamic acid; 3-prenyl-4-hydroxycinnamic acid; 4-hydroxycinnamic acid and 4-methoxy-3,5,7-trihydroxyflavone. The extract EEP (ethanolic extract of propolis) was obtained by the conventional method from raw propolis using ethanol as solvent. The extracts (SFE) were obtained by supercritical solvent extraction from the raw propolis using supercritical carbon dioxide (sc-CO 2 ), with and without the addition of ethanol as a co-solvent. The fractionated supercritical extracts (FSCE) were obtained by fractionation (extract and raffinate) of the dry EEP with sc-CO 2 . EEP yields of 39.5% were obtained and maximum global extraction yields were 7.3% for SFE with no co-solvent, 51% for SFE with 15% ethanol and 18% for the FSCE extract fraction. The concentrations of the markers in the different extracts differed as a function of the operational parameters, indicating that the addition of co-solvent and the selectivity of sc-CO 2 could be manipulated so as to obtain extracts with the yields and concentrations of interest.

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“…It has been characterized variously as an anti-bacterial, 6,7) anti-viral, 8) anti-inflammatory, 9-11) anti-oxidant, 12) and anti-carcinogenesis agent. 13,14) Obesity is caused by various environmental and genetic factors.15) One of the main environmental factors causing obesity is the intake of a high-fat diet, now common in many populations. A diet-induced obesity animal model has been developed to investigate human obesity, replicating the effects of human obesity more accurately than genetic obesity models.…”

mentioning

confidence: 99%

Propolis Prevents Diet-Induced Hyperlipidemia and Mitigates Weight Gain in Diet-Induced Obesity in Mice

Koya‐Miyata

Arai

Mizote

et al. 2009

Biological & Pharmaceutical Bulletin

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The accumulation of visceral adipose tissue usually results from an energy imbalance involving the combination of excessive calorie consumption with insufficient energy expenditure. Increased visceral adiposity can induce insulin resistance and lead to type 2 diabetes mellitus, dyslipidemia, hypertension, and cardiovascular disease.1) "Metabolic syndrome" is the combination of multiple cardiovascular risk factors, including visceral obesity, dyslipidemia, glucose intolerance, and hypertension in one individual.2,3) Obesity resulting from an accumulation of visceral adiposity is a primary cause of metabolic syndrome.Propolis is a sticky, resinous substance collected by honey bees (Apis mellifera) from the sap, leaves, and buds of plants, and then mixed with secreted beeswax. The chemical constituents of propolis are mainly flavonoids, phenolic compounds, caffeoylquinic acids, cinnamic acid derivatives, diterpenoic acid, lignan, coumarin acid and other compounds. 4,5) Propolis has been used as a folk medicine in many countries from ancient times especially in Brazil and Eastern Europe. It has been characterized variously as an anti-bacterial, 6,7) anti-viral, 8) anti-inflammatory, 9-11) anti-oxidant, 12) and anti-carcinogenesis agent. 13,14) Obesity is caused by various environmental and genetic factors.15) One of the main environmental factors causing obesity is the intake of a high-fat diet, now common in many populations. A diet-induced obesity animal model has been developed to investigate human obesity, replicating the effects of human obesity more accurately than genetic obesity models.16) Mice that are fed a high-fat diet, develop obesity, hyperglycemia, and hyperlipidemia, and differ from those fed a normal diet in the expression levels of specific genes transcripts.17) Recent studies have reported that propolis prevented and mitigated diabetes and hypertension, [18][19][20][21][22] but it remains unclear whether propolis similarly prevents and mitigates the accumulation of visceral adipose tissues and hyperlipidemia. In this study we examined the effect of propolis on visceral fat and hyperlipidemia induced in a high-fat dietinduced obesity mouse model, and analyzed hepatic gene expression involved in lipid metabolism. MATERIALS AND METHODS Preparation of Propolis ExtractPropolis used in this study was obtained from Apiai, Sao Paulo in Brazil. Propolis (1 kg) was treated with 50% ethanol (3 l) at room temperature for 24 h, and filtered. This extract included 10.8% of solid contents of propolis. Total flavonoids content in the extract was determined as amounts of quercetin by using the aluminum nitrate method as described previously.23) In addition, the extract was subjected to reversed-phase column chromatography using following conditions: column, Shim Pack CLC-ODS (6 mm i.d.ϫ150 mm, Shimadzu, Japan); column temperature, 50°C; gradient system, A solvent (30% MeOH, 70% H 2 O and 1% AcOH) and B solvent (75% MeOH, 25% H 2 O and 1% AcOH), 0-20 min 100% A isocratic, 20-55 min 100% B isocratic, 55-75 min 100% ...

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Renal carcinogenesis induced by ferric nitrilotriacetate in mice, and protection from it by Brazilian propolis and Artepillin C

Cited by 53 publications

References 18 publications

An in vitro and in vivo investigation of the cytotoxic effects of caffeic acid (3,4-dihydroxycinnamic acid) phenethyl ester and bortezomib in multiple myeloma cells

An in vitro and in vivo investigation of the cytotoxic effects of caffeic acid (3,4-dihydroxycinnamic acid) phenethyl ester and bortezomib in multiple myeloma cells

Supercritical CO2 extraction of raw propolis and its dry ethanolic extract

Propolis Prevents Diet-Induced Hyperlipidemia and Mitigates Weight Gain in Diet-Induced Obesity in Mice

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