Brazilian Red Propolis Extract Research Articles

Inhibition of DMBA-induced Oral Squamous Cells Carcinoma Growth by Brazilian Red Propolis in Rodent Model.

We investigated the effect of oral administration of hydroalcoholic extract of Brazilian red propolis (HERP) on DMBA-induced oral squamous cell carcinomas (OSCC) in rodents. The chemical components of the HERP were assessed by high-performance liquid chromatography (HPLC). Carcinogenesis was topically induced in the lower lip of 25 rats using 9,10-dimethyl-1,2-benzanthracene (DMBA); the tumour was treated with saline (TUM1) and Tween 80 (TUM2) as well as HERP at 10, 50 and 100 mg/kg (HERP10, HERP50 and HERP100, respectively) for 20 weeks. Topical application of saline and oral administration of 100 mg/kg HERP was used in five rats as a control group (CTR). After 26 weeks, the histological malignancy grading and immunohistochemical expression of Ki-67 and p16(INK4A) were assessed in the tumours/tissue samples. The compounds identified were propyl gallate, daidzein, catechin, epicatechin, formononetin and biochanin A. Formononetin, daidzein and biochanin A showed concentration of 23.29, 0.38 and 0.67 mg/g of HERP, respectively. HERP at doses of 50 and 100 mg/kg inhibited 40% of OSCC growth and promoted a 3-week delay in development of clinically detectable tumours. Epithelial dysplasia was observed in all samples with no clinical tumour, except in CTR. No significant difference in the immunoexpression of Ki-67 and p16(INK4A) was observed between HERP-treated and saline/Tween 80-treated groups (p > 0.05). Our results suggest that HERP exerts chemopreventive activity on the progression of DMBA-induced epithelial dysplasia to OSCC in an experimental model of labial carcinogenesis; however, this effect is not associated with Ki-67 and p16(INK4A) immunoexpression.

Comparison of the in vitro efficiency of supplementary bee propolis extracts of different origin in enhancing the ruminal degradability of organic matter and mitigating the formation of methane

The current study was conducted to compare the effects of ethanolic extracts of Brazilian red propolis (BRP) and Egyptian brown propolis (EBP) characterized by different individual compounds on the ruminal degradation of nutrients and methanogenesis. The utility of propolis as a natural alternative to the ionophore antibiotic monensin, which was used as a positive control, was also tested. The propolis extract was incubated with 0 (negative control), 125, 250, or 500μg per 500mg of dietary dry matter. A semi-automatic in vitro gas production (GP) system was operated with three batches of rumen fluid in three replicates per batch for each treatment. The major compounds of the BRP extract were isoflavonoids and chalcones, which represented 0.43 of the total. Isoflavonoids and saturated fatty acids made up 0.53 of the EBP extract. Extract of BRP25μg enhanced the true organic matter degradability (TDOM) (P<0.05) compared with negative control. All doses of BRP and EBP25μg enhanced (P<0.05) TDOM compared with monensin while no differences were observed among the propolis extract treatments. Compared with the negative control, the treatment suppressing (P<0.05) methane (CH4) and total GP was monensin. The propolis extracts were only half or less than half as effective as monensin against CH4 production. Both the BRP and EBP extracts increased (P<0.05) the production of total and all major (acetate, propionate, butyrate) short-chain fatty acids (SCFA). Monensin enhanced (P<0.05) only propionate production, clearly reduced (P<0.05) the acetate-to-propionate ratio compared with the negative control. Ruminal ammonia remained unaffected by the treatments, but the propolis extracts reduced (P<0.05) the protozoal count. This study demonstrated the efficiency of two types of propolis extracts, although they were less effective than monensin in mitigating CH4 emissions. It also showed that propolis with very different compositions seemed to act in a similar way and that the efficiency of the two types of propolis in modifying the ruminal degradation of nutrients and mitigating methane formation was comparable. The most active component(s) in propolis still have to be identified.

Modulatory activity of brazilian red propolis on chemically induced dermal carcinogenesis

To evaluate modulatory effects of a hydroalcoholic extract of Brazilian red propolis (HERP) on dermal carcinogenesis using a murine model. The HERP was used at concentrations of 10, 50 and 100 mg/kg (PROP10, PROP50 and PROP100, respectively) to modulate dermal carcinogenesis induced by the application of 9,10-dimetil-1,2-benzatraceno (DMBA) on the backs of animals. The chemical compounds identified in HERP included propyl gallate, catechin, epicatechin and formononetin. PROP100 treatment resulted in significantly decreased tumor multiplicity throughout the five weeks of tumor promotion (p<0.05), and this concentration also resulted in the highest frequency of verrucous tumors (p<0.05). All of the tumors that developed in DMBA-treated animals were regarded as squamous cell carcinomas and were either diagnosed as non-invasive verrucous carcinomas or invasive squamous cell carcinomas (SCCs). The average score for malignancy was significantly lower in the PROP100-treated group than the non-treated group (p<0.05), but there was no difference between the other groups (p>0.05). The oral administration of hydroalcoholic extract of Brazilian red propolis at a dose of 100 mg/kg had a significant modulatory effect on the formation, differentiation and progression of chemically induced squamous cell carcinoma in a murine experimental model.

Ethanol Extract of Brazilian Red Propolis Induces Apoptosis in Human Breast Cancer MCF-7 Cells through Endoplasmic Reticulum Stress

Propolis, a natural product collected from plants by honey bees, is commonly used in folk medicines. Endoplasmic reticulum (ER) stress is known to induce apoptosis through the induction of CCAAT/enhancer-binding protein homologous protein (CHOP). Here, we investigated whether ethanol extracts of propolis and caffeic acid phenethyl ester (CAPE) induce apoptosis, mitochondrial dysfunction, and ER stress in human breast cancer MCF-7 cells and human fibroblasts. Among several ethanol extracts of propolis and CAPE, Brazilian red propolis (BRP) significantly reduced MCF-7 cell viability through the induction of mitochondrial dysfunction, caspase-3 activity, and DNA fragmentation but did not affect those of fibroblasts. Moreover, treatment with BRP significantly induced CHOP expression in MCF-7 cells compared to fibroblasts. Further, pretreatment with a chemical chaperone, 4-phenylbutyric acid, suppressed BRP-triggered MCF-7 cell death. Overall, we revealed that an ethanol extract of BRP induces MCF-7 cell apoptosis through, at least in part, ER stress-related signaling.

Constituents of Brazilian red propolis and their preferential cytotoxic activity against human pancreatic PANC-1 cancer cell line in nutrient-deprived condition

Human pancreatic cancer cells such as PANC-1 are known to exhibit marked tolerance to nutrition starvation that enables them to survive for prolonged period of time even under extremely nutrient-deprived conditions. Thus, elimination of this tolerance to nutrition starvation is regarded as a novel approach in anticancer drug development. In this study, the MeOH soluble extract of Brazilian red propolis was found to kill 100% PANC-1 cells preferentially in the nutrient-deprived condition at the concentration of 10 μg/mL. Further phytochemical investigation led to the isolation of 43 compounds including three new compounds, (6a S,11a S)-6a-ethoxymedicarpan ( 1), 2-(2′,4′-dihydroxyphenyl)-3-methyl-6-methoxybenzofuran ( 2), and 2,6-dihydroxy-2-[(4-hydroxyphenyl)methyl]-3-benzofuranone ( 3). Among them, (6a R,11a R)-3,8-dihydroxy-9-methoxypterocarpan ( 21, DMPC) displayed the most potent 100% preferential cytotoxicity (PC 100) at the concentration of 12.5 μM. Further study on the mode of cell death induced by DMPC against PANC-1 cells indicated that killing process was not accompanied by DNA fragmentation, rather through a nonapoptotic pathway accompanied by necrotic-type morphological changes.