NZ Honey fights MPI over alleged health claims
Monday, 28 September 2015
The New Zealand Herald
MPI has been cracking down on the manuka honey industry amid international criticism there was more manuka honey coming out of the country than New Zealand actually produces.
By Suze Metherell
New Zealand Honey International, the closely-held honey products maker, wants a judicial declaration on whether its trademarks Manuka Doctor and Manuka Pharm amount to health claims after the Ministry of Primary Industries withdrew export approvals, blocking the firm's sales into certain markets.
MPI has been cracking down on the manuka honey industry amid international criticism there was more manuka honey coming out of the country than New Zealand actually produces.
With no industry consensus on what constitutes manuka honey, MPI introduced an interim labelling guideline in July 2014 to give the industry clarity and protect consumers from false claims, as well as to try to improve credibility of the manuka products.
The regulator cancelled NZ Honey's export assurance in May, saying the company's brand names Manuka Doctor and Manuka Pharm breached food labelling standards.
Wednesday, September 30, 2015
Tuesday, September 29, 2015
A Fatty Acid from Royal Jelly with Multiple Biological Activities
Chem Biodivers. 2015 Sep;12(9):1307-12. doi: 10.1002/cbdv.201500048.
5-Fluorouridine (1) - a nucleoside antimetabolite with strong cancerostatic properties - was protected i) at the 2'- and 3'-OH groups with a heptan-4-ylidene residue and ii) at the 5'-OH group with a (4-methoxyphenyl)(diphenyl)methyl residue.
This fully protected compound, 3, was submitted to a Mitsunobu reaction with the N-hydroxysuccinimide (NHS) ester, 5, of (2E)-10-hydroxydec-2-enoic acid (4) which gave nucleolipid 6. The latter was detritylated with Cl2 CHCOOH to yield the co-drug 7 as NHS ester.
Monday, September 28, 2015
Nigerian Propolis Protects Liver and Pancreas from Damage Caused by Diabetes
Hepatoprotective and Pancreatoprotective Properties of the Ethanolic Extract of Nigerian Propolis
J Intercult Ethnopharmacol. 2015 Apr-Jun;4(2):102-8
Increased oxidative stress is associated with the progression of diabetic mellitus. In the present study, we investigated the effects of the ethanolic extract of Nigerian propolis (N. propolis) on markers of oxidative stress, histology of the liver and pancreas and glycaemia in alloxan-induced diabetic rats.
MATERIALS AND METHODS:
Alloxan-induced hyperglycemic Wistar rats were treated with either metformin (150 mg/kg/d) or N. propolis (200 mg/kg/d and 300 mg/kg/d) for 28 days. At the end of the treatment period, the rats were sacrificed; blood was collected for biochemical analysis while their pancreases and liver were excised and processed for histological studies.
RESULTS:
Serum oxidative stress markers and blood glucose concentration were compared between the treated and control rats. In contrast to the non-treated diabetic rats, blood glucose concentration were not significantly different between treated rats and control (P < 0.05) at 28 days of treatment with N. propolis and metformin. Serum malondialdehyde levels was reduced while superoxide dismutase levels were elevated in the N. propolis group; these levels were converse in the diabetic group, these differences are statistically significant (P<0 .05="" compared="" control.="" group.="" group="" histologically="" improvement="" in="" p="" the="" there="" to="" treated="" untreated="" was="" when="" with="">
CONCLUSION:
These findings suggest that the N. propolis confers protection against hyperglycemia-induced oxidative stress in both liver and pancreas of adult Wistar rats.
J Intercult Ethnopharmacol. 2015 Apr-Jun;4(2):102-8
Increased oxidative stress is associated with the progression of diabetic mellitus. In the present study, we investigated the effects of the ethanolic extract of Nigerian propolis (N. propolis) on markers of oxidative stress, histology of the liver and pancreas and glycaemia in alloxan-induced diabetic rats.
MATERIALS AND METHODS:
Alloxan-induced hyperglycemic Wistar rats were treated with either metformin (150 mg/kg/d) or N. propolis (200 mg/kg/d and 300 mg/kg/d) for 28 days. At the end of the treatment period, the rats were sacrificed; blood was collected for biochemical analysis while their pancreases and liver were excised and processed for histological studies.
RESULTS:
Serum oxidative stress markers and blood glucose concentration were compared between the treated and control rats. In contrast to the non-treated diabetic rats, blood glucose concentration were not significantly different between treated rats and control (P < 0.05) at 28 days of treatment with N. propolis and metformin. Serum malondialdehyde levels was reduced while superoxide dismutase levels were elevated in the N. propolis group; these levels were converse in the diabetic group, these differences are statistically significant (P<0 .05="" compared="" control.="" group.="" group="" histologically="" improvement="" in="" p="" the="" there="" to="" treated="" untreated="" was="" when="" with="">
CONCLUSION:
These findings suggest that the N. propolis confers protection against hyperglycemia-induced oxidative stress in both liver and pancreas of adult Wistar rats.
Sunday, September 27, 2015
Royal Jelly Helps Hydrate Skin
Epidermal Hydration Is Improved by Enhanced Ceramide Metabolism in Aged C57BL/6J Mice After Dietary Supplementation of Royal Jelly
J Med Food. 2015 Sep;18(9):999-1006
Epidermal hydration is maintained by the epidermal lipid barrier, of which ceramide (Cer) is the major constituent. We examined the dietary effect of royal jelly (RJ) on epidermal hydration in aged mice.
Altered Cer metabolism was further determined by measuring epidermal levels of individual Cer, glucosylceramide (GC), and sphingomyelin (SM) species, and of Cer-metabolizing enzymes. Aged C57BL/6J mice were fed a control diet (group AGED) or diets with 1% RJ harvested from two different areas (groups AGED+RJ1:AGED+RJ2) for 16 weeks. Aged C57BL/6J mice with no dietary intervention (the control group: group C) represented the onset of aging. In group AGED, epidermal levels of hydration, Cer1/2/5/6/7, GC-A/B/C/D, SM1/2/3, and β-glucocerebrosidase (GCase) protein, an enzyme of GC hydrolysis for Cer generation, were lower than in group C; these levels, as well as those of Cer3/4 and acidic sphingomyelinase (aSMase) protein, an enzyme of SM hydrolysis for Cer generation, were higher in group AGED+RJ1 than in group AGED. Despite increases in GC-B, SM1/2/3, and serine palmitoyltransferase2 protein, an enzyme of de novo Cer synthesis, in group AGED+RJ2 to levels higher than in group AGED, epidermal levels of hydration, Cer1-7, GC-A/C/D, GCase, and aSMase proteins were similar in these two groups. Expression of GCase and aSMase mRNAs, and of Cer synthase3 and ceramidase proteins, enzymes of de novo Cer synthesis and degradation, did not differ among groups.
Dietary RJ1 improved epidermal hydration by enhancing Cer metabolism with increased levels of all Cer, GC, and SM species, and of GCase and aSMase proteins.
J Med Food. 2015 Sep;18(9):999-1006
Epidermal hydration is maintained by the epidermal lipid barrier, of which ceramide (Cer) is the major constituent. We examined the dietary effect of royal jelly (RJ) on epidermal hydration in aged mice.
Altered Cer metabolism was further determined by measuring epidermal levels of individual Cer, glucosylceramide (GC), and sphingomyelin (SM) species, and of Cer-metabolizing enzymes. Aged C57BL/6J mice were fed a control diet (group AGED) or diets with 1% RJ harvested from two different areas (groups AGED+RJ1:AGED+RJ2) for 16 weeks. Aged C57BL/6J mice with no dietary intervention (the control group: group C) represented the onset of aging. In group AGED, epidermal levels of hydration, Cer1/2/5/6/7, GC-A/B/C/D, SM1/2/3, and β-glucocerebrosidase (GCase) protein, an enzyme of GC hydrolysis for Cer generation, were lower than in group C; these levels, as well as those of Cer3/4 and acidic sphingomyelinase (aSMase) protein, an enzyme of SM hydrolysis for Cer generation, were higher in group AGED+RJ1 than in group AGED. Despite increases in GC-B, SM1/2/3, and serine palmitoyltransferase2 protein, an enzyme of de novo Cer synthesis, in group AGED+RJ2 to levels higher than in group AGED, epidermal levels of hydration, Cer1-7, GC-A/C/D, GCase, and aSMase proteins were similar in these two groups. Expression of GCase and aSMase mRNAs, and of Cer synthase3 and ceramidase proteins, enzymes of de novo Cer synthesis and degradation, did not differ among groups.
Dietary RJ1 improved epidermal hydration by enhancing Cer metabolism with increased levels of all Cer, GC, and SM species, and of GCase and aSMase proteins.
Saturday, September 26, 2015
Bee Venom Protects Against Neuron Cell Death
Bee Venom Protects against Rotenone-Induced Cell Death in NSC34 Motor Neuron Cells
Toxins (Basel). 2015 Sep 21;7(9):3715-3726
Rotenone, an inhibitor of mitochondrial complex I of the mitochondrial respiratory chain, is known to elevate mitochondrial reactive oxygen species and induce apoptosis via activation of the caspase-3 pathway.
Bee venom (BV) extracted from honey bees has been widely used in oriental medicine and contains melittin, apamin, adolapin, mast cell-degranulating peptide, and phospholipase A₂. In this study, we tested the effects of BV on neuronal cell death by examining rotenone-induced mitochondrial dysfunction. NSC34 motor neuron cells were pretreated with 2.5 μg/mL BV and stimulated with 10 μM rotenone to induce cell toxicity. We assessed cell death by Western blotting using specific antibodies, such as phospho-ERK1/2, phospho-JNK, and cleaved capase-3 and performed an MTT assay for evaluation of cell death and mitochondria staining. Pretreatment with 2.5 μg/mL BV had a neuroprotective effect against 10 μM rotenone-induced cell death in NSC34 motor neuron cells. Pre-treatment with BV significantly enhanced cell viability and ameliorated mitochondrial impairment in rotenone-treated cellular model. Moreover, BV treatment inhibited the activation of JNK signaling and cleaved caspase-3 related to cell death and increased ERK phosphorylation involved in cell survival in rotenone-treated NSC34 motor neuron cells.
Taken together, we suggest that BV treatment can be useful for protection of neurons against oxidative stress or neurotoxin-induced cell death.
Toxins (Basel). 2015 Sep 21;7(9):3715-3726
Rotenone, an inhibitor of mitochondrial complex I of the mitochondrial respiratory chain, is known to elevate mitochondrial reactive oxygen species and induce apoptosis via activation of the caspase-3 pathway.
Bee venom (BV) extracted from honey bees has been widely used in oriental medicine and contains melittin, apamin, adolapin, mast cell-degranulating peptide, and phospholipase A₂. In this study, we tested the effects of BV on neuronal cell death by examining rotenone-induced mitochondrial dysfunction. NSC34 motor neuron cells were pretreated with 2.5 μg/mL BV and stimulated with 10 μM rotenone to induce cell toxicity. We assessed cell death by Western blotting using specific antibodies, such as phospho-ERK1/2, phospho-JNK, and cleaved capase-3 and performed an MTT assay for evaluation of cell death and mitochondria staining. Pretreatment with 2.5 μg/mL BV had a neuroprotective effect against 10 μM rotenone-induced cell death in NSC34 motor neuron cells. Pre-treatment with BV significantly enhanced cell viability and ameliorated mitochondrial impairment in rotenone-treated cellular model. Moreover, BV treatment inhibited the activation of JNK signaling and cleaved caspase-3 related to cell death and increased ERK phosphorylation involved in cell survival in rotenone-treated NSC34 motor neuron cells.
Taken together, we suggest that BV treatment can be useful for protection of neurons against oxidative stress or neurotoxin-induced cell death.
Friday, September 25, 2015
2-AP Together with MGO Can Be a Suitable Parameter for the Quality Control of Manuka Honey
Identification and Quantitation of 2-Acetyl-1-pyrroline in Manuka Honey (Leptospermum scoparium)
J. Agric. Food Chem., Article ASAP
Publication Date (Web): September 12, 2015
Manuka honey from New Zealand is known for its exceptional antibacterial activity, which is due to high amounts of the 1,2-dicarbonyl compound methylglyoxal (MGO). MGO in manuka honey is formed via non-enzymatic dehydration from dihydroxyacetone (DHA) during honey maturation. MGO and DHA are highly reactive substances, leading to a variety of unique chemical reactions. During Strecker reaction between proline and MGO, 2-acetyl-1-pyrroline (2-AP), an important aroma compound, is formed.
Using liquid–liquid extraction and gas chromatography–mass spectrometry analysis, 2-AP was identified unambiguously in manuka honey for the first time. Quantitation was carried out via external matrix calibration, using a synthetic 2-AP standard and artificial honey. The 2-AP concentration in 11 commercial samples of manuka honey ranged from 0.08 to 0.45 mg/kg. For manuka honey samples containing MGO in concentrations above 250 mg/kg, significantly higher amounts of 2-AP were found when compared to non-manuka honeys.
When high amounts of MGO were artificially added to non-manuka multifloral honey, an increase of the 2-AP concentration from 0.07 to 0.40 mg/kg after 12 weeks of storage at 37 °C was observed, concomitant with a significant increase in the concentration of 5-hydroxymethylfurfural (HMF). No increase of 2-AP was found during storage at ambient temperature. 2-AP together with MGO can be a suitable parameter for the quality control of manuka honey.
Thursday, September 24, 2015
Manuka Honey Helps Treat Corneal Edema
Standardised antibacterial Manuka honey in the management of persistent post-operative corneal oedema: a case series
Clin Exp Optom. 2015 Sep;98(5):464-72
BACKGROUND:
Corneal oedema is a common post-operative problem that delays or prevents visual recovery from ocular surgery. Honey is a supersaturated solution of sugars with an acidic pH, high osmolarity and low water content. These characteristics inhibit the growth of micro-organisms, reduce oedema and promote epithelialisation. This clinical case series describes the use of a regulatory approved Leptospermum species honey ophthalmic product, in the management of post-operative corneal oedema and bullous keratopathy.
METHODS:
A retrospective review of 18 consecutive cases (30 eyes) with corneal oedema persisting beyond one month after single or multiple ocular surgical procedures (phacoemulsification cataract surgery and additional procedures) treated with Optimel Antibacterial Manuka Eye Drops twice to three times daily as an adjunctive therapy to conventional topical management with corticosteroid, aqueous suppressants, hypertonic sodium chloride five per cent, eyelid hygiene and artificial tears. Visual acuity and central corneal thickness were measured before and at the conclusion of Optimel treatment.
RESULTS:
A temporary reduction in corneal epithelial oedema lasting up to several hours was observed after the initial Optimel instillation and was associated with a reduction in central corneal thickness, resolution of epithelial microcysts, collapse of epithelial bullae, improved corneal clarity, improved visualisation of the intraocular structures and improved visual acuity. Additionally, with chronic use, reduction in punctate epitheliopathy, reduction in central corneal thickness and improvement in visual acuity were achieved. Temporary stinging after Optimel instillation was experienced. No adverse infectious or inflammatory events occurred during treatment with Optimel.
CONCLUSIONS:
Optimel was a safe and effective adjunctive therapeutic strategy in the management of persistent post-operative corneal oedema and warrants further investigation in clinical trials.
Clin Exp Optom. 2015 Sep;98(5):464-72
BACKGROUND:
Corneal oedema is a common post-operative problem that delays or prevents visual recovery from ocular surgery. Honey is a supersaturated solution of sugars with an acidic pH, high osmolarity and low water content. These characteristics inhibit the growth of micro-organisms, reduce oedema and promote epithelialisation. This clinical case series describes the use of a regulatory approved Leptospermum species honey ophthalmic product, in the management of post-operative corneal oedema and bullous keratopathy.
METHODS:
A retrospective review of 18 consecutive cases (30 eyes) with corneal oedema persisting beyond one month after single or multiple ocular surgical procedures (phacoemulsification cataract surgery and additional procedures) treated with Optimel Antibacterial Manuka Eye Drops twice to three times daily as an adjunctive therapy to conventional topical management with corticosteroid, aqueous suppressants, hypertonic sodium chloride five per cent, eyelid hygiene and artificial tears. Visual acuity and central corneal thickness were measured before and at the conclusion of Optimel treatment.
RESULTS:
A temporary reduction in corneal epithelial oedema lasting up to several hours was observed after the initial Optimel instillation and was associated with a reduction in central corneal thickness, resolution of epithelial microcysts, collapse of epithelial bullae, improved corneal clarity, improved visualisation of the intraocular structures and improved visual acuity. Additionally, with chronic use, reduction in punctate epitheliopathy, reduction in central corneal thickness and improvement in visual acuity were achieved. Temporary stinging after Optimel instillation was experienced. No adverse infectious or inflammatory events occurred during treatment with Optimel.
CONCLUSIONS:
Optimel was a safe and effective adjunctive therapeutic strategy in the management of persistent post-operative corneal oedema and warrants further investigation in clinical trials.
Tuesday, September 22, 2015
Bee Venom Protects Motor Neuron Cells
Bee Venom Protects against Rotenone-Induced Cell Death in NSC34 Motor Neuron Cells
Toxins 2015, 7(9), 3715-3726
Rotenone, an inhibitor of mitochondrial complex I of the mitochondrial respiratory chain, is known to elevate mitochondrial reactive oxygen species and induce apoptosis via activation of the caspase-3 pathway. Bee venom (BV) extracted from honey bees has been widely used in oriental medicine and contains melittin, apamin, adolapin, mast cell-degranulating peptide, and phospholipase A2.
In this study, we tested the effects of BV on neuronal cell death by examining rotenone-induced mitochondrial dysfunction. NSC34 motor neuron cells were pretreated with 2.5 μg/mL BV and stimulated with 10 μM rotenone to induce cell toxicity.
We assessed cell death by Western blotting using specific antibodies, such as phospho-ERK1/2, phospho-JNK, and cleaved capase-3 and performed an MTT assay for evaluation of cell death and mitochondria staining. Pretreatment with 2.5 μg/mL BV had a neuroprotective effect against 10 μM rotenone-induced cell death in NSC34 motor neuron cells.
Pre-treatment with BV significantly enhanced cell viability and ameliorated mitochondrial impairment in rotenone-treated cellular model. Moreover, BV treatment inhibited the activation of JNK signaling and cleaved caspase-3 related to cell death and increased ERK phosphorylation involved in cell survival in rotenone-treated NSC34 motor neuron cells.
Taken together, we suggest that BV treatment can be useful for protection of neurons against oxidative stress or neurotoxin-induced cell death.
Toxins 2015, 7(9), 3715-3726
Rotenone, an inhibitor of mitochondrial complex I of the mitochondrial respiratory chain, is known to elevate mitochondrial reactive oxygen species and induce apoptosis via activation of the caspase-3 pathway. Bee venom (BV) extracted from honey bees has been widely used in oriental medicine and contains melittin, apamin, adolapin, mast cell-degranulating peptide, and phospholipase A2.
In this study, we tested the effects of BV on neuronal cell death by examining rotenone-induced mitochondrial dysfunction. NSC34 motor neuron cells were pretreated with 2.5 μg/mL BV and stimulated with 10 μM rotenone to induce cell toxicity.
We assessed cell death by Western blotting using specific antibodies, such as phospho-ERK1/2, phospho-JNK, and cleaved capase-3 and performed an MTT assay for evaluation of cell death and mitochondria staining. Pretreatment with 2.5 μg/mL BV had a neuroprotective effect against 10 μM rotenone-induced cell death in NSC34 motor neuron cells.
Pre-treatment with BV significantly enhanced cell viability and ameliorated mitochondrial impairment in rotenone-treated cellular model. Moreover, BV treatment inhibited the activation of JNK signaling and cleaved caspase-3 related to cell death and increased ERK phosphorylation involved in cell survival in rotenone-treated NSC34 motor neuron cells.
Taken together, we suggest that BV treatment can be useful for protection of neurons against oxidative stress or neurotoxin-induced cell death.
Monday, September 21, 2015
Honey and Black Seed Oil Can Help Treat Indigestion
Efficacy and safety of Honey based formulation of nigella sativa seed oil in functional dyspepsia: A double blind randomized controlled clinical trial
J Ethnopharmacol. 2015 Sep 16. pii: S0378-8741(15)30147-1
ETHNOPHARMACOLOGICAL RELEVANCE:
A honey based formulation from Nigella sativa L. (N. sativa) has been used in Traditional Persian Medicine for upper gastrointestinal symptoms. Considering the traditional use of this formulation and its ingredients known pharmacologic effects, this study aimed to evaluate the efficacy and safety of N. sativa seed oil mixed with honey in treatment of patients with functional dyspepsia.
METHODS AND MATERIALS:
Seventy patients diagnosed with functional dyspepsia according to ROME III criteria and confirmed by upper gastrointestinal endoscopy were selected to receive a traditional honey based formulation of Nigella sativa (5mlN. sativa oil orally daily) or placebo for 8 weeks in a double-blind randomized placebo-controlled clinical trial using a parallel design with a 1:1 allocation ratio. Patients were evaluated prior to and following 8 weeks of the intervention in terms of the Hong Kong index of dyspepsia severity, presence of H. pylori infection based on urease test, scores in different domains of short form (SF-36) health survey, and any observed adverse events.
RESULTS:
The mean scores of Hong Kong index of dyspepsia severity sores and the rate of H. pylori infection were significantly lower in the N. sativa group comparing the placebo group after the intervention (P < 0.001). No serious adverse event was reported.
CONCLUSION:
This study showed that adjuvant supplementation of honey based formulation of N. sativa can cause significant symptomatic improvement of patients with functional dyspepsia whom received the standard anti-secretory therapy. The results should be investigated further in studies with longer duration and larger sample size.
J Ethnopharmacol. 2015 Sep 16. pii: S0378-8741(15)30147-1
ETHNOPHARMACOLOGICAL RELEVANCE:
A honey based formulation from Nigella sativa L. (N. sativa) has been used in Traditional Persian Medicine for upper gastrointestinal symptoms. Considering the traditional use of this formulation and its ingredients known pharmacologic effects, this study aimed to evaluate the efficacy and safety of N. sativa seed oil mixed with honey in treatment of patients with functional dyspepsia.
METHODS AND MATERIALS:
Seventy patients diagnosed with functional dyspepsia according to ROME III criteria and confirmed by upper gastrointestinal endoscopy were selected to receive a traditional honey based formulation of Nigella sativa (5mlN. sativa oil orally daily) or placebo for 8 weeks in a double-blind randomized placebo-controlled clinical trial using a parallel design with a 1:1 allocation ratio. Patients were evaluated prior to and following 8 weeks of the intervention in terms of the Hong Kong index of dyspepsia severity, presence of H. pylori infection based on urease test, scores in different domains of short form (SF-36) health survey, and any observed adverse events.
RESULTS:
The mean scores of Hong Kong index of dyspepsia severity sores and the rate of H. pylori infection were significantly lower in the N. sativa group comparing the placebo group after the intervention (P < 0.001). No serious adverse event was reported.
CONCLUSION:
This study showed that adjuvant supplementation of honey based formulation of N. sativa can cause significant symptomatic improvement of patients with functional dyspepsia whom received the standard anti-secretory therapy. The results should be investigated further in studies with longer duration and larger sample size.
Sunday, September 20, 2015
Topical Application of Propolis Significantly Enhanced Closure of Diabetic Wounds
Topical Application of Propolis Enhances Cutaneous Wound Healing by Promoting TGF-Beta/Smad-Mediated Collagen Production in a Streptozotocin-Induced Type I Diabetic Mouse Model
Cell Physiol Biochem. 2015 Sep 18;37(3):940-954
BACKGROUND/AIMS:
Impaired wound healing is considered to be one of the most serious complications associated with diabetes as it significantly increases the susceptibility of patients to infection. Propolis is a natural bee product used extensively in foods and beverages that has significant benefits to human health. In particular, propolis has antioxidant, anti-inflammatory and analgesic effects that could be useful for improving wound healing. In this study, we investigated the effects of topical application of propolis on the healing and closure of diabetic wounds in a streptozotocin (STZ)-induced type I diabetic mouse model.
METHODS:
Sixty male mice were distributed equally into 3 experimental groups: group 1, non-diabetic control mice; group 2, diabetic mice; and group 3, diabetic mice treated daily with a topical application of propolis.
RESULTS:
We found that diabetic mice exhibited delayed wound closure characterized by a significant decrease in the levels of TGF-β1 and a prolonged elevation of the levels of inflammatory cytokines (IL-1β, IL-6 and TNF-α) and MMP9 in wound tissues compared with control non-diabetic mice. Moreover, the wound tissues of diabetic mice showed a marked reduction in the phosphorylation of Smad2 and Smad3 as well as a marked reduction in collagen production. Interestingly, compared with untreated diabetic mice, topical application of propolis significantly enhanced the closure of diabetic wounds and decreased the levels of IL-1β, IL-6, TNF-α and MMP9 to near normal levels. Most importantly, compared with untreated diabetic mice, the treatment of diabetic mice with propolis significantly enhanced the production of collagen via the TGF-β1/Smad2,3 signaling axis in wounded tissues.
CONCLUSION:
Our findings reveal the molecular mechanisms underlying the improved healing and closure of diabetic wounds following topical propolis application.
Cell Physiol Biochem. 2015 Sep 18;37(3):940-954
BACKGROUND/AIMS:
Impaired wound healing is considered to be one of the most serious complications associated with diabetes as it significantly increases the susceptibility of patients to infection. Propolis is a natural bee product used extensively in foods and beverages that has significant benefits to human health. In particular, propolis has antioxidant, anti-inflammatory and analgesic effects that could be useful for improving wound healing. In this study, we investigated the effects of topical application of propolis on the healing and closure of diabetic wounds in a streptozotocin (STZ)-induced type I diabetic mouse model.
METHODS:
Sixty male mice were distributed equally into 3 experimental groups: group 1, non-diabetic control mice; group 2, diabetic mice; and group 3, diabetic mice treated daily with a topical application of propolis.
RESULTS:
We found that diabetic mice exhibited delayed wound closure characterized by a significant decrease in the levels of TGF-β1 and a prolonged elevation of the levels of inflammatory cytokines (IL-1β, IL-6 and TNF-α) and MMP9 in wound tissues compared with control non-diabetic mice. Moreover, the wound tissues of diabetic mice showed a marked reduction in the phosphorylation of Smad2 and Smad3 as well as a marked reduction in collagen production. Interestingly, compared with untreated diabetic mice, topical application of propolis significantly enhanced the closure of diabetic wounds and decreased the levels of IL-1β, IL-6, TNF-α and MMP9 to near normal levels. Most importantly, compared with untreated diabetic mice, the treatment of diabetic mice with propolis significantly enhanced the production of collagen via the TGF-β1/Smad2,3 signaling axis in wounded tissues.
CONCLUSION:
Our findings reveal the molecular mechanisms underlying the improved healing and closure of diabetic wounds following topical propolis application.
Saturday, September 19, 2015
Speaker: Maria Spivak, University of Minnesota
When (Date/Time) November 13, 2015, 11:15 AM - 12:05 PM
Where 107 Forest Resources Bldg.
Penn State University
Friday, September 18, 2015
Bee Pollen is Safe and Has Good Nutritional Quality
Microbiological Assessment, Nutritional Characterization and Phenolic Compounds of Bee Pollen from Mellipona mandacaia
Molecules. 2015 Jul 9;20(7):12525-12544
This study aims to assess the microbiological parameters and the chemical composition of 21 samples of stingless bee pollen (Melipona mandacaia) from two regions of Bahia, Brazil (João Dourado and Uibaí), with particular emphasis on the nutritional value, total phenols and flavonoids and fatty acids composition.
Regarding the microbiological quality, the studied microorganisms (moulds and yeasts, coliforms, Escherichia coli, Staphylococcus aureus, Salmonella sp., psychrotrophic and sulfite-reducing Clostridia) were absent in all samples. On the other hand, the values obtained for the aerobic mesophilic microorganism ranged from 11.0 ± 1.0 to 1.32 ± 1.2 cfu∙g-¹ (JD samples) and from 282 ± 3.82 to 688 ± 10.1 cfu∙g-¹ (U samples). The nutritional parameters (moisture, ash, water activity, pH, total acidity, protein, fiber, total phenolic, flavonoids and reducing sugars) were within the stipulated by law, except for pH and moisture content, which presented superior and inferior values, respectively. Polyunsaturated fatty acids (54.1%) were significantly higher than saturated (42.18%) and monounsaturated (3.71%).
It was found that the bee pollen is safe from the microbiological point of view and has a good nutritional quality. The influence of the geographical origin on the assessed parameters was evident, especially concerning the fatty acid profile.
Molecules. 2015 Jul 9;20(7):12525-12544
This study aims to assess the microbiological parameters and the chemical composition of 21 samples of stingless bee pollen (Melipona mandacaia) from two regions of Bahia, Brazil (João Dourado and Uibaí), with particular emphasis on the nutritional value, total phenols and flavonoids and fatty acids composition.
Regarding the microbiological quality, the studied microorganisms (moulds and yeasts, coliforms, Escherichia coli, Staphylococcus aureus, Salmonella sp., psychrotrophic and sulfite-reducing Clostridia) were absent in all samples. On the other hand, the values obtained for the aerobic mesophilic microorganism ranged from 11.0 ± 1.0 to 1.32 ± 1.2 cfu∙g-¹ (JD samples) and from 282 ± 3.82 to 688 ± 10.1 cfu∙g-¹ (U samples). The nutritional parameters (moisture, ash, water activity, pH, total acidity, protein, fiber, total phenolic, flavonoids and reducing sugars) were within the stipulated by law, except for pH and moisture content, which presented superior and inferior values, respectively. Polyunsaturated fatty acids (54.1%) were significantly higher than saturated (42.18%) and monounsaturated (3.71%).
It was found that the bee pollen is safe from the microbiological point of view and has a good nutritional quality. The influence of the geographical origin on the assessed parameters was evident, especially concerning the fatty acid profile.
Thursday, September 17, 2015
Which Australian species of Leptospermum produce honey with high antibacterial qualities?
Honey healing: medicinal honey potential has Australian researchers on the hunt for more liquid gold
ABC Rural, 9/16/2015
As spring kicks in, honey researchers are stepping up their efforts to study how native trees can increase the value of honey that has healing properties.
Manuka honey is known for its medicinal and healing qualities, with New Zealand product currently dominating the lucrative market.
The honey is produced with the pollen from Leptospermum tree species. New Zealand only has two of these species, but Australia has about 86.
Professor Liz Harry from the ithree institute, at the University of Technology Sydney, wants Australian beekeepers to send her samples of their honey.
It is part of a research project that aims to establish which Australian species of Leptospermum produce honey with high antibacterial qualities to rival new Zealand's Manuka product.
"On the Sunshine Coast, in Queensland, there is quite a lot of Leptospermum species, and it is very potent in killing bacteria and has similar chemical properties to the New Zealand Manuka honey," Ms Harry said...
Wednesday, September 16, 2015
A Parameter for Quality Control of Manuka Honey
Identification and Quantitation of 2-Acetyl-1-pyrroline in Manuka Honey (Leptospermum scoparium)
J Agric Food Chem. 2015 Sep 12
Manuka honey from New Zealand is known for its exceptional antibacterial activity, which is due to high amounts of the 1,2-dicarbonyl compound methylglyoxal (MGO). MGO in manuka honey is formed via non-enzymatic dehydration from dihydroxyacetone (DHA) during honey maturation. MGO and DHA are highly reactive substances, leading to a variety of unique chemical reactions.
During Strecker degradation of proline and MGO, 2-acetyl-1-pyrroline (2-AP), an important aroma compound, is formed. Using liquid-liquid extraction and GC-MS analysis, 2-AP was identified unambiguously in manuka honey for the first time. Quantitation was carried out via external matrix calibration, using a synthetic 2-AP standard and artificial honey. The 2-AP concentration in 11 commercial samples of manuka honey ranged from 0.08 to 0.45 mg/kg. For manuka honey samples containing MGO in concentrations above 250 mg/kg, significantly higher amounts of 2-AP were found when compared to non-manuka honeys.
When high amounts of MGO were artificially added to non-manuka multifloral honey, an increase of the 2-AP concentration from 0.07 to 0.40 mg/kg after 12 weeks of storage at 37 °C was observed, concomitant with a significant increase in the concentration of 5-hydroxymethylfurfural (HMF). No increase of 2-AP was found during storage at ambient temperature. 2-AP together with MGO can be a suitable parameter for the quality control of manuka honey.
J Agric Food Chem. 2015 Sep 12
Manuka honey from New Zealand is known for its exceptional antibacterial activity, which is due to high amounts of the 1,2-dicarbonyl compound methylglyoxal (MGO). MGO in manuka honey is formed via non-enzymatic dehydration from dihydroxyacetone (DHA) during honey maturation. MGO and DHA are highly reactive substances, leading to a variety of unique chemical reactions.
During Strecker degradation of proline and MGO, 2-acetyl-1-pyrroline (2-AP), an important aroma compound, is formed. Using liquid-liquid extraction and GC-MS analysis, 2-AP was identified unambiguously in manuka honey for the first time. Quantitation was carried out via external matrix calibration, using a synthetic 2-AP standard and artificial honey. The 2-AP concentration in 11 commercial samples of manuka honey ranged from 0.08 to 0.45 mg/kg. For manuka honey samples containing MGO in concentrations above 250 mg/kg, significantly higher amounts of 2-AP were found when compared to non-manuka honeys.
When high amounts of MGO were artificially added to non-manuka multifloral honey, an increase of the 2-AP concentration from 0.07 to 0.40 mg/kg after 12 weeks of storage at 37 °C was observed, concomitant with a significant increase in the concentration of 5-hydroxymethylfurfural (HMF). No increase of 2-AP was found during storage at ambient temperature. 2-AP together with MGO can be a suitable parameter for the quality control of manuka honey.
Tuesday, September 15, 2015
Romanian Apitherapy Congress October 30 - November 2, 2015
November 2 (Monday): Practical Workshop at University Hospital CFR Iasi
Optional:
Dinner, Saturday, October 31, 8:30 p.m. to 10 p.m.
For questions contact: drstangaciu@gmail.com
Dr Stefan Stangaciu
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