Protective Effect Of Honey Research Articles

Protective Effect of Honey Against Zinc Oxide Nanoparticles' Toxicity in Maternal and Foetal Livers of Rat

Protective Effect of Honey Against Zinc Oxide Nanoparticles' Toxicity in Maternal and Foetal Livers of Rat

The effect of Anzer honey on X-ray induced genotoxicity in human lymphocytes: An in vitro study.

Anzer honey is well known in Turkey and used for its medicinal properties, especially for pharyngitis, tonsillitis, ulcers and cancer. In this study, we investigated whether Anzer honey, which is shown to have antioxidant, anti-tumoral, and anti-inflammatory properties, has a protective effect against X-ray induced genotoxic damage by cytogenetic methods. Peripheral blood lymphocytes isolated from 20 healthy volunteers were divided into two groups and cultivated by conventional methods. Study group lymphocytes were treated with 10% diluted honey while those in the control group were not. Both groups were exposed to a high dose (2 Gy) X-ray at the 48th hour of culture. Conventional cytogenetic staining and Giemsa banding methods were applied to evaluate chromosomal breakage and ring formation. Micronucleus frequencies were determined by the cytokinesis-block micronucleus (CBMN) assay. Paired sample t test was used to compare groups. Anzer honey, which was analyzed melissopalynologically, was used. Micronucleus frequency was significantly decreased in the study group (CI=348.75 ± 31, median 326, min. 98, max. 704) compared to the control group (CI=489.10 ± 27, median 500, min. 216, max. 645) (p=.001). Chromosomal breakage was also significantly decreased in the study group (CI=118.70 ± 16, median 109, min. 12, max. 316) compared to the control group (CI=233.60± 25, median 225, min. 65, max. 492) (p < .0001). This is the first study indicating that genotoxic damage in the peripheral blood lymphocytes of healthy volunteers induced by X-radiation may be prevented or alleviated by adding Anzer honey in vitro. These results encourage further research about the protective effects of honey. RESEARCH HIGHLIGHTS: Anzer honey has a genoprotective effect against radiation-induced genotoxicity, probably by preventing oxidation damage.

Protective effects of honey and bee venom against lipopolysaccharide and carbon tetrachloride-induced hepatoxicity and lipid peroxidation in rats.

In the present study, the protective effects of honey and bee venom (BV) either independently or in combination against lipopolysaccharide (LPS) and carbon tetrachloride (CCl4)-induced hepatoxicity, lipid peroxidation, and hematological alterations in male albino rats were investigated. In addition, histopathological alterations of hepatic tissues induced by LPS/CCL4 were recorded. Sixty-four of male albino rats of average weight 120-150g were included in this study. Rats were divided into eight equal groups of eight. The obtained results demonstrated that treatment with LPS/CCl4 caused an increase in the levels of alpha-fetoprotein, which was accompanied by changes in the hepatic function biomarkers that characterized by the increased levels of transaminases (AST, ALT). The results showed oxidative stress as assigned by the increase in lipid peroxide. Meantime detraction in the antioxidants, including glutathione peroxidase was observed. Interruptions in biochemical parameters accompanied by disturbances in hematological parameters and liver histopathology were resulted due to exposure to LPS/CCl4. This study showed the use of honey and BV provided a protective effect on hepatotoxicity induced by LPS/CCl4. This might have been occurred through the reduction of hepatic transaminases and the "Alpha-fetoprotein" in serum and the equilibration of the antioxidation system, thereby, inhibiting the reactive oxygen species accumulation. Honey and BV administration reestablish disturbed hematological parameters and liver histopathology persuaded by LPS/CCl4. More interesting, we demonstrated that using a combination of the honey and BV showed promising enhancement in their protective effects over the use of just one of the two reagents.

Protective effect of honey on learning and memory impairment, depression and neurodegeneration induced by chronic unpredictable mild stress

Introduction: Chronic stress, which has been prevalent in human life, induce structural changes in the hippocampus. Depression and impairment of memory are serious comorbidities of chronic stress. In this study, we evaluated the impact of an Iranian honey pretreatment on memory deficit, depression and the hippocampal neuronal loss in the chronic unpredictable mild stress (CUMS) model. Methods: Adult male Wistar rats were divided into the control groups that received water or honey (0.2 or 2g/kg) and CUMS groups that subjected different, randomly and unpredictable mild stressors for 4 weeks. Ten days before starting the CUMS procedures, the animals received honey (0.2 or 2g/kg, daily, orally), which was continued until sacrificing. Morris water maze and sucrose performance tests were used to evaluate the spatial learning and memory and depressive-like behavior in the animals respectively. Hippocampus and whole brain samples were collected for further biochemical and histological analysis. Results: Honey reversed the depression-like behavior and ameliorated the spatial memory deficit induced by CUMS. Also, honey decreased cell death in the hippocampus and reduced the malondialdehyde level in treated animals. Conclusion: These results revealed that honey diminished learning and memory deficits and depression in chronic stress conditions.

Protective effects of honey by bees (Apis dorsata) on decreased cortical thickness and bone impact strength of ovariohysterectomized rats as models for menopause.

Aim:This study aimed to determine the potential of honey as anti-osteoporosis by evaluating its effectiveness in increasing bone impact strength and cortical thickness, through scanning electron microscopy (SEM) examination.Materials and Methods:Forty-five female rats at 3 months of age, weighing 150-200 g were used in the study. They were placed in individual cages and adapted to food and environment for 10 days. On the 11th day, after the animals were adapted for 10 days, the animals were randomly divided into five treatment groups (n=9): Sham operation group (SH); ovariohysterectomized (OVX) group with no treatment; OVX with treatment Apis dorsata 1 g/kg BW (AD-1); OVX with treatment A. dorsata 2 g/kg BW (AD-2); and OVX with treatment A. dorsata 4 g/kg BW (AD-3). Furthermore, those nine rats in each treatment group were divided into three groups. Three of them were observed at months 1st, 2nd, and 3rd so that in each observation taken three rats in each treatment group. At the end of the study, the rats were euthanized and necropsy for taking their second femoral bone, i.e. dexter region for examining their bone impact strength, while the sinister region was used for measure the cortical thickness of the femoral diaphysis and examining their bone microarchitecture using SEM analysis.Results:Based on results of the ANOVA test, the cortical thickness measurements of femoral diaphyseal can be seen that from month 1 to month 3 the lowest result was found in the group of rats that were OVX-I. Meanwhile, the highest result was found in the group of rats that were not OVX (SH-III). It was significantly different from the other treatment groups (p<0.05). The groups of rats were OVX with honey supplementation at doses of 2 g/kg BW had shown an increasing pattern in the cortical bone thickness from month 1 to month 3. Even on the observation of the 3rd month, the cortical bone thickness in the AD-2 (AD-2-III) group was not significantly different (p>0.05) from that in the group of rats was not OVX in month 1 (SH-I). The results of the bone impact strength measurement from month 1 to month 3 indicated that the groups of rats were OVX without the administration of honey supplements had the lowest value. The highest bone impact strength was found in the group of rats that was not OVX, but not significantly different (p>0.05) with the groups of rats that were OVX administered honey supplement with a dose of 2 g/kg BW (AD-2) and 4 g/kg BW (AD-3).Conclusion:The supplement of honey A. dorsata at doses of 2 g/kg BW in the group of rats was that OVX can inhibit the decreasing of the cortical bone thickness and repair damage in microarchitecture to generate bone impact strength. As a result, bones are not easily broken.

Protective Effects of Honey and Spirulina Platensis on Acetic Acid-Induced Ulcerative Colitis in Rats

Background: Overproduction of reactive oxygen species (ROS) causes increased lipid peroxidation, decreased intestinal epithelial barrier integrity, and ultimately mucosal disruption and ulceration. Several studies have confirmed the antioxidant, anti-inflammatory, and immunomodulatory properties of Spirulina Platensis (SP), edible blue - green algae, in various inflammatory diseases. In addition, natural honey, a source of phenolic and flavonoid compounds, is a powerful antioxidant, which can help prevent chronic oxidative stress and subsequent inflammation. Objectives: In this study, we examined and compared the protective effects of SP and honey on ulcerative colitis induced by acetic acid (AA) in rats. Methods: Forty male rats were allocated into five groups (N = 8) and received pretreatment for 32 consecutive days. The administrations were as follows: group 1 (control) and group 2 (AA-colitis group): normal saline, group 3: 1 ml honey/day, group 4: 1 ml honey/day plus 1 g/kg SP, and group 5: 1 g/kg SP. Colitis was induced on the 30th day in groups 2 to 5. On day 32, the clinical activity score was determined and anesthetized animals were sacrificed. Serum interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNF-α), glutathione peroxidase (GPx), reduced glutathione (GSH), total antioxidant capacity (TAC), superoxide dismutase (SOD), myeloperoxidase (MPO), prostaglandin E2 (PGE2), malondialdehyde (MDA), nitric oxide (NO), and colonic weight/length ratio were determined. In addition, histopathological changes of the colon were observed microscopically. Results: The inflammatory markers (PGE2, MDA, NO, IL-6, IL-1β, MPO, and TNF-α) were significantly lower in the pretreatment groups than in the AA-colitis group (P values < 0.05). PGE2 [median (IQR)] of the honey, SP + honey, and SP groups was [0.76 (0.33)], [0.75 (0.40)], and [0.87 (0.86)], respectively, compared to the AA-colitis group [2.60 (2.23)] (P values < 0.041). MDA values were [6.52 (3.57)], [6.09 (3.59)], and [5.85 (4.92)] vs. [16.60 (12.03)] (P values < 0.046) and IL-1β values were [42.20 (8.2)], [41.76 (18.10)], and [42.93 (14.09)] vs. [79.54 (40.79)] (P values < 0.044). Also, SOD, GSH, GPx, and TAC [median (IQR)] were significantly higher in the pretreatment groups than in the AA- colitis group (P values < 0.05). For example, TAC values of the honey, SP + honey, and SP groups were [0.164 (0.08)], [0.14 (0.05)], and [0.16 (0.10)], respectively, vs. the AA-colitis group [0.08 (0.01)] (P values < 0.028). Conclusions: Honey and SP are favorable foods in preventing oxidative stress and inflammatory diseases such as ulcerative colitis.

PROTECTIVE ROLE OF HONEY AFTER LEAD TOXICITY EFFECT ON ALBINO RATS LINGUAL PAPILLAE

INTRODUCTION: Studies concerning exposure of human to lead during daily activities are sometimes leading to many complications. Lead is a poisonous heavy metal, it’s toxicity can change the antioxidant balance in biological tissues. Honey is rich in phenolic acids and flavonoids, which exhibit a wide range of biological effects and act as natural antioxidants.OBJECTIVES: (1) To investigate the histological changes in lingual papillae following lead toxicity in experimental rats. (2) To assess the possible protective effects of honey using scanning electron microscopy (SEM).MATERIALS AND METHODS: Thirty two adult male albino rats were divided into four groups, eight rats/ group. Group I (control): 1ml distilled water. Group II (control + honey): 50 mg/kg honey + 1ml distilled water. Group III (lead): 16.5 mg lead acetate. Group IV (honey + lead): 16.5 mg lead acetate + 50 mg/kg honey. All doses were given by oral intubations daily /6 weeks. After 6 weeks, rats were sacrificed, and tongues were dissected out and processed for SEM.RESULTS: In Group II: Increased papillary density of the filiform papillae was noticed. In Group III the filiform papillae were distorted. Some appeared shorter while others had eroded tips and hyperkeratosis. Complete loss of papillae were seen in some samples. Disfigured fungiform papillae with swollen taste buds were seen. In Group IV, filiform and fungiform papillae appeared close to normal with minimal changes.CONCLUSIONS: The atrophy observed in Group III could be explained by lead-induced oxidative stress. Lead toxicity had a dual effect where increased free radical formation together with depletion of endogenous antioxidant enzymes resulted in inflammation and increased cell injury. Lead causes anemia and decreased salivary secretion, which may explain the epithelial erosion. Honey exerted its protective role through restoring enzymatic activity and through its antioxidant mechanism.

Organic honey supplementation reverses pesticide-induced genotoxicity by modulating DNA damage response.

Glyphosate (GLY) and organophosphorus insecticides such as chlorpyrifos (CPF) may cause DNA damage and cancer in exposed individuals through mitochondrial dysfunction. Polyphenols ubiquitously present in fruits and vegetables, have been viewed as antioxidant molecules, but also influence mitochondrial homeostasis. Here, honey containing polyphenol compounds was evaluated for its potential protective effect on pesticide-induced genotoxicity. Honey extracts from four floral organic sources were evaluated for their polyphenol content, antioxidant activity, and potential protective effects on pesticide-related mitochondrial destabilization, reactive oxygen and nitrogen species formation, and DNA damage response in human bronchial epithelial and neuronal cells. The protective effect of honey was, then evaluated in a residential population chronically exposed to pesticides. The four honey types showed a different polyphenol profile associated with a different antioxidant power. The pesticide-induced mitochondrial dysfunction parallels ROS formation from mitochondria (mtROS) and consequent DNA damage. Honey extracts efficiently inhibited pesticide-induced mtROS formation, and reduced DNA damage by upregulation of DNA repair through NFR2. Honey supplementation enhanced DNA repair activity in a residential population chronically exposed to pesticides, which resulted in a marked reduction of pesticide-induced DNA lesions. These results provide new insight regarding the effect of honey containing polyphenols on pesticide-induced DNA damage response.

Protective effects of honey against cadmium-induced alteration of some biochemical parameters in rats

The objective of this study is to elucidate on the effect of honey on plasma and organ biochemical parameters of albino rats exposed to acute and sub-chronic dose of cadmium chloride. Uric acid levels, activities of plasma lactate dehydrogenase (LDH), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, organ (liver, lungs, and kidney) AST, ALT, superoxide dismutase (SOD), and catalase (CAT) were determined. Plasma uric acid and glucose levels, plasma LDH, AST, and ALT activities were significantly decreased; activities of organ SOD, CAT, AST, and ALT activities were increased in rats administered sub-chronically and acutely with cadmium (Cd). Treatment with honey restored their levels to normal.

The effect of lead toxicity on albino rats' filiform and fungiform papillae and the possible protective role of honey and black seed

Aims: (1) To investigate the histological changes in lingual papillae following lead toxicity in experimental rats. (2) To assess the possible protective effects of honey and black seed using light microscopy (LM) and scanning electron microscopy (SEM). Materials and Methods: Forty adult male albino rats were divided into four groups, 10 rats/group. Group I (control): 1 ml distilled water. Group II (lead): 16.5 mg lead acetate. Group III (honey + lead): 16.5 mg lead acetate + 50 mg/kg honey. Group IV (black seed + lead): 16.5 mg lead acetate + 50 mg/kg black seed aqueous suspension. All doses were given by oral intubation daily/6 weeks. After 6 weeks, rats were terminated, and tongues were decimated for LM and SEM. Results: True filiform papillae in Group II were distorted. Some appeared shorter while others had eroded tips and hyperkeratosis. Areas of epithelial erosion with complete loss of papillae and keratin were seen in some samples. Disfigured fungiform papillae with swollen taste buds were seen. In Group III, filiform and fungiform papillae appeared close to normal with minimal changes. However, in Group IV papillae were distorted with hyperkeratosis and limited areas of epithelial erosions were seen. Conclusion: The atrophy observed in Group II could be explained by lead-induced oxidative stress. Lead toxicity had a dual effect where increased free radical formation together with depletion of endogenous antioxidant enzymes resulted in inflammation and increased cell injury. Lead causes anemia and decreased salivary secretion, which may explain the epithelial erosion. Honey exerted its protective role through restoring enzymatic activity and through its antioxidant mechanism. Black seed offered lower protection than honey. Increased dose and/or duration of co-administration of black seed may improve protection.

Histological changes in male accessory reproductive organs in rats exposed to cigarette smoke and the protective effect of honey supplementation

The effect of cigarette smoke (CS) on histology of male accessory reproductive organs and the possible protective effect of honey supplementation in rats were investigated in this study. Rats received distilled water, honey, CS exposure or honey plus CS exposure. Honey (1.2 g/kg body weight/day) was administered by gavage and CS exposure (3 times per day) was done in a chamber for 13 weeks. CS exposure significantly increased relative weight of epididymis and ventral prostate. There were also significantly increased number of clear cells and epithelial height of cauda epididymis as well as severe interstitial oedema and decreased epithelial height of prostate gland. However, with the supplementation of honey, these histological changes were significantly reversed suggesting the protective effect of honey against the toxic effect of CS on male accessory reproductive organs in rats.

The Possibility of Using Honey as Cytoprotective Against Pathological Effect of Doxorubicin Morphological Changes, Toxilogical Symptoms, Histological Structure and Functions of Mice Liver

Doxorubicin (DOX) is one of the most important cytotoxic drugs in cancer chemotherapy. However, it causes pathological effects on many organs. The aim of the present study was to investigate the possible protective effect of honey. Albino mice of MF1 (mus musculus) strain weighting 37±3 g were obtained from king Fahd medical research center. Mice body and liver weight , morphological and behavior changes as well as liver function and pathological effects on liver were recorded. Administration of DOX to mice induced weakness in general activities of animals with several morphological changes during experiment such as bleeding, ulcerations, dermatitis, alopecia, abnormal limbs, and bosselation. Toxicity study of DOX showed that the LD50 and LD were 20 and 30 mg/kg of DOX, respectively. The results of honey administration to mice reduce pathological symptoms caused DOX as indicates by body weights and liver, which were higher than that of DOX only. In addition, daily administration of honey for seven weeks decreased these histopathological changes, the structure of liver and hepatocytes appearance was more or less similar to control group as well its function. The present results indicate that honey may play an important role as Cytoprotective and pave the way for further studies on the possible use of honey.

English

&nbsp; Lactic acid bacteria (LAB):&nbsp;Streptococcus thermophilus&nbsp;TA 040 andLactobacillus delbrueckii&nbsp;spp.&nbsp;bulgaricus&nbsp;Lb 340, were cultured in reconstituted (10%, w/v) skimmed milk with 5 or 10% (w/v) polyfloral or unifloral honey. Inoculated samples were incubated aerobically at 42&deg;C until milk coagulation. Samples were collected at 2 h intervals and examined for biomass and pH changes. Cell viability and post-acidifying activity of both strains during 28 days of storage at 4&deg;C were also measured.&nbsp;A higher increase&nbsp;(P&lt;0.05)&nbsp;in growth and acidifying activity of&nbsp;S. thermophilus&nbsp;monocultures was observed when 10% honey was added. However,&nbsp;L. bulgaricus&nbsp;did not show such a marked increase in its growth capacity. In associated cultures, LAB growth was slightly inhibited, whereas curdling time was prolonged by an hour when 10% honey was added and yogurt acidity was moderate. Cell viability improved by 5 to 6.6% for&nbsp;S. thermophilus&nbsp;and 10% for&nbsp;L. bulgaricus&nbsp;in pure honey-sweetened cultures over 28 days of refrigerated storage.&nbsp;This protective effect of honey on LAB cell viability was also observed in associated cultures (10 to 12% comparatively to the control). &nbsp; Key words:&nbsp;&nbsp;Streptococcus thermophilus,&nbsp;Lactobacillus bulgaricus,&nbsp;honey, growth, viability.

Prevention of Ethanol-Induced Gastric Lesions in Rats by Natural Honey, and Its Possible Mechanism of Action

The effects and the mechanism of natural honey on absolute ethanol-induced gastric lesions were studied in rats. Drugs and/or honey were administered subcutaneously or orally to 48-h fasted animals at different time intervals before oral administration of ethanol (0.5 ml/100 g). Mucosal damage and pH were measured 1 h later. Honey afforded protection against gastric damage and reversed the changes in pH induced by ethanol. The effects of honey were dose- and time-dependent. Thus, pretreatment with honey (1.25 g/kg) 30 min before ethanol provided more than 80% protection. On the other hand, administration of honey simultaneously with or 5 min after ethanol failed to offer protection. The cyclooxygenase inhibitor indomethacin (IND) did not alter the protective effects when given before or after honey. The protective effects of honey could be reversed by treatment with the sulfhydryl (SH) blocker N-ethylmaleimide (NEM). Combined IND and NEM treatment caused greater reduction of the protective effects, but the values were not significantly different from those obtained with NEM alone. Thus, the gastroprotective effects of honey appeared to be mediated through SH-sensitive processes. Furthermore, the protective effects were supported by both macroscopic and microscopic findings. It is suggested that honey may be used clinically in preventing/reducing ethanol-induced gastric lesions in humans.