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NATURAL HONEY AND H. PYLORI INFECTION
- Thread starter ginfreely
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NATURAL HONEY AND H. PYLORI INFECTION
H. pylori infection represents the most common risk factor underlying chronic inflammation and gastric cancer[64,65]. H. pylori can lead to mucosal inflammation and cancer development through several mechanisms including H. pylori virulence factors such as CagA and VacA genotypes and inflammatory mediators that induce cellular signalling alterations in gastric cells[65]. The intake of honey also helps treat H. pylori infection [66]. Natural honey from New Zealand and Saudi Arabia at concentrations 20% (v/v) inhibited the growth of H. pylori in vitro[67,68]. Honey had an inhibitory effect on H. pylori in vitro at solutions of both 10% and 20% honey[671. al Somal et al[59] also found that Manuka honey from New Zealand, at concentrations as low as 5% v/v, completely inhibit the growth of H. pylori, and that 2.5% v/v partially inhibits the growth of H. pylori[68]. Osmotic effects were shown to be the most important parameter for killing H. pylori as all carbohydrate solutions > or = 15% (v/v) inhibited 100% of the H. pylori. The therapeutic effect of honey was attributed to the antibacterial properties [68,69].
Osato et al[70] also reported that commercial honeys and the artificial solution were effective as Manuka honey in inhibiting growth of all H. pylori isolates at concentrations 15% v/v. It has also been reported that the use of honey with triple therapy regimen may help shorten the time required to eliminate H. pylori from stomach lining of patients with gastritis or duodenal ulcer caused by H. pylori infection[71].
H. pylori infection represents the most common risk factor underlying chronic inflammation and gastric cancer[64,65]. H. pylori can lead to mucosal inflammation and cancer development through several mechanisms including H. pylori virulence factors such as CagA and VacA genotypes and inflammatory mediators that induce cellular signalling alterations in gastric cells[65]. The intake of honey also helps treat H. pylori infection [66]. Natural honey from New Zealand and Saudi Arabia at concentrations 20% (v/v) inhibited the growth of H. pylori in vitro[67,68]. Honey had an inhibitory effect on H. pylori in vitro at solutions of both 10% and 20% honey[671. al Somal et al[59] also found that Manuka honey from New Zealand, at concentrations as low as 5% v/v, completely inhibit the growth of H. pylori, and that 2.5% v/v partially inhibits the growth of H. pylori[68]. Osmotic effects were shown to be the most important parameter for killing H. pylori as all carbohydrate solutions > or = 15% (v/v) inhibited 100% of the H. pylori. The therapeutic effect of honey was attributed to the antibacterial properties [68,69].
Osato et al[70] also reported that commercial honeys and the artificial solution were effective as Manuka honey in inhibiting growth of all H. pylori isolates at concentrations 15% v/v. It has also been reported that the use of honey with triple therapy regimen may help shorten the time required to eliminate H. pylori from stomach lining of patients with gastritis or duodenal ulcer caused by H. pylori infection[71].
H. pylori has been shown to activate mitogen-activated protein kinases and transcription factors such as AP-1 and NF-KB that regulate cell proliferation and differentiation in gastric epithelial cells using several different bacterial components and host signaling pathways|72,73]. NF-KB and activator protein-1 (AP-1) are key regulators of inflammation and signaling cascades that lead to carcinogenesis.
There are numerous agents including honey have been reported to suppress NF-KB activation and act as potential chemopreventive agents for inflammation and cancer[74]. CAPE blocked H. pylori-induced NF-KB and AP-1 expression in gastric cancer cells, and CAPE also suppressed H. pylori-induced cell proliferation and production of the cytokines TNF-a and IL-8 and COX-2 expression[55]. Therefore, the inhibition of these molecules by CAPE could result in suppression of many genes during H. pylori-induced inflammation. Wu et al[75] demonstrated that the activity of NF-KB and the expression of matrix metalloproteinase-9, IL-beta, and IL-8 in gastric cancer cells by H. pylori significantly reversed by CAPE treatment, which suggested that CAPE could be promising adjuvant agent against gastric cancer. In Monogolian gerbils, CAPE treatment elicited anti-inflammatory effects on H. pylori-induced chronic gastritis. CAPE significantly inhibited H. pylori-stimulated NF-B activation and mRNA expression of several inflammatory factors in a dose-dependent manner, and prevented degradation of IkB-alpha and phosphorylation of p65 in gastric cancer cells[76].
There are numerous agents including honey have been reported to suppress NF-KB activation and act as potential chemopreventive agents for inflammation and cancer[74]. CAPE blocked H. pylori-induced NF-KB and AP-1 expression in gastric cancer cells, and CAPE also suppressed H. pylori-induced cell proliferation and production of the cytokines TNF-a and IL-8 and COX-2 expression[55]. Therefore, the inhibition of these molecules by CAPE could result in suppression of many genes during H. pylori-induced inflammation. Wu et al[75] demonstrated that the activity of NF-KB and the expression of matrix metalloproteinase-9, IL-beta, and IL-8 in gastric cancer cells by H. pylori significantly reversed by CAPE treatment, which suggested that CAPE could be promising adjuvant agent against gastric cancer. In Monogolian gerbils, CAPE treatment elicited anti-inflammatory effects on H. pylori-induced chronic gastritis. CAPE significantly inhibited H. pylori-stimulated NF-B activation and mRNA expression of several inflammatory factors in a dose-dependent manner, and prevented degradation of IkB-alpha and phosphorylation of p65 in gastric cancer cells[76].
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Potential mechanisms of honey actions were found to include regulation of cell cycle, induction of apoptosis, activation of mitochondrial pathway, inhibition of angiogenesis and modulation of oxidative stress. Honey can inhibit the development of cancer by blocking the three stages of carcinogenesis (initiation, promotion and progression). The inhibitory effect of honey on carcinogenesis can be attributed to the presence of its active components, especially flavonoids and phenolic constituents. Honey plays an important role in preventing inflammatory tissues from producing free radicals[42]. Caffeic acid phenethyl ester (CAPE), an active component of propolis, has many biological and pharmacological activities including antioxidant, antiinflammatory, antiviral action, anti-proliferative effect, apoptosis-inducing effect and anticancer effect[43-46]. Caffeic acid esters have been shown to have an inhibitory effect on tumor cell proliferation and transformation by the down regulation of many cellular enzymatic pathways including protein tyrosine kinase, cycloxygenase and ornithine decarboxylase pathways[47-50].
Abdel-Latif MM. Chemoprevention of gastrointestinal cancers by natural honey. World J Pharmacol 2015; 4(1): 160-167 [DOI: 10.5497/wjp.v4.i1.160]
Abdel-Latif MM. Chemoprevention of gastrointestinal cancers by natural honey. World J Pharmacol 2015; 4(1): 160-167 [DOI: 10.5497/wjp.v4.i1.160]
Propolis or bee glue is a resinous mixture that honey bees produce by mixing saliva and beeswax with exudate gathered from tree buds, sap flows, or other botanical sources. It is used as a sealant for unwanted open spaces in the beehive. Wikipedia
NATURAL HONEY AND GASTROINTESTINAL INFLAMMATION
Inflammation plays an important role in the development of several diseases including gastrointestinal diseases and cancer[51,52]. Inflammation is recognized as a risk factor for gastric inflammation and Helicobacter pylori (H. pylori) infection and clinical intervention by natural products such as honey may provide an approach for reducing inflammation and H. pylori-associated diseases, particularly gastric cancer. Honey contains many phenolic compounds such as ellagic acid, gallic acid, caffeic acid, quercetin and chrysin, which correlated to its antioxidant and anti-inflammatory activities[36,52,53]. It was suggested that honey and its components can inhibit inflammation via inactivation of nuclear factor kappa-B (NF-κB) and inhibition of transcription of genes for pro-inflammatory mediators such as COX-2, tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6) and inducible nitric oxide synthase[54,55]. Gelam honey has shown to have anti-inflammatory effects by reducing the edema size and inhibiting the production of the pro-inflammatory mediators nitric oxide, prostaglandin E2, TNF-α, and IL-6 in rats[56]. Honey has been reported to potentiate the gastric protection effects of sucralfate against ammonia-induced gastric lesions in rats[57]. Alagwu has reported that honey intake caused cytoprotection on the gastric mucosa of albino rats[58]. Oral administration of honey has been reported to protect against gastrointestinal infection such as gastritis, duodenitis and gastric ulcer caused by bacteria[59-61]. Nasutia et al[62] demonstrated that oral pretreatment of honey prevented indomethacin-induced gastric lesions in rats. Perfusion of the stomach with isotonic honey resulted in a marked reduction of the lesions caused by ethanol and indomethacin in rats[38,63].
Abdel-Latif MM. Chemoprevention of gastrointestinal cancers by natural honey. World J Pharmacol 2015; 4(1): 160-167 [DOI: 10.5497/wjp.v4.i1.160]
Inflammation plays an important role in the development of several diseases including gastrointestinal diseases and cancer[51,52]. Inflammation is recognized as a risk factor for gastric inflammation and Helicobacter pylori (H. pylori) infection and clinical intervention by natural products such as honey may provide an approach for reducing inflammation and H. pylori-associated diseases, particularly gastric cancer. Honey contains many phenolic compounds such as ellagic acid, gallic acid, caffeic acid, quercetin and chrysin, which correlated to its antioxidant and anti-inflammatory activities[36,52,53]. It was suggested that honey and its components can inhibit inflammation via inactivation of nuclear factor kappa-B (NF-κB) and inhibition of transcription of genes for pro-inflammatory mediators such as COX-2, tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6) and inducible nitric oxide synthase[54,55]. Gelam honey has shown to have anti-inflammatory effects by reducing the edema size and inhibiting the production of the pro-inflammatory mediators nitric oxide, prostaglandin E2, TNF-α, and IL-6 in rats[56]. Honey has been reported to potentiate the gastric protection effects of sucralfate against ammonia-induced gastric lesions in rats[57]. Alagwu has reported that honey intake caused cytoprotection on the gastric mucosa of albino rats[58]. Oral administration of honey has been reported to protect against gastrointestinal infection such as gastritis, duodenitis and gastric ulcer caused by bacteria[59-61]. Nasutia et al[62] demonstrated that oral pretreatment of honey prevented indomethacin-induced gastric lesions in rats. Perfusion of the stomach with isotonic honey resulted in a marked reduction of the lesions caused by ethanol and indomethacin in rats[38,63].
Abdel-Latif MM. Chemoprevention of gastrointestinal cancers by natural honey. World J Pharmacol 2015; 4(1): 160-167 [DOI: 10.5497/wjp.v4.i1.160]
NATURAL HONEY AND GASTROINTESTINAL CANCERS
There are many research studies support the use of natural honey for cancer prevention and treatment, especially cancers of the gastrointestinal tract. Nutritional studies have indicated that consumption of honey modulates the risk of the development of gastric cancer, and also honey induced apoptosis in gastric mucosa[77]. It was postulated that CAPE may be a promising adjuvant treatment in gastric cancer[78]. The chemopreventive actions of honey and its components have been also studied in various colon cancer models. Gelam and Nenas honeys suppressed the growth of HT 29 colon cancer cells by inducing DNA damage and apoptosis and suppressing inflammation[79]. Jaganathan also demonstrated the anti-proliferative effect of Caffeic acid, one of the phenolic constituents of honey, inhibited in the colon cancer cells HCT15 and HT29[80]. Honey induced apoptosis by causing the depletion of intracellular non-protein thiols and reduced the mitochondrial membrane potential and increased generation of reactive oxygen species. Furthermore, honey constituents induced apoptosis in colon cancer cells[81]. Orsolić et al[82] showed that honey exerted anti-metastatic effect in a murine tumor model with colon carcinoma. Supplementation of diet with honey and Nigella sativa had a protective effect against methylnitrosourea-induced oxidative stress, inflammatory response and carcinogenesis in Sprague Dawely rats[83]. Caffeic acid esters derivatives inhibited azoxymethane-induced colonic colonie preneoplastic lesions, ornithine decarboxylase, tyrosine protein kinase, and lipoxygenase activities and aberrant crypt foci formation, which are relevant to colon carcinogenesis in rat colon[50]. Caffeic acid and its ester are potent inhibitors of human colon adenocarcinoma cell growth[84]. Dietary administration of phenylethyl-3-methylcaffeate significantly inhibited the incidence and multiplicity of invasive, noninvasive adenocarcinomas of the colon, and also suppressed the colon tumor volume by 43% compared to the control diet, and also inhibited the formation in colonic tumors by 15%-30% in the animals[48]. Gribel’ et al[85] indicated that honey possessed moderate antitumor effect and pronounced antitumor activity of 5-flurouracil and cyclophosphamide against five different strains of rat and mouse tumors. Furthermore, honey potentiated the antitumor activity of the chemotherapeutic drugs 5-fluorouracil and cyclophosphamide in colorectal cancer cells[86,87]. The anticancer effects of natural honey and its components on liver cancer cells have been investigated in a number of studies[88-90]. Treatment of hepatocellular carcinoma HepG2 cells with bee honey and Nigella sativa led to a significant decrease in both the number of viable HepG2 cells and the levels of nitric oxide and improved the total antioxidant status and caspase-3 activity, especially in HepG2 cells treated with higher doses of bee honey Nigella sativa (20% and 5000 μg/mL)[88]. It has been reported that Spanish honeys were most effective in protecting against food mutagen-induced DNA damage in HepG2 cells, which was attributed to its antioxidant and free radical scavenging properties[89]. Gelam honey was selectively cytotoxic to liver cancer cells and found that the IC50 value of gelam honey towards HepG2 was 25% whereas it was 70% for normal human hepatocytes (WRL-68)[90]. Abdel Aziz et al[91] reported that honey extracts exerted cytotoxic, antimetastatic and anti-angiogenic effects in HepG2 cells. Treatment with diethylnitrosamine induced hepatic cancer in rats and the neoplastic hepatic cells were reduced in the liver of honey-treated DEN-induced rats[92]. These studies indicate that honey has an anticancer effect on various types of cancer cells and exerts its protective effect against the development of cancer by modulating the molecular and cellular mechanisms of carcinogenesis stages. Some of the mechanisms by which honey may exert its anticancer effects are cell cycle arrest, activation of mitochondrial pathway, induction of mitochondrial outer membrane permeabilization, induction of apoptosis, modulation of oxidative stress, amelioration of inflammation, modulation of insulin signaling, and inhibition of angiogenesis[37]. The effect of honey was also investigated in pancreatic cancer. Caffeic acid phenethyl ester induced apoptosis in human pancreatic cancer cells by activation of caspase-3/caspase-7 and mitochondrial dysfunction[93]. Treatment with CAPE slightly restored the expression of E-cadherin and markedly reversed the transforming growth factor-β-induced overexpression of vimentin at 24 h in Human pancreatic cancer cells (PANC-1) cells. CAPE suppressed the expression of Twist 2 and growth of PANC-1 xenografts without significant toxicity in an orthotopic pancreatic cancer model. These data suggest that CAPE could suppress the epithelial-mesenchymal transition in pancreatic cancer[94].
Abdel-Latif MM. Chemoprevention of gastrointestinal cancers by natural honey. World J Pharmacol 2015; 4(1): 160-167 [DOI: 10.5497/wjp.v4.i1.160]
There are many research studies support the use of natural honey for cancer prevention and treatment, especially cancers of the gastrointestinal tract. Nutritional studies have indicated that consumption of honey modulates the risk of the development of gastric cancer, and also honey induced apoptosis in gastric mucosa[77]. It was postulated that CAPE may be a promising adjuvant treatment in gastric cancer[78]. The chemopreventive actions of honey and its components have been also studied in various colon cancer models. Gelam and Nenas honeys suppressed the growth of HT 29 colon cancer cells by inducing DNA damage and apoptosis and suppressing inflammation[79]. Jaganathan also demonstrated the anti-proliferative effect of Caffeic acid, one of the phenolic constituents of honey, inhibited in the colon cancer cells HCT15 and HT29[80]. Honey induced apoptosis by causing the depletion of intracellular non-protein thiols and reduced the mitochondrial membrane potential and increased generation of reactive oxygen species. Furthermore, honey constituents induced apoptosis in colon cancer cells[81]. Orsolić et al[82] showed that honey exerted anti-metastatic effect in a murine tumor model with colon carcinoma. Supplementation of diet with honey and Nigella sativa had a protective effect against methylnitrosourea-induced oxidative stress, inflammatory response and carcinogenesis in Sprague Dawely rats[83]. Caffeic acid esters derivatives inhibited azoxymethane-induced colonic colonie preneoplastic lesions, ornithine decarboxylase, tyrosine protein kinase, and lipoxygenase activities and aberrant crypt foci formation, which are relevant to colon carcinogenesis in rat colon[50]. Caffeic acid and its ester are potent inhibitors of human colon adenocarcinoma cell growth[84]. Dietary administration of phenylethyl-3-methylcaffeate significantly inhibited the incidence and multiplicity of invasive, noninvasive adenocarcinomas of the colon, and also suppressed the colon tumor volume by 43% compared to the control diet, and also inhibited the formation in colonic tumors by 15%-30% in the animals[48]. Gribel’ et al[85] indicated that honey possessed moderate antitumor effect and pronounced antitumor activity of 5-flurouracil and cyclophosphamide against five different strains of rat and mouse tumors. Furthermore, honey potentiated the antitumor activity of the chemotherapeutic drugs 5-fluorouracil and cyclophosphamide in colorectal cancer cells[86,87]. The anticancer effects of natural honey and its components on liver cancer cells have been investigated in a number of studies[88-90]. Treatment of hepatocellular carcinoma HepG2 cells with bee honey and Nigella sativa led to a significant decrease in both the number of viable HepG2 cells and the levels of nitric oxide and improved the total antioxidant status and caspase-3 activity, especially in HepG2 cells treated with higher doses of bee honey Nigella sativa (20% and 5000 μg/mL)[88]. It has been reported that Spanish honeys were most effective in protecting against food mutagen-induced DNA damage in HepG2 cells, which was attributed to its antioxidant and free radical scavenging properties[89]. Gelam honey was selectively cytotoxic to liver cancer cells and found that the IC50 value of gelam honey towards HepG2 was 25% whereas it was 70% for normal human hepatocytes (WRL-68)[90]. Abdel Aziz et al[91] reported that honey extracts exerted cytotoxic, antimetastatic and anti-angiogenic effects in HepG2 cells. Treatment with diethylnitrosamine induced hepatic cancer in rats and the neoplastic hepatic cells were reduced in the liver of honey-treated DEN-induced rats[92]. These studies indicate that honey has an anticancer effect on various types of cancer cells and exerts its protective effect against the development of cancer by modulating the molecular and cellular mechanisms of carcinogenesis stages. Some of the mechanisms by which honey may exert its anticancer effects are cell cycle arrest, activation of mitochondrial pathway, induction of mitochondrial outer membrane permeabilization, induction of apoptosis, modulation of oxidative stress, amelioration of inflammation, modulation of insulin signaling, and inhibition of angiogenesis[37]. The effect of honey was also investigated in pancreatic cancer. Caffeic acid phenethyl ester induced apoptosis in human pancreatic cancer cells by activation of caspase-3/caspase-7 and mitochondrial dysfunction[93]. Treatment with CAPE slightly restored the expression of E-cadherin and markedly reversed the transforming growth factor-β-induced overexpression of vimentin at 24 h in Human pancreatic cancer cells (PANC-1) cells. CAPE suppressed the expression of Twist 2 and growth of PANC-1 xenografts without significant toxicity in an orthotopic pancreatic cancer model. These data suggest that CAPE could suppress the epithelial-mesenchymal transition in pancreatic cancer[94].
Abdel-Latif MM. Chemoprevention of gastrointestinal cancers by natural honey. World J Pharmacol 2015; 4(1): 160-167 [DOI: 10.5497/wjp.v4.i1.160]
CONCLUSION
Natural honey has many therapeutic benefits and medical uses. The different effects of natural honey including anti-inflammatory antioxidants and anticancer effects highlight its importance in the prevention of gastrointestinal cancers and improvement of cancer therapies. Some evidence of the anticancer effects of honey has been reported from in-vitro and in-vivo studies in gastrointestinal cancers, however, further investigation of anticancer effects of honey in animal and clinical studies are required to prove its therapeutic efficacy in chemoprevention strategies.
Abdel-Latif MM. Chemoprevention of gastrointestinal cancers by natural honey. World J Pharmacol 2015; 4(1): 160-167 [DOI: 10.5497/wjp.v4.i1.160]
Natural honey has many therapeutic benefits and medical uses. The different effects of natural honey including anti-inflammatory antioxidants and anticancer effects highlight its importance in the prevention of gastrointestinal cancers and improvement of cancer therapies. Some evidence of the anticancer effects of honey has been reported from in-vitro and in-vivo studies in gastrointestinal cancers, however, further investigation of anticancer effects of honey in animal and clinical studies are required to prove its therapeutic efficacy in chemoprevention strategies.
Abdel-Latif MM. Chemoprevention of gastrointestinal cancers by natural honey. World J Pharmacol 2015; 4(1): 160-167 [DOI: 10.5497/wjp.v4.i1.160]
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