Role of oregano and Citrus species-based essential oil preparation for the control of coccidiosis in broiler chickens.

BACKGROUND: Due to presence of drug-resistant Eimeria strains and raised public health safety concerns about drug residues in the meat, there is renewed interest in the search for natural alternatives to the coccidiosis control agents. This study was conducted to test the anticoccidial efficacy of oregano and Citrus spp.-based essential oils for broilers. METHODS: A total of 280 7-day-old broiler chicks were fed a control diet or diets with salinomycin or essential oils for up to 35 d of age. On d 14, half of the control groups and the treated groups were orally challenged with a coccidiosis vaccine at 25 times higher than the recommended vaccine dose. Control diet-fed chickens that were gavaged with phosphate-buffered saline were considered non-challenged control group. RESULTS: Eimeria challenge or dietary additives failed to affect growth performance during the 7 to 20 d growth period although essential oil-fed chickens exhibited the lowest body wight gain (P = 0.332) and the highest feed conversion ratio (P = 0.062). Oocysts in the litter were detected in the challenged control diet group and the challenged/essential oil-fed groups at 21 and 35 d, respectively. Superoxide dismutase activity in the serum was elevated (P = 0.059) in the salinomycin-fed chickens compared to the challenged controls. Alpha-1-acid glycoprotein was decreased by 28.7% in the salinomycin-fed chickens but increased by 38.1% in the essential oil group compared with the challenged control group. Challenged control group exhibited a significantly higher cooking loss of the thigh meat, compared to the non-challenged control diet group, which was marginally mitigated by dietary supplementation with essential oils. Chickens fed essential oil-added diet had the highest branched-chain fatty acids contents in the cecum. CONCLUSIONS: In conclusion, this study shows that oregano and Citrus-based essential oil preparation did not affect growth performance in broiler chickens challenged with the coccidiosis vaccine nor did Eimeria-specific duodenal lesion. However, dietary essential oil preparation lowered oocysts present in litter materials and altered branched-chain fatty acids in cecal digesta. Beneficial findings of the essential oil preparation on volatile fatty acids and oocysts output may warrant further research into assessing its effectiveness and its efficacy in pathogenic field-isolate Eimeria spp.-induced coccidiosis disease model.

Nafamostat mesilate attenuates transient focal ischemia/reperfusion-induced brain injury via the inhibition of endoplasmic reticulum stress.

Nafamostat mesilate (NM), a serine protease inhibitor, has a broad range of clinical applications that include use as an anticoagulant during hemodialysis in cerebral hemorrhage patients, as a hemoperfusion anticoagulant for patients with intravascular coagulation, hemorrhagic lesions, and hemorrhagic tendencies, and for the improvement of acute pancreatitis. However, the effects of NM on acute cerebral ischemia have yet to be investigated. Thus, the present study utilized a rat model in which transient middle cerebral artery occlusion (MCAO) was used to induce ischemic injury to investigate the effects of NM on infarct volume and histological and biological changes. NM (1mg/kg) was intravenously administered prior to and after the MCAO procedure. Compared to control rats, the administration of NM significantly decreased infarct size and the extent of brain edema after the induction of focal ischemia via MCAO. Additionally, NM treatment attenuated MCAO-induced neuronal degeneration and activation of microglia and astrocytes. NM treatment also inhibited the MCAO-induced expression levels of glucose-regulated protein 78 (GRP78), CATT/EBP homologous protein (CHOP), and p-eukaryotic initiation factor 2α (eIF2α), which are endoplasmic reticulum (ER) stress markers, in the cerebral cortex. The present findings demonstrate that NM exerts neuroprotective effects in the brain following focal ischemia via, at least in part, the inhibition of ER stress.

Rg3-enriched Korean Red Ginseng improves vascular function in spontaneously hypertensive rats.

BACKGROUND: Panax ginseng has distinct and impressive health benefits, such as improved blood pressure and immune system functioning. Rg3-enriched Korean Red Ginseng (REKRG) isolated from Korean Red Ginseng contains a high percentage of Rg3. METHODS: In this study, we examined the effects of REKRG on endothelial cell nitric oxide synthase (eNOS) activation and adhesion molecules in endothelial cells and vascular function in rats. RESULTS: REKRG dose-dependently increased eNOS phosphorylation and nitric oxide (NO) production in endothelial cells. In addition, REKRG markedly inhibited the tumor necrosis factor-α (TNF-α)-mediated induction of intercellular adhesion molecule (ICAM)-1 and cyclooxygenase (COX)-2 expressions in endothelial cells. REKRG improved endothelium-dependent vasorelaxation in the Wistar-Kyoto (WKY) rat and spontaneously hypertensive rats (SHRs) compared with controls. Furthermore, REKRG treatment for 6 weeks increased serum NO levels and reduced the mean aortic intima-media thickness compared with controls. CONCLUSION: Taken together, these results suggest that REKRG increased vascular function and improved immune system functioning. Therefore, REKRG is a very useful food for preventing or improving various cardiovascular diseases.

CRIF1 deficiency induces p66shc-mediated oxidative stress and endothelial activation.

Mitochondrial dysfunction has been implicated in the pathophysiology of various cardiovascular diseases. CRIF1 is a protein present in the mitochondria associated with large mitoribosomal subunits, and CRIF1 knockdown induces mitochondrial dysfunction and promotes ROS production. p66shc is a redox enzyme implicated in mitochondrial ROS generation and translation of oxidative signals and, therefore, is a key factor for oxidative stress in endothelial cells. In this study, we investigated whether mitochondrial dysfunction induced by CRIF1 knockdown induces p66shc stimulation and plays any role in mitochondrial dysfunction-induced endothelial activation. Knockdown of CRIF1 decreased the expression of mitochondrial oxidative phosphorylation (OXPHOS) complexes I, III and IV, leading to increased mitochondrial ROS (mtROS) and hyperpolarization of the mitochondrial membrane potential. Knockdown of CRIF1 also stimulated phosphorylation of p66shc and increased cytosolic ROS in endothelial cells. Furthermore, the expression of vascular cell adhesion molecule-1 and endoplasmic reticulum stress proteins were increased upon CRIF1 knockdown in endothelial cells. However, p66shc knockdown blunted the alteration in mitochondrial dynamics and ROS production in CRIF1 knockdown endothelial cells. In addition, p66shc knockdown reduced the CRIF1 knockdown-induced increases in adhesion between monocytes and endothelial cells. Taken together, these results suggest that CRIF1 knockdown partially induces endothelial activation via increased ROS production and phosphorylation of p66shc.

Docosahexaenoic acid improves vascular function via up-regulation of SIRT1 expression in endothelial cells.

n-3-Polyunsaturated fatty acids (PUFAs) protect against myocardial infarction, arteriosclerosis and high blood pressure by stimulating endothelial nitric oxide synthase (eNOS) to increase nitric oxide (NO) production. However, the mechanism remains to be elucidated. This study investigated the role of SIRT1 in the protective effects of docosahexaenoic acid (DHA) in vascular endothelial cells. Exposure of human umbilical vein endothelial cells (HUVECs) to 0.3-30 µM DHA did not affect cell viability, and DHA treatment dose-dependently increased SIRT1 expression. The DHA-mediated increase in SIRT1 expression induced eNOS deacetylation, increasing endothelial NO. However, inhibition of SIRT1 inhibited DHA-mediated increases in NO production. This effect was mediated via deacetylation of lysines 496 and 506 in the eNOS calmodulin-binding domain. The effects of DHA were also demonstrated in rat aortic rings, in which DHA treatment increased SIRT1 expression and bioavailable NO. Our results demonstrate that SIRT1 plays an important role in DHA-mediated increases in bioavailable NO via decreased eNOS acetylation.