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Trophocytes and fat cells of honeybees have been used for cellular senescence studies, but their oxidative stress and antioxidant enzyme activities with aging in workers is unknown. Here, we assayed reactive oxygen species and the activities of antioxidant enzymes in the trophocytes and fat cells of young and old workers. Young workers had higher reactive oxygen species levels, higher superoxide dismutase and thioredoxin reductase activities as well as lower catalase and glutathione peroxidase activities compared to old workers. Adding these results up, we propose that oxidative stress decreases with aging in the trophocytes and fat cells of workers.

Queen honeybees (Apis mellifera) have much longer lifespans than worker bees. Although the expression of age-related molecules in the trophocytes and fat cells of young and old workers have been determined, the expression of age-related molecules in queens is unknown. In this study, we examined the expression of age-related molecules in the trophocytes and fat cells of young and old queens. Molecular analyses detected no differences in telomerase activity or telomere lengths between trophocytes and fat cells from young and old queens, indicating that these cells do not divide in adulthood. Further assays showed that old queens has higher non-homogeneous cellular morphology, senescence-associated β-galactosidase (SA-β-Gal) activity, accumulation of lipofuscin granules, lipid peroxidation, and protein oxidation compared to young queens. These results demonstrate that age-related molecules can be used to evaluate aging in the trophocytes and fat cells of queens and to lay the foundation for further study of the mechanisms that delay cellular aging in the trophocytes and fat cells of queens.aging / trophocyte / fat cell / queen / honeybee

Trophocytes and fat cells of queen honeybees have been used for delayed cellular senescence studies, but their oxidative stress and anti-oxidant enzyme activities with advancing age are unknown. In this study, we assayed reactive oxygen species (ROS) and anti-oxidant enzymes in the trophocytes and fat cells of young and old queens. Young queens had lower ROS levels, lower superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, and higher thioredoxin reductase (TR) activity compared to old queens. These results show that oxidative stress and anti-oxidant enzyme activities in trophocytes and fat cells increase with advancing age in queens and suggest that an increase in oxidative stress and a consequent increase in stress defense mechanisms are associated with the longevity of queen honeybees.

Although stress is one of the risk factors of diabetes, few studies have assessed the effects of stress on diabetic rats. This study, therefore, analyzed differences in cardiovascular-related factors among control, nonstressed diabetic, and stressed diabetic rats as well as assessed the effects of linalyl acetate (LA) on stressed diabetic rats. Male Sprague-Dawley rats were subjected to immobilization stress throughout the experimental period, and diabetes was induced on day 15 by a single injection of streptozotocin. After confirming the induction of diabetes, stressed diabetic rats were administered LA (10 or 100 mg/kg) or metformin (500 mg/kg) for the last 7 days. Compared with nonstressed diabetic rats, stressed diabetic rats had significantly lower body weight, body fat percentage, ACh-induced vasorelaxation, systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), and NF-κB expression as well as increased serum nitrite concentration. Although metformin increased serum insulin concentration significantly, 100 mg/kg LA showed only an increasing tendency. However, treatment with 100 mg/kg LA not only reduced serum glucose and NF-κB expression, but also restored ACh-induced vasorelaxation, SBP, DBP, HR, AMP-activated protein kinase expression, and serum nitrite almost to control levels. Importantly, 100 mg/kg LA was more effective than metformin in ameliorating serum glucose, endothelial nitric oxide synthase expression, HR, and serum nitrite. These findings suggest that chronic stress can aggravate endothelial dysfunction and hemodynamic alterations in diabetes and that LA may have potent therapeutic efficacy in diabetic patients with cardiovascular disease complications or chronic stress. NEW & NOTEWORTHY To our knowledge, this is the first study to assess the effects of linalyl acetate (LA) on cardiovascular-related factors in diabetic rats exposed to chronic stress. Treatment with LA restored acetylcholine-induced vasorelaxation, blood pressure, heart rate, and AMP-activated protein kinase and serum nitrite levels. The present results suggest that LA may have potent therapeutic efficacy in diabetic patients with complications of cardiovascular disease or chronic stress.

Ischemic stroke remains an important cause of disability and mortality. Hypertension is a critical risk factor for the development of ischemic stroke. Control of risk factors, including hypertension, is therefore important for the prevention of ischemic stroke. Linalyl acetate (LA) has been reported to have therapeutic effects in ischemic stroke by modulating intracellular Ca2+ concentration and having anti-oxidative properties. The preventive efficacy of LA has not yet been determined. This study therefore investigated the preventive efficacy of LA in rat aortas exposed to hypertension related-ischemic injury, and the mechanism of action of LA.Hypertension was induced in vivo following ischemic injury to the aorta induced by oxygen-glucose deprivation and reoxygenation in vitro. Effects of LA were assayed by western blotting, by determining concentrations of lactate dehydrogenase (LDH) and reactive oxygen species (ROS) and by vascular contractility assays. LA significantly reduced systolic blood pressure in vivo. In vitro, LA suppressed ischemic injury-induced expression of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit p47phox, as well as ROS production, LDH release, and ROS-induced endothelial nitric oxide synthase suppression. These findings indicate that LA has anti-hypertensive properties that can prevent hypertension-related ischemic injury and can prevent NADPH oxidase-induced production of ROS.

Calcium-related ischemic injury (CRII) can damage cells of the neurovascular unit (NVU). Here, we investigate the protective effects of linalyl acetate (LA) against CRII-induced NVU damage and evaluate the underlying mechanisms. The protective effects of LA in cell lines representative of NVU components (BEND, SH-SY5Y, BV2, and U373 cells) were evaluated following exposure to oxygen-glucose deprivation/reoxygenation alone (OGD/R-only) or OGD/R in the presence of 5 mM extracellular calcium ([Ca2+]o) to mimic CRII. LA reversed damage under OGD/R-only conditions by blocking p47phox/NADPH oxidase (NOX) 2 expression, reactive oxygen species (ROS) production, nitric oxide (NO) abnormality, and lactate dehydrogenase (LDH) release only in the BEND cells. However, under CRII-mimicking conditions, LA reversed NO abnormality and matrix metalloproteinase (MMP)-9 activation in the BEND murine brain endothelial cells; inhibited p47phox expression in the human SH-SY5Y neural-like cells; decreased NOX2 expression and ROS generation in the BV2 murine microglial cells; and reduced p47phox expression in the U373 human astrocyte-like cells. Importantly, LA protected against impairment of the neural cells, astrocytes, and microglia, all of which are cellular components of the NVU induced by exposure to CRII-mimicking conditions, by reducing LDH release. We found that LA exerted a protective effect in the BEND cells that may differ from its protective effects in other NVU cell types, following OGD/R-induced damage in the context of elevated [Ca2+]o.

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