Influence of waste of lubricating oil on the intensity of its aging in a marine trunk diesel engine

Представлены результаты моделирования старения моторного масла в судовом тронковом дизеле при разном его угаре с идентификацией влияния на степень окисления, срабатывание присадок (по щелочности), накопление нерастворимых продуктов, рост кислотности и смолообразования форсировки двигателя и качества применяемых горюче-смазочных материалов. Показана рациональность исследования процесса старения смазочного масла в циркуляционной системе смазки одноцилиндрового отсека дизеля в лабораторных условиях, что позволяет выдерживать контролируемые параметры комплекса «дизель – топливо – масло» (ДТМ) и снизить затраты на моторные испытания. По результатам расчетно-эксперементального исследования получена модель старения смазочного масла по удельным, приходящимся на единицу мощности двигателя показателям, которая позволяет прогнозировать его состояние в зависимости от срока службы и своевременно отбраковывать. Показана адекватность модели старения по экспериментальным данным использования моторного масла в судовом полноразмерном тронковом дизеле повышенной форсировки. Разработанная модель по указанным направлениям старения позволяет определить состав и режимы функционирования комплекса ДТМ, при которых обеспечивается ресурсосберегающее маслоиспользование в двигателях внутреннего сгорания. This paper presents the results of an engine oil aging model in a marine trunk diesel engine under different combustion conditions with characterization of the effect on the oxidation rate, the actuation of additives (by alkalinity), the accumulation of non-soluble products, an increase in acidity and gumming of the engine boost and the quality of the utilized fuels and lubricants. The efficiency of the lubricating oil aging process study in the circulating lubrication system of a single-cylinder diesel compartment in laboratory conditions is also shown in the article, this allows to maintain the controlled parameters of the «diesel – fuel – oil» system and to reduce the cost of motor tests. Based on the results of a computational-experimental study a lubricating oil aging model was obtained in terms of specific indicators per unit of engine power, which allows to predict its condition depending on the operating life and to promptly discard it. The adequacy of the aging model is based on experimental data of the engine oil use in a ship's full-size trunk diesel engine with increased boost. The developed model of the indicated directions of aging makes it possible to determine the composition and operating modes of the «engine-fuel-oil» system, which ensures resource-saving oil use in internal combustion engines.

Extracts of Different Organs of Macadamia Nut Tree (Macadamia Integrifolia) Ameliorate Oxidative Damage in D-Galactose Accelerated Aging Model in Rats

Macadamia nut tree, Macadamia integrifolia (Maiden & Betche), is cultivated for the production of the edible macadamia nuts, which are a good source of monounsaturated fatty acids. We investigated the effect of ethanolic extracts of leaves, nuts, and nutshells of macadamia in D-galactose accelerated aging model in rats. Administration of D-galactose (150 mg/kg) in rats for 60 days resulted in impairment of cognitive function and motor coordination and caused an increase in oxidative stress and deterioration of liver and kidney functions. Macadamia nut extract ameliorated cognitive impairment induced by D-galactose as inferred from Morris water maze test and balance test using rotarod. Also, nut extract was superior to leaves and shell extract in reducing serum levels of malondialdehyde (50%), alanine transaminase (63%), aspartate transaminase (63%), total bilirubin (24%), creatinine (38%), and urea (16%) compared to animals that received no treatment. Chemical analysis showed that macadamia nut extract has a high percentage of oleic acid (81%) followed by palmitoleic acid (6.9%). This study encourages further investigation of the health benefits of macadamia nuts and the underlying mechanism of these effects.

Peanut meal extract fermented with Bacillus natto attenuates physiological and behavioral deficits in a D-galactose-induced aging rat model

Our previous studies have shown that the nutritional properties of peanut meal after fermentation are markedly improved. In this study, in order to facilitate the further utilization of peanut meal, we investigated the effects of its fermentation extract by Bacillus natto (FE) on cognitive ability, antioxidant activity of brain, and protein expression of hippocampus of aging rats induced by D-galactose. Seventy-two female SD rats aged 4-5 months were randomly divided into six groups: normal control group (N), aging model group (M), FE low-dose group (FL), FE medium-dose group (FM), FE high-dose group (FH) and vitamin E positive control group (Y). Morris water maze (MWM) test was performed to evaluate their effects on learning and memory ability in aging rats. SOD activity and malondialdehyde (MDA) content of brain, HE staining and the expression of γ-aminobutyric acid receptor 1 (GABABR1) and N-methyl-D-aspartic acid 2B receptor (NMDAR2B) in the hippocampus of rats were measured. The results show that FE supplementation can effectively alleviate the decrease of thymus index induced by aging, decrease the escape latency of MWM by 66.06%, brain MDA by 28.04%, hippocampus GABABR1 expression by 7.98%, and increase brain SOD by 63.54% in aging model rats. This study provides evidence for its anti-aging effects and is a research basis for potential nutritional benefits of underutilized food by-products.

The Gut Microbiota Metabolite Urolithin B Improves Cognitive Deficits by Inhibiting Cyt C-Mediated Apoptosis and Promoting the Survival of Neurons Through the PI3K Pathway in Aging Mice

Background: Despite considerable advances in pharmacotherapy, more effective therapeutic interventions for aging-related neurodegenerative disorders (NDs), such as Alzheimer’s disease (AD), remain limited. Urolithin B (UB), one of the major subcategories of urolithins (microbiota metabolites) found in various tissues after ellagitannin consumption, has been shown to possess antioxidant, anti-inflammatory, and antiapoptotic effects. However, the neuroprotective effect of UB on brain aging in mice and its potential mechanisms were still unknown.Methods: In the current research, we first assessed the ameliorative effects of UB on oxidative injury and apoptosis induced by H2O2 in neuro-2a cells. Then a subcutaneous injection of D-galactose in mice for 8 weeks was used to establish the aging model to evaluate the protective effects of UB. The capacity of memory and learning, alterations of hippocampus histology and corresponding molecular mechanisms were all evaluated.Results: The D-gal-induced accelerated aging model in vivo demonstrated that UB could significantly ameliorate deficits in learning and memory by inhibiting the accumulation of advanced glycation end products (AGEs) and elevating the expression and activity of Cu, Zn-SOD and CAT. Furthermore, UB downregulated the c-Jun N-terminal kinase (JNK) signaling pathway and prevented cytochrome c release from isolated mitochondria, thereby inhibiting neuronal apoptosis during the aging process. More importantly, UB stimulation of aging mice activated ERK and phosphoinositide 3-kinase (PI3K), leading to neuronal survival along with Akt and p44/42 mitogen-activated protein kinase (MAPK) phosphorylation and activation.Conclusion: In summary, UB effectively alleviated cognitive deficits and ameliorated brain aging-related conditions and could be considered a healthcare product to prevent aging-associated NDs such as AD.