Environmental filtering and biotic interactions act on different facets of the diversity of benthic assemblages associated with eelgrass.

Eelgrass supports diverse benthic communities that ensure a variety of ecosystem functions. To better understand the ecological processes that shape community composition in eelgrass at local and regional scales, taxonomic and functional α- and ß-diversity were quantified for communities inhabiting five meadows in France. The extent to which environmental factors affected local and regional benthic communities was quantified by considering their direct and indirect effects (through morphological traits of eelgrass) using piecewise structural equation modeling (pSEM). Communities supported by eelgrass had higher species abundances, as well as taxonomic and functional diversity compared to nearby bare sediments. No significant differences were found between communities from the center relative to the edges of meadows, indicating that both habitats provide similar benefits to biodiversity. The presence of a few abundant species and traits suggests moderate levels of habitat filtering and close associations of certain species with eelgrass. Nevertheless, high turnover of a large number of rare species and traits was observed among meadows, resulting in meadows being characterized by their own distinct communities. High turnover indicates that much of the community is not specific to eelgrass, but rather reflects local species pools. pSEM showed that spatial variation in community composition (ß-diversity) was primarily affected by environmental conditions, with temperature, current velocity, and tidal amplitude being the most significant explanatory variables. Local richness and abundance (α-diversity) were affected by both environment and morphological traits. Importantly, morphological traits of Zostera marina were also influenced by environmental conditions, revealing cascading effects of the environment on assemblages. In sum, the environment exerted large effects on community structure at both regional and local scales, while plant traits were only pertinent in explaining local diversity. This complex interplay of processes acting at multiple scales with indirect effects should be accounted for in conservation efforts that target the protection of biodiversity.

Serum Biomarkers to Mild Cognitive Deficits in Children and Adolescents.

Intellectual disability (ID) is a condition characterized by significant limitations in both cognitive development and adaptive behavior. The diagnosis is made through clinical assessment, standardized tests, and intelligence quotient (IQ). Genetic, inflammation, oxidative stress, and diet have been suggested to contribute to ID, and biomarkers could potentially aid in diagnosis and treatment. Study included children and adolescents aged 6-16 years. The ID group (n = 16) and the control group (n = 18) underwent the Wechsler Intelligence Scale for Children (WISC-IV) test, and blood samples were collected. Correlations between biomarker levels and WISC-IV test scores were analyzed. The ID group had an IQ score below 75, and the values of four domains (IQ, IOP, IMO, and IVP) were lower compared to the control group. Serum levels of FKN, NGF-ß, and vitamin B12 were decreased in the ID group, while DCFH and nitrite levels were increased. Positive correlations were found between FKN and the QIT and IOP domains, NGF and the QIT and IMO domains, and vitamin B12 and the ICV domain. TNF-α showed a negative correlation with the ICV domain. Our study identified FKN, NGF-ß, and vitamin B12 as potential biomarkers specific to ID, which could aid in the diagnosis and treatment of ID. TNF-α and oxidative stress biomarkers suggest that ID has a complex etiology, and further research is needed to better understand this condition and develop effective treatments. Future studies could explore the potential implications of these biomarkers and develop targeted interventions based on their findings.

Capsicum baccatum Red Pepper Prevents Cardiometabolic Risk in Rats Fed with an Ultra-Processed Diet.

Metabolic syndrome is a serious health condition reaching epidemic proportions worldwide and is closely linked to an increased risk of cardiovascular problems. The lack of appropriate treatment paves the way for developing new therapeutic agents as a high priority in the current research. In this study, we evaluated the protective effects of Capsicum baccatum red pepper on metabolic syndrome scenarios induced by an ultra-processed diet in rats. After four months, the ultra-processed diet increased central obesity, triglycerides, total cholesterol, LDL-cholesterol plasma levels, and impaired glucose tolerance. The oral administration of C. baccatum concomitantly with the ultra-processed diet avoided the accumulation of adipose tissue in the visceral region, reduced the total cholesterol and LDL fraction, and improved glucose homeostasis, factors commonly associated with metabolic syndrome. The data presented herein reveal an important preventive action of C. baccatum in developing metabolic disorders among animals fed a hypercaloric diet, significantly reducing their cardiometabolic risk. Allied with the absence of toxic effects after chronic use, our study suggests C. baccatum red pepper as a secure and enriched source of bioactive compounds promising to protect against pathological processes associated with metabolic syndrome.

Effects of Avocado Oil Supplementation on Insulin Sensitivity, Cognition, and Inflammatory and Oxidative Stress Markers in Different Tissues of Diet-Induced Obese Mice.

Obesity induces insulin resistance, chronic inflammation, oxidative stress, and neurocognitive impairment. Avocado oil (AO) has antioxidants and anti-inflammatory effects. This study evaluated the effect of AO supplementation on obese mice in the adipose tissue, muscle, liver, and hippocampus. Male C57BL/6J mice received a standard and high-fat diet (20 weeks) and then were supplemented with AO (4 mL/kg of body weight, 90 days) and divided into the following groups: control (control), control + avocado oil (control + AO), diet-induced obesity (DIO), and diet-induced obesity + avocado oil (DIO + AO) (n = 10/group). AO supplementation was found to improve insulin sensitivity and decrease hepatic fat accumulation and serum triglyceride levels in DIO mice. AO improved cognitive performance and did not affect mood parameters. Oxidative marker levels were decreased in DIO + AO mice in all the tissues and were concomitant with increased catalase and superoxide dismutase activities in the epididymal adipose tissue and quadriceps, as well as increased catalase activity in the liver. AO in obese animals further induced reductions in TNF-α and IL-1ß expressions in the epididymal adipose tissue and quadriceps. These results suggest that AO supplementation has the potential to be an effective strategy for combating the effects of obesity in rats, and human studies are needed to confirm these findings.

Behavioral, genetic and biochemical changes in the brain of the offspring of female mice treated with caffeine during pregnancy and lactation.

The intrauterine environment is a critical location for exposure to exogenous and endogenous factors that trigger metabolic changes through fetal programming. Among the external factors, chemical compounds stand out, which include caffeine, since its consumption is common among women, including during pregnancy. Thereby, the aim of the present study was to evaluate the behavioral, genetic, and biochemical parameters in the offspring of female mice treated with caffeine during pregnancy and lactation. Swiss female mice (60 days old) received tap water or caffeine at 0.3 or 1.0 mg/mL during copulation (7 days), pregnancy (21 days) and lactation (21 days). After the end of the lactation period, the offspring were divided into groups (water, caffeine 0.3 or 1.0 mg/mL) with 20 animals (10 animals aged 30 days and 10 animals aged 60 days per group per sex). Initially, the offspring were submitted to behavioral tasks and then euthanized for genetic and biochemical analysis in the brain (cortex, striatum, and hippocampus). Behavioral changes in memory, depression, and anxiety were observed in the offspring: 30-day-old female offspring at 1.0 mg /mL dose presented anxiogenic behavior and male offspring the 0.3 mg/mL dose at 30 days of age did not alter long-term memory. Furthermore, an increase in DNA damage and oxidative stress in the brain were observed in the offspring of both sexes. Furthermore, there were changes in Ape-1, BAX, and Bcl-2 in the female offspring hippocampus at 30 days of life. Thus, with this study, we can suggest genotoxicity, oxidative stress, and behavioral changes caused by caffeine during pregnancy and lactation in the offspring that were not treated directly, but received through their mothers; thus, it is important to raise awareness regarding caffeine consumption among pregnant and lactating females.

Resistance Exercise Training Improves Metabolic and Inflammatory Control in Adipose and Muscle Tissues in Mice Fed a High-Fat Diet.

This study investigates whether ladder climbing (LC), as a model of resistance exercise, can reverse whole-body and skeletal muscle deleterious metabolic and inflammatory effects of high-fat (HF) diet-induced obesity in mice. To accomplish this, Swiss mice were fed for 17 weeks either standard chow (SC) or an HF diet and then randomly assigned to remain sedentary or to undergo 8 weeks of LC training with progressive increases in resistance weight. Prior to beginning the exercise intervention, HF-fed animals displayed a 47% increase in body weight (BW) and impaired ability to clear blood glucose during an insulin tolerance test (ITT) when compared to SC animals. However, 8 weeks of LC significantly reduced BW, adipocyte size, as well as glycemia under fasting and during the ITT in HF-fed rats. LC also increased the phosphorylation of AktSer473 and AMPKThr172 and reduced tumor necrosis factor-alpha (TNF-α) and interleukin 1 beta (IL1-ß) contents in the quadriceps muscles of HF-fed mice. Additionally, LC reduced the gene expression of inflammatory markers and attenuated HF-diet-induced NADPH oxidase subunit gp91phox in skeletal muscles. LC training was effective in reducing adiposity and the content of inflammatory mediators in skeletal muscle and improved whole-body glycemic control in mice fed an HF diet.

Involvement of Multiple Variants of Soluble CD146 in Systemic Sclerosis: Identification of a Novel Profibrotic Factor.

OBJECTIVE: Systemic sclerosis (SSc) is an autoimmune disorder characterized by excessive fibrosis, immune dysfunction, and vascular damage, in which the expression of many growth factors is deregulated. CD146 was recently described as a major actor in SSc. Since CD146 also exists as a circulating soluble form (sCD146) that acts as a growth factor in numerous angiogenic- and inflammation-related pathologies, we sought to identify the mechanisms underlying the generation of sCD146 and to characterize the regulation and functions of the different variants identified in SSc. METHODS: We performed in vitro experiments, including RNA-Seq and antibody arrays, and in vivo experiments using animal models of bleomycin-induced SSc and hind limb ischemia. RESULTS: Multiple forms of sCD146, generated by both shedding and alternative splicing of the primary transcript, were discovered. The shed form of sCD146 was generated from the cleavage of both long and short membrane isoforms of CD146 through ADAM-10 and TACE metalloproteinases, respectively. In addition, 2 novel sCD146 splice variants, I5-13-sCD146 and I10-sCD146, were identified. Of interest, I5-13-sCD146 was significantly increased in the sera of SSc patients (P < 0.001; n = 117), in particular in patients with pulmonary fibrosis (P < 0.01; n = 112), whereas I10-sCD146 was decreased (P < 0.05; n = 117). Further experiments revealed that shed sCD146 and I10-sCD146 displayed proangiogenic activity through the focal adhesion kinase and protein kinase Cε signaling pathways, respectively, whereas I5-13-sCD146 displayed profibrotic effects through the Wnt-1/ß-catenin/WISP-1 pathway. CONCLUSION: Variants of sCD146, and in particular the novel I5-13-sCD146 splice variant, could constitute novel biomarkers and/or molecular targets for the diagnosis and treatment of SSc and other angiogenesis- or fibrosis-related disorders.

Dietary omega-3 fatty acids prevent neonatal seizure-induced early alterations in the hippocampal glutamatergic system and memory deficits in adulthood.

OBJECTIVE: We investigated the influence of dietary omega-3 polyunsaturated fatty acids (n-3 PUFAs) on glutamatergic system modulation after a single episode of neonatal seizures and their possible effects on seizure-induced long-lasting behavioral deficits. METHODS: Male Wistar rats receiving an omega-3 diet (n-3) or an n-3 deficient diet (D) from the prenatal period were subjected to a kainate-induced seizure model at P7. Glutamate transporter activity and immunocontents (GLT-1 and GLAST) were assessed in the hippocampus at 12, 24, and 48 h after the seizure episode. Fluorescence intensity for glial cells (GFAP) and neurons (NeuN) was assessed 24 h after seizure in the hippocampus. Behavioral analysis (elevated-plus maze and inhibitory avoidance memory task) was performed at 60 days of age. RESULTS: The D group showed a decrease in glutamate uptake 24 h after seizure. In this group only, the GLT1 content increased at 12 h, followed by a decrease at 24 h. GLAST increased up to 24 h after seizure. GFAP fluorescence was higher, and NeuN fluorescence decreased, in the D group independent of seizures. In adulthood, the D group presented memory deficits independent of seizures, but short-term memory (1.5 h after a training session) was abolished in the D group treated with kainate. SIGNIFICANCE: N-3 PUFA positively influenced the glutamatergic system during seizure and prevented seizure-related memory deficits in adulthood.

Effects of Low-Intensity Transcranial Pulsed Ultrasound Treatment in a Model of Alzheimer's Disease.

Alzheimer's disease (AD) is the most common neurodegenerative disease. One of the main pathology markers of AD is the beta-amyloid plaques (ßA1-42) created from residues of the badly processed amyloid precursor protein. The accumulation of these plaques can induce neuroinflammation and oxidative stress and impair antioxidant mechanisms, culminating in cognitive and memory deficits. New therapies are necessary to treat AD as the approved drugs do not treat the progress of the disease. Transcranial low-intensity pulsed ultrasound (LIPUS) affects brain metabolism and could be tested as a treatment for AD. This study was aimed at evaluating the LIPUS treatment in a model of AD induced by ßA1-42 intracerebroventricularly (ICV) and its effects on learning memory, neurotrophins, neuroinflammation and oxidative status. ßA1-42 was administered ICV 24 h before the start of a 5-wk LIPUS treatment. The treatment with LIPUS improved recognition memory, as well as increasing nerve growth factor ß and brain-derived neurotrophic factor levels in the hippocampus and cortex. There was a decrease in protein damage in the hippocampus treated with LIPUS. Neuroinflammation and oxidative stress were not present in the AD model used. The results indicated that LIPUS is a novel and promising adjuvant strategy for treatment of the late stage of AD.

Physical Exercise Training Improves Judgment and Problem-Solving and Modulates Serum Biomarkers in Patients with Alzheimer's Disease.

Alzheimer's disease (AD) is characterized by progressive impairment of memory, with an etiology involving oxidative stress and inflammation. Exercise training is a safe, efficacious, and economic approach to manage neurodegenerative diseases. In AD, the biomarkers of oxidative damage to lipids, proteins, and DNA are elevated. In the present study, we aimed to evaluate whether exercise is effective in patients with AD by assessing the serum biomarkers associated with the redox status, neurotrophin levels, and inflammatory system. This nonrandomized clinical study (n = 15) involved 22 training sessions performed twice a week (60 min/session) in patients diagnosed with AD. The cognitive and self-awareness tests were performed 48 h before and after the physical training session. In patients with AD, physical training significantly improved the judgment and problem-solving domains of the memory score; however, general mental health, memory, orientation, and home/hobby domains were improved slightly, and the neurotrophin levels remained unaltered. Significantly, the markers of protein integrity also increased following exercise. Furthermore, catalase activity and ROS levels decreased, nitrite levels increased, and interleukin-4 level increased following physical training in patients with AD. Although proinflammatory cytokines remained unaltered, the levels of neuron-specific enolase, a marker of neuronal damage, decreased following exercise training in these patients. In conclusion, physical exercise training could be a safe and effective method for blocking the AD progression and improving the antioxidant capacity and anti-inflammatory system, whereas certain assessed biomarkers could be utilized to monitor AD therapy.

Effects of Zingiber officinale extract supplementation on metabolic and genotoxic parameters in diet-induced obesity in mice.

Obesity is an epidemic associated with many diseases. The nutraceutical Zingiber officinale (ZO) is a potential treatment for obesity; however, the molecular effects are unknown. Swiss male mice were fed a high-fat diet (59 % energy from fat) for 16 weeks to generate a diet-induced obesity (DIO) model and then divided into the following groups: standard diet + vehicle; standard diet + ZO; DIO + vehicle and DIO + ZO. Those in the ZO groups were supplemented with 400 mg/kg per d of ZO extract (oral administration) for 35 d. The animals were euthanised, and blood, quadriceps, epididymal fat pad and hepatic tissue were collected. DIO induced insulin resistance, proinflammatory cytokines, oxidative stress and DNA damage in different tissues. Treatment with ZO improved insulin sensitivity as well as decreased serum TAG, without changes in body weight or adiposity index. TNF-α and IL-1ß levels were lower in the liver and quadriceps in the DIO + ZO group compared with the DIO group. ZO treatment reduced the reactive species and oxidative damage to proteins, lipids and DNA in blood and liver in obese animals. The endogenous antioxidant activity was higher in the quadriceps of DIO + ZO. These results in the rat model of DIO may indicate ZO as an adjuvant on obesity treatment.

Microbiological and physicochemical characteristics of buffalo milk used for dairy products in southern Brazil.

In Brazil, the buffalo milk market has been growing. However, identity and quality standards have not been established for this raw material, nor have proper distinctions between buffalo milk and bovine milk been defined. Currently, the State of Rio Grande do Sul (RS) has only three producers that supply raw material for officially marketed derivatives. The aim of this study was to determine the identity and quality standards of raw buffalo milk in this region. Samples were obtained biweekly from three farm cooling tanks between June 2017 and August 2018, to reach a total of 69 samples. The averages for the results of the physicochemical parameters fat, protein, lactose, total solids, SNF (solids-not-fat), calcium, density, FP, acidity and SCC were 5.5 g/100 g, 4.06 g/100 g, 5.07 g/100 g, 15.5 g/100 g, 9.96 g/100 g, 0.161 g/100 g, 1.034 g/ml, -0.527°C, 16°D and 95 × 103 cells/ml, respectively. With reference to the microbiological parameters, the mean of the Standard Plate Count (SPC) and thermotolerant coliforms were 9,0 × 104 CFU/ml and 1.6 × 102 MPN/ml, respectively. Regarding coagulase-positive staphylococci, 36 samples tested positive (52% of total). Neither Salmonella spp. nor Listeria monocytogenes, nor antibiotic or antiparasitic residues were detected in any sample. In conclusion, the buffalo milk used as raw material for dairy products in southern Brazil demonstrated satisfactory physicochemical and microbiological characteristics, in accordance with recent scientific literature.

Methodology for elemental analysis of a mineral fertilizer, some of its raw materials and limestone using microwave-induced plasma optical emission spectrometry (MIP OES).

The elemental analysis of complex matrices such as superphosphate-fertilizers and agricultural inputs by means of microwave-induced plasma optical emission has been evaluated in the present study. A commercial single superphosphate-fertilizer and three certified reference materials - CRMs (multi-nutrient, phosphate rock and dolomitic limestone) were analysed. Samples were submitted for three different analyte extraction or decomposition procedures; microwave assisted digestion (MAD), extraction by heating on a metallic plate and ultrasound assisted extraction (US). Analyte recovery tests were carried out to evaluate dilutions of the obtained sample solutions to reduce or avoid matrix effects. Better results were obtained for samples submitted for MAD and the concentration values found agreed with those certified or known for the CRMs. Inductively coupled plasma optical emission spectrometry (ICP OES) was employed as an independent technique for analyte determination in the superphosphate-fertilizer submitted for MAD. The concentrations found by both techniques were in agreement with each other for most of the investigated elements. As such, MIP OES has demonstrated good performance for the determination of 19 elements.

Insulin activates microglia and increases COX-2/IL-1ß expression in young but not in aged hippocampus.

Brain insulin resistance and neuroinflammation are known to increase with age. Insulin exerts metabolic roles on neurons and astrocytes, but its effects on microglia is unclear. In this study we investigated whether insulin affected microglia in the hippocampus of young and aged rats. We injected intracerebroventricular (i.c.v.) insulin (20 mU) or vehicle for five days and evaluated microglial inflammatory markers in the hippocampus of young (3 months) Wistar rats. Increased microglial activation (Iba-1+CD68+cells) and COX-2/IL-1ß levels in the hippocampus were found. Since the aged brain is an experimental model for brain insulin resistance and chronic neuroinflammation we submitted aged rats (22 months) to i.c.v. insulin/vehicle administration and found no significant increase in Iba-1+CD68+ microglia or COX-2/IL-1ß levels. To further investigate whether insulin triggered transient or persistent proinflammatory responses, young rats were evaluated eight-days after the last insulin injection. Microglia were persistently activated, and COX-2 levels remained elevated in the hippocampus, which paralleled increased spatial memory performance in the Morris Water Maze behavioral task. To determine if microglia were directly responsive to insulin, primary microglia were challenged with insulin and increased Akt Ser473 phosphorylation, a protein activated by the insulin receptor, was detected. These data suggest that microglia in the hippocampus integrate insulin signaling and neuroinflammatory responses and that this signal is disrupted during chronic inflammation. In our concept, the disruption between microglia activation by insulin signaling is a new pathological mechanism behind insulin resistance in the aging brain.

Ginger and avocado as nutraceuticals for obesity and its comorbidities.

Obesity is a worldwide epidemic and is one of the factors involved in the etiology of type 2 diabetes mellitus. Obesity induces low-grade inflammation and oxidative stress. The treatment for obesity involves changes in diet, physical activity, and even medication and surgery. Currently, the use of nutraceutical compounds is associated with health benefits. Ginger and avocado are used for many people all around the world; however, its effect as a nutraceutical compound is less known by the general population. For this reason, we searched information of the literature to point its effects on distinct mechanisms of defense against the obesity its comorbidities. The present review aimed showing that these nutraceuticals may be useful in obesity treatment. Reports have shown that ginger and avocado induce antioxidant and anti-inflammatory effects by improving enzymatic activity and modulating obesity-related impairments in the anti-inflammatory system in different tissues, without side effects. Furthermore, ginger and avocado were found to be effective in reversing the harmful effects of obesity on blood lipids. In conclusion, on the basis of the positive effects of ginger and avocado in in vitro, animal, and human studies, these nutraceuticals may be useful in obesity treatment.

Therapeutic effects of iontophoresis with gold nanoparticles in the repair of traumatic muscle injury.

Studies have shown the benefits of gold nanoparticles (GNPs) in muscle and epithelial injury models. In physiotherapy, the use of the microcurrent apparatus is associated with certain drugs (Iontophoresis) to increase the topical penetration and to associate the effects of both therapies. Therefore, the objective of this study was to investigate the effects of iontophoresis along with GNPs in the skeletal muscle of rats exposed to a traumatic muscle injury. We utilised 50 Wistar rats randomly divided in to five experimental groups (n = 10): Control group (CG); Muscle injury group (MI); MI + GNPs (20 nm, 30 mg kg-1); MI + Microcurrent (300 µA); and MI + Microcurrent + GNPs. The treatment was performed daily for 7 days, with the first session starting at 24 h after the muscle injury. The animals were sacrificed and the gastrocnemius muscle was surgically removedand stored for the proper evaluations. The group that received iontophoresis with GNPs showed significant differences in inflammation and oxidative stress parameters and in the histopathological evaluation showed preserved morphology. In addition, we observed an improvement in the locomotor response and pain symptoms of these animals. These results suggest that the association of boththerapies accelerates the inflammatory response of the injured limb.

Intranasal insulin treatment modulates the neurotropic, inflammatory, and oxidant mechanisms in the cortex and hippocampus in a low-grade inflammation model.

The inflammatory process plays a critical role in the development of neurodegenerative diseases. Insulin is used in preclinical and clinical studies of neurological disorders. Its intranasal (IN) administration directly in the brain allows for its peripheral metabolic effects to be avoided. Swiss male mice were injected with lipopolysaccharide (LPS) (0.1 mg/kg) to induce low-grade inflammation. IN insulin treatment was initiated 4 h later at a dose of 1.7 IU once daily for 5 days. LPS induced cognitive deficits, which the IN insulin treatment reversed. LPS significantly decreased, whereas IN insulin significantly increased the levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor-ß in the cortex. In the hippocampus, IN insulin significantly decreased the BDNF level. LPS significantly increased the interleukin (IL)-6 levels in the cortex, while IN Insulin significantly decreased its levels in the hippocampus. The tumor necrosis factor-α levels were significantly decreased by IN insulin both in the cortex and hippocampus. Moreover, IN insulin significantly increased the IL-10 levels in the cortex. The levels of oxidative and nitrosative stress were significantly higher in the LPS-treated mice; however, IN insulin had a modulatory effect on both. LPS significantly increased the antioxidant enzyme activity both in the cortex and hippocampus, whereas IN insulin significantly increased the activity of both superoxide dismutase and catalase in the hippocampus and that of catalase in the cortex. The hydrogen peroxide levels revealed that LPS significantly affected the electron transport chain. Therefore, IN insulin could be useful in the treatment of neuroinflammatory diseases.

Gold Nanoparticles Treatment Reverses Brain Damage in Alzheimer's Disease Model.

Alzheimer's disease (AD) is characterized by amyloid (A)ß peptide accumulation and intracellular neurofibrillary tangles. New hypotheses have suggested that AD involves neuroinflammation and oxidative stress. Gold nanoparticles (AuNP) presents anti-inflammatory and antioxidant characteristics. The present study evaluated the AuNP treatment on an AD model (okadaic acid, OA). Male Wistar rats were injected intracerebroventricularly with OA (100 µg); 24 h later they were treated with 20-nm AuNP (at a dose 2.5 mg/kg) every 48 h for 21 days. The following groups were separated (n = 12/group): Sham, AuNP, OA, and OA + AuNP. OA increases Tau phosphorylation in the cortex and hippocampus, while AuNP treatment maintained it as normal. Spatial memory was impaired by OA, and AuNP treatment prevented this deficit. Neurotrophic factors (BDNF and NGF- ß) in the cortex and hippocampus were decreased by OA. The OA and OA + AuNP groups showed increased interleukin (IL)-1 ß in the hippocampus and cortex, and the AuNP group showed increased IL-1 ß in the hippocampus. In both groups, S100 levels in the cortex and hippocampus were increased by OA. IL-4 was increased in OA + AuNP animals. AuNPs prevented oxidative stress (sulfhydryl and nitrite levels) in brain structures induced by OA. Moreover, OA modulated ATP synthase activity, and AuNP maintained normal brain mitochondrial function. The antioxidant capacities were reduced by OA, and AuNP restored antioxidant status (SOD, catalase activities and GSH levels) on brain. OA-induced damage on brain tissues, and long-term AuNP treatment prevented the neuroinflammation, modulation of mitochondrial function, and impaired cognition induced by AD model, showing that AuNPs may be a promising treatment for neurodisease caused by these elements.

Insulin treatment protects the brain against neuroinflammation by reducing cerebral cytokines and modulating mitochondrial function.

In the central nervous system, glial cells protect the brain against neuronal stress by inducing inflammatory responses; namely, intracellular signaling and cytokine production. However, chronic inflammation is often associated with degenerative diseases that can damage hormone signaling and mitochondrial function. Lipopolysaccharide (LPS) induces neuroinflammation by stimulating the production of interleukin-1beta (IL-1ß) and tumor necrosis factor-alpha (TNF-α); moreover, it generates oxidative stress and impairs cognitive functions. The aim of the present study was to assess the therapeutic efficacy of intracerebroventricular (i.c.v.) injections of insulin against neuroinflammation. Inflammation was first induced in male Wistar rats (60 days old, n = 12/group) through an intraperitoneal injection of 0.1 mg/kg LPS. The i.c.v. insulin treatment at a 0.5 mU dose was initiated 4 h later and administered once a day for 5 days. Thereafter, the spatial memory of the rats was assessed, and the hippocampus and cortex were later dissected for biochemical analyses. Our results showed that LPS induced cognitive function impairments, but the insulin treatment reversed these effects. Whereas the levels of brain-derived neurotrophic factor and beta-nerve growth factor in the hippocampus were not altered by LPS, they were decreased in the cortex by insulin. The IL-1ß and TNF-α levels were increased in the cortex and hippocampus following exposure to LPS, but insulin reversed these effects. Evaluation of the H2O2levels and mitochondrial membrane potential revealed that LPS modulated mitochondrial function, an effect that was also reversed by insulin. Moreover, LPS induced oxidative stress by decreasing the superoxide dismutase and catalase activities and glutathione and sulfhydryl levels. Furthermore, the levels of oxidative stress probes/markers (i.e.,2',7'-dichlorodihydrofluoresceindiacetateand nitrite) were higher in the LPS-treated rats. These effects were all reversed in the cortex and hippocampus by insulin treatment. Our results suggest a potential role for insulin as a therapeutic drug against inflammatory diseases associated with mitochondrial dysfunction in the brain.