Aging and age-related diseases with a focus on therapeutic potentials of young blood/plasma.

Aging is accompanied by alterations in the body with time-related to decline of physiological integrity and functionality process, responsible for increasing diseases and vulnerability to death. Several ages associated with biomarkers were observed in red blood cells, and consequently plasma proteins have a critical rejuvenating role in the aging process and age-related disorders. Advanced age is a risk factor for a broad spectrum of diseases and disorders such as cardiovascular diseases, musculoskeletal disorders and liver, chronic kidney disease, neurodegenerative diseases, and cancer because of loss of regenerative capacity, correlated to reduced systemic factors and raise of pro-inflammatory cytokines. Most studies have shown that systemic factors in young blood/plasma can strongly protect against age-related diseases in various tissues by restoring autophagy, increasing neurogenesis, and reducing oxidative stress, inflammation, and apoptosis. Here, we focus on the current advances in using young plasma or blood to combat aging and age-related diseases and summarize the experimental and clinical evidence supporting this approach. Based on reports, young plasma or blood is new a therapeutic approach to aging and age-associated diseases.

The Impact of Cerebral Ischemia on Antioxidant Enzymes Activity and Neuronal Damage in the Hippocampus.

Cerebral ischemia and subsequent reperfusion, leading to reduced blood supply to specific brain areas, remain significant contributors to neurological damage, disability, and mortality. Among the vulnerable regions, the subcortical areas, including the hippocampus, are particularly susceptible to ischemia-induced injuries, with the extent of damage influenced by the different stages of ischemia. Neural tissue undergoes various changes and damage due to intricate biochemical reactions involving free radicals, oxidative stress, inflammatory responses, and glutamate toxicity. The consequences of these processes can result in irreversible harm. Notably, free radicals play a pivotal role in the neuropathological mechanisms following ischemia, contributing to oxidative stress. Therefore, the function of antioxidant enzymes after ischemia becomes crucial in preventing hippocampal damage caused by oxidative stress. This study explores hippocampal neuronal damage and enzymatic antioxidant activity during ischemia and reperfusion's early and late stages.

Tau Protein Biosensors in the Diagnosis of Neurodegenerative Diseases.

Tau protein plays a crucial role in diagnosing neurodegenerative diseases. However, performing an assay to detect tau protein on a nanoscale is a great challenge for early diagnosis of diseases. Enzyme-linked immunosorbent assay (ELISA), western-blotting, and molecular-based methods, e.g., PCR and real-time PCR, are the most widely used methods for detecting tau protein. These methods are subject to certain limitations: the need for advanced equipment, low sensitivity, and specificity, to name a few. With the above said, it is necessary to discover advanced and novel methods for monitoring tau protein. Counted among remarkable approaches adopted by researchers, biosensors can largely eliminate the difficulties and limitations associated with conventional methods. The main objective of the present study is to review the latest biosensors developed to detect the tau protein. Furthermore, the problems and limitations of conventional diagnosis methods were discussed in detail.

Profiling inflammatory mechanisms, hyperphosphorylated tau of hippocampal tissue and spatial memory following vitamin D3 treatment in the mice model of vascular dementia.

BACKGROUND: The aim of this study was to investigate the effect of vitamin D3 (VitD3) on inflammatory mechanisms, hyperphosphorylated tau (p-tau) in the hippocampus, and cognitive impairment of the mouse model of vascular dementia (VaD). METHODS: In this study, 32 male mice were randomly assigned to the control, VaD, VitD3 (300 IU/Kg/day), and VitD3 (500 IU/Kg/day) groups. VaD and VitD3 groups were gavaged daily for 4 weeks with a gastric needle. For biochemical assessments, blood samples and the hippocampus were isolated. IL-1ß and TNF-α were analyzed by ELISA, and p-tau and other inflammatory molecules were measured by western blot. RESULTS: VitD3 supplements significantly (P < 0.05) decreased the level of inflammatory factors in the hippocampus and prevented apoptosis. However, regarding p-tau in hippocampal tissue, this decrease was not statistically significant (P > 0.05). The results of behavioral assessments showed that VitD3 significantly improved the spatial memory of treated mice. CONCLUSION: These results suggest that the neuroprotective effects of VitD3 are mainly associated with their anti-inflammatory effects.

Biosensors technology for anti-epileptic drugs.

A broad group of antiepileptic drugs (AEDs) often controls the frequency of seizures. Given the variability of pharmacokinetics, narrow target range, and the difficulty of identifying signs of toxicity from laboratory responses, therapeutic monitoring of AEDs plays a vital role in optimizing drug administration. Nanomaterials, especially biosensor-based methods, can facilitate the analysis of these agents with unique advantages such as rapid analysis, sensitivity, selectivity, and low cost. This review describes recent advances in biosensors developed to analyze AEDs. First, we described common electrochemical measurement techniques and types of deposited electrode substrates. Additionally, various chemical and biological modifiers to improve the sensitivity and selectivity of the sensor have been categorized and briefly described. Finally, the prospects for developing an electrochemical platform for quantifying AEDs are presented.

Effects of the Oral Ingestion of Probiotics on Brain Damage in a Transient Model of Focal Cerebral Ischemia in Mice.

BACKGROUND: Probiotics are microorganisms that may influence brain function via altering brain neurochemistry. New research evidence suggests that probiotic bacteria might protect tissue damage through diminishing the production of free radicals and/or inflammatory cytokines. Therefore, this study was designed to evaluate the effects of probiotic bacteria on the prevention or reduction of brain damage in an experimental model of stroke in mice. METHODS: In this study, 30 male BLC57 mice were randomly divided into 6 equal groups. Focal cerebral ischemia was induced via middle cerebral artery occlusion for 45 minutes, followed by 24 hours of reperfusion, in the mice. Probiotics at a concentration of 107 CFU/mL were administered by oral gavage daily for 14 days before ischemia. Infarct size, neurological outcome, and biochemical markers were measured 24 hours after brain ischemia. Statistical analysis were performed using the one-way ANOVA and/or Kruskal-Wallis ANOVA on rank by Sigma Stat (2.0; Jandel Scientific) software. RESULTS: Our results indicated that pretreatment with probiotics significantly reduced infarct size by 52% (P=0.001) but could not improve neurological function (P=0.26). Moreover, the administration of probiotics significantly decreased the malondialdehyde content (P=0.001) and the tumor necrosis factor-alpha level (P=0.004) in the ischemic brain tissue. CONCLUSION: The findings of the present study showed that probiotic supplements might be useful in the prevention or attenuation of brain ischemic injury in patients at risk of stroke. Probiotics may open new therapeutic alternatives for the prevention of stroke. More preclinical and clinical studies are, however, needed to clarify their efficacy in cerebral stroke.

Lavandula Reduces Heart Injury via Attenuating Tumor Necrosis Factor-Alpha and Oxidative Stress in A Rat Model of Infarct-Like Myocardial Injury.

OBJECTIVE: Lavender is used in herbal medicine for different therapeutic purposes. Nonetheless, potential therapeutic effects of this plant in ischemic heart disease and its possible mechanisms remain to be investigated. MATERIALS AND METHODS: In this experimental study, lavender oil at doses of 200, 400 or 800 mg/kg was administered through gastric gavage for 14 days before infarct-like myocardial injury (MI). The carotid artery and left ventricle were cannulated to record arterial blood pressure (BP) and cardiac function. At the end of experiment, the heart was removed and histopathological alteration, oxidative stress biomarkers as well as tumor necrosis factor-alpha (TNF-α) level were evaluated. RESULTS: Induction of M.I caused cardiac dysfunction, increased levels of lipid peroxidation, TNF-α and troponin I in heart tissue (P<0.001). Pretreatment with lavender oil at doses of 200 and 400 mg/kg significantly reduced myocardial injury, troponin I and TNF-α. In addition, it improved cardiac function and antioxidant enzyme activity (P<0.01). CONCLUSION: Our finding showed that lavender oil has cardioprotective effect through inhibiting oxidative stress and inflammatory pathway in the rat model with infarct-like MI. We suggest that lavender oil may be helpful in prevention or attenuation of heart injury in patients with high risk of myocardial infarction and/or ischemic heart disease.

Protective Effects of Enriched Environment Against Transient Cerebral Ischemia-Induced Impairment of Passive Avoidance Memory and Long-Term Potentiation in Rats.

INTRODUCTION: Enriched Environment (EE), a complex novel environment, has been demonstrated to improve synaptic plasticity in both injured and intact animals. The present study investigated the capacity of an early environmental intervention to normalize the impairment of passive avoidance memory and Long-Term Potentiation (LTP) induced by transient bilateral common carotid artery occlusion (2-vessel occlusion, 2VO) in rats. METHODS: After weaning, young Wistar rats (22 days old) were housed in EE or Standard Environment (SE) for 40 days. Transient (30-min) incomplete forebrain ischemia was induced 4 days before the passive avoidance memory test and LTP induction. RESULTS: The transient forebrain ischemia led to impairment of passive avoidance memory and LTP induction in the Perforant Path-Dentate Gyrus (PP-DG) synapses. Interestingly, housing and growing in EE prior to 2VO was found to significantly reverse 2VO-induced cognitive and LTP impairments. CONCLUSION: Our results suggest that early housing and growing in EE exhibits therapeutic potential to normalize cognitive and LTP abnormalities induced by 2VO ischemic model in rats.

The Effect of Oral Consumption of Probiotics in Prevention of Heart Injury in a Rat Myocardial Infarction Model: a Histopathological, Hemodynamic and Biochemical Evaluation.

BACKGROUND: Despite the emerging evidence on beneficial effects of probiotics on the cardiovascular system, their impact on the management of ischemic heart diseases and its possible mechanism have not been elucidated. METHODS: Four viable probiotics bacterial strains, including Bifidobacterium breve, Lactobacillus casei, Lactobacillus bulgaricus and Lactobacillus acidophilus, at the concentrations of 2×106 colony-forming units/ml were orally administered to the rats daily for 14 days before the induction of infarct-like myocardial injury using isoproterenol. Subsequently, 24 h after myocardial injury, the right carotid artery and the left ventricle were catheterized for recording blood pressure and cardiac parameters. At the end of the experiment, the heart was removed for the evaluation of histopathological and biochemical parameters, as well as tumor necrosis factor-alpha (TNF-α) assay. RESULTS: The induction of acute myocardial injury resulted in significant (P≤0.01) left ventricular (LV) dysfunction, as shown by an increase in LV end-diastolic pressure and a decrease in LV dp/dt max, LV dp/dt min, LV systolic pressure, and blood pressure, as compared with normal rats. Pretreatment with viable probiotics significantly reduced lipid peroxidation and TNF-α level and improved cardiac function (P<0.01). CONCLUSION: This study shows that viable probiotics have a cardioprotective effect on infarct-like myocardial injury through suppressing TNF-α and oxidative stress damage in a rat model. Probiotic supplements may be used as a new option for prophylaxis in patients at the risk of ischemic heart disease in future.