Neuropeptide Levels Research Articles

Gingival Crevicular Fluid Levels of Neurokinin A and Substance P in Patients with Symptomatic Irreversible Pulpitis: A Systematic Review and Meta-Analysis.

The levels of neuropeptides neurokinin A (NKA) and substance P (SP) in the gingival crevicular fluid of patients with symptomatic irreversible pulpitis (SIP) were evaluated using a comprehensive review and meta-analysis. The data bases of Pubmed, Scopus, EBSCOhost, Science Direct, Proquest and Cochrane library databases were thoroughly searched. The quality of the study was evaluated using the Joanna Briggs Criteria. Twenty four studies were listed following a thorough search of full texts, abstracts, and removal of duplicates. Only two of these papers were eligible for inclusion in the meta-analysis. Since the results obtained were in mean and standard deviation, the levels of neuropeptides in the test and control groups were examined using the meta-analysis. When compared with healthy teeth, NKA was not significantly elevated in GCF of individuals with SIP (P = 0.06; odd ratio = 1.34 [-0.05 to 2.74] at 95% confidence interval [CI]). Additionally, there was no evidence of an association between SP and SIP (P = 0.08; odds ratio = 0.84 [-0.10 to 1.77] at 95% CI). This systematic research demonstrated that in individuals with SIP, NKA, and SP are not substantially linked. However, the lack of study in this area makes it evident that additional research is needed, particularly in relation to pulpal disorders and NKA.

Raynaud's Phenomenon: A Brush Up!

Raynaud's Phenomenon: A Brush Up!

Relationships of orexigenic and anorexigenic hormones with body fat distribution in patients with obstructive sleep apnea syndrome.

We aimed to examine the relationships of disease activity and risk factors with serum levels of orexigenic and anorexigenic hormones in patients with obstructive sleep apnea syndrome (OSAS). Fasting blood samples were taken for hormonal analysis of all participants, abdominal/neck bioimpedance measurements were recorded, and polysomnography (PSG) analyses were performed. According to the apnea-hypopnea index (AHI), 34 patients with newly diagnosed OSAS and 34 participants without OSAS were compared. The median body mass index (BMI) measured in the OSAS group was 30.39kg/m2 and AHI was 18.95 and these values were 25.40kg/m2 and 1.55 in the control group. There was a higher level of visceral adiposity and neuropeptide Y (NPY) in the moderate-to-severe OSAS group compared to the mild OSAS and control groups, and in the mild OSAS group compared to the control group (p = 0.001, p < 0.001). A positive correlation between the level of NPY and AHI and BMI (p < 0.001, p = 0.011), and a negative correlation between NPY levels and oxygen saturation (p = 0.001) was found. Oxygen saturation and desaturation rates were correlated with body fat percentage, body fat mass, abdominal adiposity, visceral adiposity, resting metabolic rate, and NPY levels. The visceral adiposity ratio and increase in NPY levels are important parameters that increase the severity of OSAS. Considering the negative effects of NPY on vascular endothelium, measurement of basal NPY level before PSG in patients with OSAS is considered a parameter related to disease severity.

Positive effect of Bifidobacterium animalis subsp. lactis VHProbi YB11 in improving gastrointestinal movement of mice having constipation.

The aim of this study was to investigate the effects of Bifidobacterium animalis subsp. lactis VHProbi® YB11 (YB11) on attenuating sucralfate-induced constipation in BALB/c mice. The strain of YB11 exhibited favorable tolerance of simulated gastrointestinal (GI) juice. Only 0.42 Log value declined when the live cells of YB11 were co-incubated with simulated GI juice. Meanwhile, this strain also displayed perfect ability to adhere the intestinal epithelium Caco-2 cells with adhesion index of 18.5. 24 of female mice were randomized into four groups. The normal group (NOR) was fed with a normal diet, whereas the placebo group (PLA), positive group (POS), and probiotic group (PRO) were fed with sucralfate to induce constipation. After first successfully establishing the constipation model, groups NOR and PLA received the oral administration of saline solutions. Meanwhile, the POS and PRO groups were orally administered phenolphthalein and YB11 suspensions, respectively. Several indices, including fecal water content, GI transit time, short-chain fatty acids (SCFAs), intestinal neuropeptides level, and histopathology of colonic tissues, were investigated. Compared with PLA, YB11 had a positive effect in increasing the fecal water content and intestinal peristalsis. Some positive trends, including the acetic and total acids level of fecal samples, and the colonic tissue histopathology, were also observed. Furthermore, YB11 had an ability to upregulate the levels of gut excitatory neuropeptides including motilin, gastrin, and substance P, whereas it downregulated the levels of inhibitory neuropeptides including endothelin-1, somatostatin, and vasoactive intestinal peptide. We conclude that the strain YB11 has a positive impact on improving gastrointestinal mobility and reducing the severity of constipation.

Lower morning levels of cortisol and neuropeptides in blood samples from patients with bipolar disorder

: Several lines of evidence indicate that circadian rhythm disruption is associated with bipolar disorder (BPD). This strong association, along with evidence from genome wide association studies (GWAS) implicating clock and clock controlled genes with BDP and efficacy of lithium treatment, suggests that BPD circadian rhythm disruption may represent a core etiology feature. Lower morning expression of the neuropeptide somatostatin (SST) has been previously reported in the brain and cerebral spinal fluid of subjects with BPD, coinciding with increased morning severity of anxiety and depression. We aimed to test the hypothesis that levels of neuropeptides involved in circadian rhythm regulation, including somatostatin (SST), neuropeptide-Y (NPY), arginine vasopressin (AVP), vasoactive intestinal peptide (VIP) and cortisol levels, are altered in blood samples collected in the morning from patients BPD. : Thirty nine patients diagnosed as BPD according to DSM-5, and 38 healthy controls were enrolled in the study. Blood were collected at 9 AM from all subjects. Serum levels of SST, NPY, AVP, VIP and cortisol were measured. : We observed significantly lower levels of SST (p=0.001), NPY (p =0.001), VIP (p=0.001) and cortisol levels (p=0.001) in the morning in subjects with BPD compared to control subjects. Significant positive effects of Young Mania Rating Scale and lithium treatment with cortisol, SST, and VIP levels were observed. : Our study suggests that lower morning levels of SST, NPY, VIP and cortisol may represent biomarkers underlying disrupted biological rhythms and behavioral and sleep disturbances observed in patients with BPD.

Plasma neuropeptide levels in patients with schizophrenia, bipolar disorder, or major depressive disorder and healthy controls: A multiplex immunoassay study.

We aimed to compare neuropeptide levels between patients with major psychiatric disorders and healthy controls and examine their association with symptoms and cognitive function. The participants were 149 patients with schizophrenia, 115 patients with bipolar disorder (BD), 186 unremitted patients with major depressive disorder (MDD), and 350 healthy controls. Psychiatric (schizophrenic, manic, and depressive) symptoms, sleep state, and cognitive (premorbid intelligence quotient, general cognitive, and memory) functions were evaluated. A multiplex immunoassay kit was used to measure cerebrospinal fluid (CSF) and plasma α-melanocyte-stimulating hormone (MSH), β-endorphin, neurotensin, oxytocin, and substance P levels. The verification assay revealed that CSF α-MSH, β-endorphin, neurotensin, oxytocin, and substance P levels were too low to be reliably measured, while plasma α-MSH, β-endorphin, neurotensin, oxytocin, and substance P levels could be successfully measured. Plasma α-MSH, β-endorphin, neurotensin, oxytocin, and substance P levels were not significantly different between patients with schizophrenia, BD, or MDD and healthy controls. Plasma α-MSH, β-endorphin, neurotensin, oxytocin, and substance P levels were not significantly correlated with psychiatric symptom scores in patients with schizophrenia, BD, or MDD and cognitive function scores in patients or healthy controls. Our data suggest that plasma neuropeptide levels do not elucidate the involvement of neuropeptides in the pathology of schizophrenia, BD, or MDD.

Betaine Attenuates Chronic Constriction Injury-Induced Neuropathic Pain in Rats by Inhibiting KIF17-Mediated Nociception.

Kinesin superfamily proteins transport a diverse range of cargo, including excitatory receptors to the dendrite and axon of a neuron via retrograde and anterograde fashions along microtubules, causing central sensitization and neuropathic pain. In this study, we have performed in silico molecular dynamics simulation to delineate the dynamic interaction of betaine with KIF17, a kinesin protein, known to be involved in neuropathic pain. The results from the molecular dynamics study suggest that the betaine-KIF17 complex is stabilized through hydrogen bonding, polar interactions, and water bridges. Findings from in vivo studies suggest a significant increase in pain hypersensitivity, oxido-nitrosative stress, and KIF17 overexpression in the sciatic nerve, dorsal root ganglion (DRG), and spinal cord of nerve-injured rats, which was significantly attenuated on treatment with betaine. Betaine treatment also restored the increased NR2B expressions and levels of proinflammatory cytokines and neuropeptides in the DRG and spinal cord of nerve-injured rats. Findings from the current study suggest that betaine attenuates neuropathic pain in rats by inhibiting KIF17-NR2B-mediated neuroinflammatory signaling.

Effect of Hyperbaric Oxygen Therapy on Sleep Quality, Drug Dosage, and Nerve Function in Patients with Sleep Disorders after Ischemic Cerebral Stroke

Objective. To explore the effects of hyperbaric oxygen therapy (HOT) on sleep quality, drug dosage, and nerve function in patients with sleep disorders after ischemic cerebral stroke (ICS). Methods. A total of 120 patients with acute ICS and sleep disorders who came to our hospital for treatment from January 2019 to October 2021 were selected and divided into control and observation groups according to the random numbering method, with 60 cases in each group. Both groups were treated with sertraline and eszopiclone for treating insomnia. The control group was given routine treatment for ICS, and the observation group was additionally treated with HOT in addition to the control group. The sleep quality, the use of sleep medication, the neurological function score, and the levels of serum tumor necrosis factor-α (TNF-α), endothelin (ET), and neuropeptide Y (NPY) before and after treatment were compared between the two groups. Results. The levels of TNF-α, ET and NPY were not significantly different between the two groups of patients before treatment ( P &gt; 0.05 ), and all of the above indicators decreased significantly in both groups after treatment, with the observation group being lower than the control group ( P &lt; 0.05 ). There was no significant difference in the sleep quality scores of PSQI, ESS, and SBQ between the two groups before treatment ( P &gt; 0.05 ), and the above indicators decreased significantly in both groups after treatment, with the observation group being lower than the control group ( P &lt; 0.05 ). There was no significant difference in the dose of sleep medication used in the first day of treatment between the two groups ( P &gt; 0.05 ), and the amount of sleep medication used in the observation group was significantly less than that in the control group after 14 d of treatment ( P &lt; 0.05 ). There was no significant difference in the NIHSS scores between the two groups before treatment ( P &gt; 0.05 ), and the scores of both groups decreased after treatment, and the scores of the observation group were significantly lower than those of the control group ( P &lt; 0.05 ). Conclusion. Compared with routine treatment, the addition of HOT to treat patients with sleep disorders after ICS can significantly improve their sleep quality, reduce dosage of sleep drugs, reduce inflammatory level of brain tissue and nerve function damage, and improve their prognosis. Trial Registration. This study was registered in the EA2019056

Release of CGRP in vivo from rat dura mater: Influence of capsaicin and topiramate

Introduction Migraine is a disease that stands out for its high prevalence with changes in the nervous system, abnormal levels of neurotransmitters, neuromodulators, and neuropeptides. The main mechanisms of action of capsaicin are chemical induction through the activation of TRPV1 channels, allowing calcium influx into neurons in the trigeminal ganglion of the dura mater, activating mast cell degranulation, releasing pro-inflammatory (e.g., histamine, oxide nitric) and vasoactive (e.g., CGRP and substance P) substances. For treatment, classes of drugs are used to act on blood vessels and to prevent vasodilation, as well as depolarization of sensory fibers of the dura mater. Objectives To better understand sterile inflammation after exposing the dura mater bilaterally, we created an experimental model to study mechanisms of action of topiramate and capsaicin in mast cell degranulation and release of CGRP in a rat skull preparation in vivo using anesthetized animals. Methods Thirty-five Wistar rats were used, divided into two groups of chronic topiramate (GTC) treated with 20mg/kg/day, gavage/10 days, and acute topiramate (GTA) in situ in the dura mater (10-3M). The animals were anesthetized and cranial windows between the coronal and lambda sutures in the hemicraniums were performed with a drill to expose the dura mater bilaterally. 10-3M capsaicin was placed on the right side and synthetic interstitial fluid on the left side and exposed to contact for 10 minutes to a small cotton ball soaked with the respective solutions so that there is no leakage of the treatment, and posteriorly kept in the freezer (-20°C) for later quantification of CGRP. The percentage of degranulated mast cells was quantified after removal of the dura mater by staining it with toluidine blue. A commercial enzyme immunoassay quantified the release of CGRP from the cranial dura mater... (Too see the complet abstract, please, check out the PDF.)

Poststroke Seizure and Epilepsy: A Review of Incidence, Risk Factors, Diagnosis, Pathophysiology, and Pharmacological Therapies

Stroke is the most common cause of epilepsy and ultimately leads to a decrease in the quality of life of those affected. Ischemic and hemorrhagic strokes can both lead to poststroke epilepsy (PSE). Significant risk factors for PSE include age < 65age less than 65 years, stroke severity measured by the National Institutes of Health Stroke Scale (NIHSS), cortical involvement, and genetic factors such as TRPM6 polymorphism. The diagnosis of PSE is made by using imaging modalities, blood biomarkers, and prognostic criteria. Electroencephalography (EEG) is currently the gold standard to diagnose PSE, while new combinations of modalities are being tested to increase diagnostic specificity. This literature review uncovers a newly found mechanism for the pathology of poststroke epilepsy. The pathogenesis of early-onset and late-onset is characterized by sequelae of neuronal cellular hypoxia and disruption of the blood-brain barrier, respectively. Interleukin-6 is responsible for increasing the activity of glial cells, causing gliosis and hyperexcitability of neurons. Epinephrine, high-mobility group protein B1, downregulation of CD32, and upregulation of HLA-DR impact the pathology of poststroke epilepsy by inhibiting the normal neuronal immune response. Decreased levels of neuropeptide Y, a neurotransmitter, act through multiple unique mechanisms, such as inhibiting intracellular Ca2+ accumulation and acting as an anti-inflammatory, also implemented in the worsening progression of poststroke epilepsy. Additionally, CA1 hippocampal resonant neurons that increase theta oscillation are associated with poststroke epilepsy. Hypertensive small vessel disease may also have an implication in the temporal lobe epilepsy by causing occult microinfarctions. Furthermore, this review highlights the potential use of statins as primary prophylaxis against PSE, with multiple studies demonstrating a reduction in incidence using statins alone, statins in combination with antiepileptic drugs (AEDs), and statins with aspirin. The evidence strongly suggests that the second generation AEDs are a superior treatment method for PSE. Data from numerous studies demonstrate their relative lack of significant drug interactions, increased tolerability, and potential superiority in maintaining seizure-free status.

Evaluation of the Circadian Rhythm Neuropeptides and Hippocampus in Rat Model of Posttraumatic Stress

ABSTRACT We investigated hippocampus weight and the levels of circadian rhythm-related neuropeptides; Somatostatin (SST), Vasoactive Intestinal Peptide (VIP), Neuropeptide Y (NPY), Melatonin (MLT), and Corticotrophin Releasing Hormone (CRH) in plasma (p) and hippocampus tissue (h) of rats with posttraumatic stress (PTS) symptoms. Thirty four healthy Spraque-Dawley rats were randomly divided into control and PTS groups. Single prolonged stress (SPS) model was used to mimic PTS. Elevated Plus Maze Test (EPMT) was used to assess anxiogenic behavior. Rats were sacrificed under anesthesia and hippocampus weight, SST, NPY, CRH, MLT, and VIP levels were measured by the Enzyme-Linked-Immuno-Sorbent-Assay method. Hippocampus weights in the PTS group were significantly lower compared to controls. NPYh and MLTh levels were significantly higher in the PTS group. NPYh and MLTh and MLTp were significantly higher in the PTS. CRH, VIP, and SST levels in hippocampus tissue and CRH, NPY, VIP, and SST in plasma did not differ between groups. A positive correlation was found between MLTh and VIPh tissue levels. There was a positive correlation between NPYh and VIPh levels, and a high degree of positive correlation between NPYp and VIPp levels. As far as we know, this is the first study in which 5 neuropeptides’ hippocampus tissue and plasma levels were evaluated together in a PTSD model. Hippocampus weights may tend to decrease in PTS. Especially, NPY and MLT from circadian rhythm neuropeptides play an important role in PTS etiology. After the 7th day of trauma exposure, the hippocampal NPY and MLT levels may increase as a stress-adaptive mechanism in PTS.

Involvement of Mechanistic Target of Rapamycin (mTOR) in Valine Orexigenic Effects in Rainbow Trout.

This study was aimed at clarifying the importance of a mechanistic target of rapamycin (mTOR) in the central orexigenic effect of valine in fish. For this, rainbow trout (Oncorhynchus mykiss) were intracerebroventricularly (ICV) injected with valine alone or in the presence of rapamycin as the mTOR inhibitor, and two experiments were performed. In the first experiment, we evaluated feed intake levels. In the second experiment, we evaluated in the hypothalamus and telencephalon the following: (1) the phosphorylation status of mTOR and its downstream effectors ribosomal protein S6 and p70 S6 kinase 1 (S6K1), (2) the abundance and phosphorylation status of transcription factors involved in appetite regulation, and (3) the mRNA levels of key neuropeptides associated with homeostatic regulation of feed intake in fish. Rising central levels of valine clearly resulted in an orexigenic response in rainbow trout. This response occurred in parallel with mTOR activation in both the hypothalamus and telencephalon, as supported by depressant changes in proteins involved in mTOR signalling (S6 and S6K1). Also, these changes disappeared in the presence of rapamycin. However, it is not clear which precise mechanisms link the activation of mTOR and the alteration in feed intake levels since we did not observe changes in mRNA levels of appetite-regulatory neuropeptides as well as in the phosphorylation status and levels of integrative proteins.

Eyestalk neuropeptide identification in the female red deep-sea crab, Chaceon quinquedens

Eyestalk-derived neuropeptides, primarily the crustacean hyperglycemic hormone (CHH) neuropeptide family, regulate vitellogenesis in decapod crustaceans. The red deep-sea crab, Chaceon quinquedens, a cold-water species inhabiting depths between 200 and 1800 m, has supported a small fishery, mainly harvesting adult males in the eastern US for over 40 years. This study aimed to understand the role of eyestalk-neuropeptides in vitellogenesis in C. quinquedens with an extended intermolt stage. Chromatography shows two CHH and one MIH peak in the sinus gland, with a CHH2 peak area four times larger than CHH1. The cDNA sequence of MIH and CHH of C. quinquedens is isolated from the eyestalk ganglia, and the qPCR assay shows MIH is significantly higher only at ovarian stages 3 than 4 and 5. However, MIH transcript and its neuropeptides do differ between stages 1 and 3. While CHH transcripts remain constant, its neuropeptide levels are higher at stages 3 than 1. Additionally, transcriptomic analysis of the de novo eyestalk ganglia assembly at ovarian stages 1 and 3 found 28 eyestalk neuropeptides. A GIH/VIH or GSH/VSH belonging to the CHH family is absent in the transcriptome. Transcripts per million (TPM) values of ten neuropeptides increase by 1.3 to 2.0-fold at stage 3 compared to stage 1: twofold for Bursicon α, followed by CHH, AKH/corazonin-like, Pyrokinin, CCAP, Glycoprotein B, PDH1, and IDLSRF-like peptide, and 1.3-fold of allatostatin A and short NP-F. WXXXRamide, the only downregulated neuropeptide, decreases TPM by ∼ 2-fold at stage 3, compared to stage 1. Interestingly, neuroparsin with the highest TPM values remains the same in stages 1 and 3. The mandibular organ-inhibiting hormone is not found in de novo assembly. We report that CHH, MIH, and eight other neuropeptides may play a role in vitellogenesis in this species.

Short-term efficacy, safety and survival of laparoscopic radical resection for colorectal cancer patients with bowel obstruction.

To investigate the short-term efficacy of laparoscopic radical resection for colorectal cancer with bowel obstruction and the effects of the surgery on inflammatory factors for improving the clinical treatment of the condition. The data of colorectal cancer patients presenting bowel obstruction (n=167) treated at our hospital from January 2019 to December 2020 were assessed. The patients were divided into a laparoscopic radical resection of colorectal cancer group (LRRCC, n=90) and open surgery group (OP, n=77). Before treatment and on the 1st, 3rd, 5th, 7th and 15th day after treatment, their serum levels of pain factors, neuropeptide Y, prostaglandin E2 and nerve growth factor were measured by a serum biochemistry analyzer, their levels of inflammatory factors including C-reactive protein, interleukin 6 (IL-6), IL-8 and tumor necrosis factor-α by ELISA, and their amount of CD3+, CD4+ and CD8+ T cell subsets were measure by flow cytometry. Anorectal motility was assessed before and 4 and 8 weeks after treatment. Survival rates were assessed using the Kaplan-Meier method. On the 1st, 3rd, 5th, 7th and 15th day after treatment, compared with the OP group, the LRRCC group had lower levels of serum pain factors, inflammatory factors and CD8+T lymphocytes, while their numbers of CD3+ and CD4+ T lymphocytes subsets were significantly increased. Further, the LRRCC group had fewer complications and significantly higher survival rates, demonstrating better efficacy than the OP group. Laparoscopic radical resection was effective and achieved superior outcomes than open surgery in treating colorectal cancer patients with bowel obstruction.

Error-prone protein synthesis recapitulates early symptoms of Alzheimer disease in aging mice.

Age-related neurodegenerative diseases (NDDs) are associated with the aggregation and propagation of specific pathogenic protein species (e.g., Aβ, α-synuclein). However, whether disruption of synaptic homeostasis results from protein misfolding per se rather than accumulation of a specific rogue protein is an unexplored question. Here, we show that error-prone translation, with its frequent outcome of random protein misfolding, is sufficient to recapitulate many early features of NDDs, including perturbed Ca2+ signaling, neuronal hyperexcitability, and mitochondrial dysfunction. Mice expressing the ribosomal ambiguity mutation Rps9 D95N exhibited disrupted synaptic homeostasis resulting in behavioral changes reminiscent of early Alzheimer disease (AD), such as learning and memory deficits, maladaptive emotional responses, epileptiform discharges, suppressed circadian rhythmicity, and sleep fragmentation, accompanied by hippocampal NPY expression and cerebral glucose hypometabolism. Collectively, our findings suggest that random protein misfolding may contribute to the pathogenesis of age-related NDDs, providing an alternative framework for understanding the initiation of AD.

Conceptual framework for the insect metamorphosis from larvae to pupae by transcriptomic profiling, a case study of Helicoverpa armigera (Lepidoptera: Noctuidae)

BackgroundInsect metamorphosis from larvae to pupae is one of the most important stages of insect life history. Relatively comprehensive information related to gene transcription profiles during lepidopteran metamorphosis is required to understand the molecular mechanism underlying this important stage. We conducted transcriptional profiling of the brain and fat body of the cotton bollworm Helicoverpa armigera (Lepidoptera: Noctuidae) during its transition from last instar larva into pupa to explore the physiological processes associated with different phases of metamorphosis.ResultsDuring metamorphosis, the differences in gene expression patterns and the number of differentially expressed genes in the fat body were found to be greater than those in the brain. Each stage had a specific gene expression pattern, which contributed to different physiological changes. A decrease in juvenile hormone levels at the feeding stage is associated with increased expression levels of two genes (juvenile hormone esterase, juvenile hormone epoxide hydrolase). The expression levels of neuropeptides were highly expressed at the feeding stage and the initiation of the wandering stage and less expressed at the prepupal stage and the initiation of the pupal stage. The transcription levels of many hormone (or neuropeptide) receptors were specifically increased at the initiation of the wandering stage in comparison with other stages. The expression levels of many autophagy-related genes in the fat body were found to be gradually upregulated during metamorphosis. The activation of apoptosis was probably related to enhanced expression of many key genes (Apaf1, IAP-binding motif 1 like, cathepsins, caspases). Active proliferation might be associated with enhanced expression levels in several factors (JNK pathway: jun-D; TGF-β pathway: decapentaplegic, glass bottom boat; insulin pathway: insulin-like peptides from the fat body; Wnt pathway: wntless, TCF/Pangolin).ConclusionsThis study revealed several vital physiological processes and molecular events of metamorphosis and provided valuable information for illustrating the process of insect metamorphosis from larvae to pupae.

НЕЙРОГЕННОЕ ВОСПАЛЕНИЕ И ОСОБЕННОСТИ ВЕГЕТАТИВНОЙ НЕРВНОЙ СИСТЕМЫ У ПАЦИЕНТОВ С БРОНХИАЛЬНОЙ АСТМОЙ В ЗАВИСИМОСТИ ОТ СТЕПЕНИ ТЯЖЕСТИ И ФЕНОТИПА ЗАБОЛЕВАНИЯ

Abstract. Bronchial asthma (BA) is a heterogeneous disease characterized by chronic airway inflammation. The central link in the pathogenesis of the disease is the inflammatory process of the bronchial wall, the maintenance of which, along with allergens, infections and toxic agents, is facilitated by "neurogenic" inflammatory factors, and imbalance in the links of the autonomic nervous system. Vasointestinal peptide is involved in bronchodilation and substance P is currently considered as the main mediator of neurogenic inflammation, capable of causing such pathophysiological reactions as pain, mucosal edema, mucus hypersecretion, and bronchoconstriction. The research available to date does not fully reflect the mechanisms and degree of influence of the imbalance of the autonomic nervous system and neurogenic inflammation in patients with severe bronchial asthma. In this regard, the study of autonomic dysfunction and it’s connection with the clinical features of severe bronchial asthma is relevant and can contribute to the improvement of a personalized approach to the treatment of patients with asthma, which is of practical interest. Our study presents the results of the level of neuropeptides depending on the type of dysfunction of the autonomic nervous system, as well as the phenotype of bronchial asthma.

Exposure to di (2-ethylhexyl) phthalate causes locomotor increase and anxiety-like behavior via induction of oxidative stress in brain

Di (2-ethylhexyl) phthalate (DEHP) is the most prevalent exposure scenario in the daily life. A growing number of significant studies showed that DEHP could exhibit long-term adverse health effects for the human body, particularly in the liver, kidneys, heart and reproductive systems. However, the impact of oral intake of DEHP on nervous system is extremely limited. In the present study, the adult C57BL/6J male mice were intragastric administered with two dosages DEHP for 35 days. The behavioral parameters were assessed using the elevated plus maze and open-field test. The mRNA expression levels of neuropeptides and the oxidative stress-associated proteins were detected by qPCR and western blot severally. The histopathologic alterations of brain were also observed by H&E and Nissl staining. The results demonstrated that oral DEHP exposure could result in neurobehavioral impairments such as locomotor increase and anxiety-like behavior. Furthermore, the pathological damages were clearly observed in cerebral cortex and hippocampus, accompanied by a decrease in neuropeptides and an increase in oxidative stress, which were all positively correlated with the dose of DEHP. Together, these findings provide valuable clues into the DEHP-induced neurotoxicity.

The effect of β-caryophyllene on food addiction and its related behaviors: A randomized, double-blind, placebo-controlled trial

Food addiction (FA) is a psychological construct that may be involved in the etiology of obesity. The cannabinoid system is involved in the addictive-like food preferences by acting on the dopaminergic pathway of the brain. β-caryophyllene is a dietary cannabinoid that is a cannabinoid type 2 (CB2) receptor agonist. This study explored the impacts of β-caryophyllene supplementation on eating behavior, appetite, mental health, anthropometric parameters, body composition, and some hormones related to appetite in women with obesity diagnosed with FA. Women with obesity and FA, diagnosed by the Yale Food Addiction Scale Score (YFAS-S) ≥3, were randomly allocated to receive a β-caryophyllene softgel (n = 26) (100 mg/daily with meal) or placebo (n = 26) for 8 weeks. Anthropometric measurements, body composition, eating behavior, biochemical markers, dietary intake, appetite, stress, anxiety, and depression were evaluated during the study period. β-caryophyllene administration significantly reduced YFAS-S compared to the placebo group (changes in FA score: 1.5 ± 0.9 vs. - 0.7 ± 1.4; corrected P = 0.05). Serum levels of orexin-A significantly decreased in the β-caryophyllene group (p = 0.02); however, no significant difference was observed compared to the placebo group (corrected P = 0.09). β-caryophyllene supplementation had no significant effect on body composition, anthropometric indices, appetite, eating behavior, dietary intake, physical activity level, mental health, and levels of oxytocin and neuropeptide Y (NPY), compared to the placebo. β-caryophyllene supplementation may have beneficial effects on improving YFAS-S in women with obesity diagnosed with FA. Trial registrationIranian Registry of Clinical Trials identifier: IRCT20200914048712N1.

Neuropeptide Y and measures of stress in a longitudinal study of women with the fibromyalgia syndrome.

Neuropeptide Y is associated with stress in animal and human laboratory studies. However, data from clinical studies are scarce and no clinical longitudinal studies have been published. The aim of this clinical study was to assess the possible association between changes in the levels of pain, depression, and stress measures, on the one hand, and plasma neuropeptide Y levels, on the other. Forty-four women with the fibromyalgia syndrome were exposed to a Cognitive Behavioral Therapy intervention. Levels of the plasma neuropeptide Y as well as pain, depression, and stress measures were obtained at the start and at the end of the intervention, and after a further six month follow-up. Based on these data, a before-and-after analysis was performed. Almost all measures of pain, depression, and stress improved during the study; specifically, variables measuring life control (coping), depression, and stress-related time urgency improved significantly. Moreover, during the same time period, the mean plasma neuropeptide Y level was reduced from 93.2±38.8fmol/mL before the Cognitive Behavioral Therapy to 75.6±42.9fmol/mL (p<0.001) at the end of the study. After exposure to a Cognitive Behavioral Therapy intervention, levels of most of the pain, depression, and stress measures improved, half of them significantly, as did the levels of neuropeptide Y. This circumstance indicates a possible functional relationship between pain-depression-stress and neuropeptide Y.