جستجوی مقالات مرتبط با کلیدواژه "inflammatory cytokines" در نشریات گروه "پزشکی"

Ulcerative colitis is a chronic inflammatory bowel disease. Immunosuppressive drugs and various salicylates improve the disease activity index in individuals with ulcerative colitis. Nonetheless, drug resistance and the side effects of these medications drive researchers toward designing studies to find complementary alternatives. Natural compounds, especially derivatives from medicinal plants, hold a special place as supplements. This study aimed to assess the anti-inflammatory effects of the aqueous extract of Pistacia atlantica gum in an experimental model of ulcerative colitis.

In this study, 20 male BALB/c mice were assigned to four equal groups. The first group served as the healthy control (negative control), the second group represented untreated colitis (positive control), the third group underwent treatment with the aqueous extract of Pistacia atlantica gum, and the fourth group was treated with mesalazine. Ulcerative colitis was induced in all treatment groups except the negative control by using 100 microliters of 4% acetic acid administered intrarectally. The treatment regimen was initiated on the 10th day of post-ulcerative colitis induction and the manifestation of disease symptoms. A week after the final treatment, the mice were euthanized, and various parameters, including levels of myeloperoxidase, nitric oxide, interleukin-1beta, interleukin-6, tumor necrosis factor-alpha, and genes, such as iNOS and COX-2, were evaluated.

The results indicated that treatment with the aqueous extract of Pistacia atlantica gum significantly decreased the activity of myeloperoxidase (P<0.01), nitric oxide (P<0.05), splenic cell proliferation (P<0.05), expression, and production of inflammatory cytokines, (P<0.05) for IL-1 ß, (P<0.01) for IL-6, and (P<0.01) for TNF-α compared to the positive control group (untreated colitis).

As evidenced by the results of this study, it appears that the aqueous extract of Pistacia atlantica gum possesses desirable anti-inflammatory properties that could potentially reduce the disease activity index and inflammatory parameters in the experimental model of ulcerative colitis. Therefore, following further supplementary experiments, it could potentially serve as a complementary therapeutic agent alongside conventional medications for the treatment of patients suffering from ulcerative colitis.

Metabolic syndrome is associated with an increase in chronic inflammation, in which exercise training may be an effective intervention for the improvement of inflammatory markers. Accordingly, this study aimed to investigate the effect of exercise training on the inflammatory markers of interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), and C-reactive protein (CRP) in patients with metabolic syndrome.

In this study, the PubMed, Scopus, and Web of Science databases were searched during June 2022 for studies addressing the effects of exercise training versus control on inflammatory factors, including IL-6, TNF-α, and CRP. The search keywords were exercise training, inflammation, and metabolic syndrome. Standardized mean difference (SMD) and 95% confidence interval were used to determine the effect size using CMA2.

Twenty-two studies including 779 subjects with metabolic syndrome were included in the meta-analysis. Exercise training significantly decreased TNF-α [-0.74 (CI: -0.24 to -1.24), p=0.003] and CRP [-0.56 (CI: -0.25 to 0.87, p=0.001); however, the effect of exercise training on the decrease of IL-6 was not significant [-0.32 (CI: 0.20 to -0.85), p=0.22].

Exercise training decreases inflammatory markers in patients with metabolic syndrome, which may be a reason for the positive effects of exercise training on improving the metabolic status and cardiovascular health in such patients.

The lifestyle in the machine world of the last century is low mobility and very little activity with the use of various types of equipment and facilities. This lifestyle is the basis of many physical and mental complications in today's humans and causes the occurrence of many chronic diseases such as diabetes and obesity, increased blood pressure, and metabolic syndrome as a whole, followed by widespread inflammation in the body. Increased inflammation in the body, especially in the central nervous system of the brain, can lead to neurological and behavioral disorders. The immune system plays an important role in regulating brain homeostasis. Even small amounts of Neuroinflammation can disrupt physiological processes that occur in the hippocampus, including neurogenesis. Inflammatory factors include inflammatory cytokines such as interleukin 6 and alpha necrosis factor. In recent years, human and animal studies have shown that the increase of these two cytokines in the body and brain can lead to a decrease in memory. However, its exact mechanisms are not fully understood. Recent findings also show that IL-6 is involved in cognitive functions and memory, and increasing its level in brain areas such as the hippocampus may lead to a decrease in memory, on the other hand, anti-inflammatory factors such as IL-10 (potential role in immunotherapy and prevention) And progress or recurrence of neuropathy play a role in the body. Interleukin 10 prevents the production and secretion of inflammatory cytokines. This cytokine is secreted to suppress pro-inflammatory effects in stressful situations. The most important brain region involved in cognitive functions and memory is the hippocampus. Any damage to nerve cells in this area of ​​the brain can be directly related to cognitive disorders. Exercise is known as a risk modulating factor for reducing memory and learning in neurological diseases and even Alzheimer's disease. It is assumed that neurological and vascular adaptation to exercise and physical activity improves cognitive function through neurogenesis, reducing pro-inflammatory processes and reducing cell damage. Physical activity can modulate microglial activation in the CNS. Low-intensity exercise is sufficient to induce an anti-microglial activation effect by regulating the expression of various factors. Some of these factors (eg, Myokines) can directly prevent microglial activation through various mechanisms that prevent Neuroinflammation in the CNS. Be secreted from different sources (such as damaged neurons, astrocytes, and microglia). According to past research and since the effect of swimming exercise on the amount of pro-inflammatory and inflammatory cytokines such as IL-6 and IL-10 and as a result on the amount of spatial memory in adult rats has not been investigated, this research was conducted in order to make its results for patients suffering from memory loss. It should be implemented in clinics as a suggested non-pharmacological and effective treatment, especially in elderly people who have been diagnosed with Alzheimer's disease.

C57BL6 male mice (approximate age 10-11 weeks) and (weight 18-21 grams) were obtained from Pasteur Institute of Iran and kept under light conditions of 12 hours of light and 12 hours of darkness (8 am to 8 pm) and a temperature of 1±23 degrees Celsius and humidity of 40-50% and enough water and food were freely available to them. The data were analyzed using t-test analysis and P<0.05 was considered significant. SPSS software was used for analysis and GraphPad Prism software (V8.5) was used for drawing graphs.

Mice who have experienced swimming showed a higher level of the cytokine interleukin 10 in their hippocampus compared to the control group (p=0.002) and the significant effect of swimming training on spatial memory was confirmed and swimming led to a decrease in hippocampal inflammation. Through the reduction of interleukin 6 levels compared to control group mice (p=0.025).

In this study, the effect of swimming training on the amount of inflammatory and anti-inflammatory factors and spatial memory was investigated, and according to the tests and results obtained, it was determined that swimming training has a significant effect on the reduction of the inflammatory factor interleukin-6 and the increase of the anti-inflammatory factor interleukin-10. It is effective in reducing the number of cognitive disorders, including spatial memory. Aerobic exercise can partially reverse the cognitive decline associated with diabetes by reducing the oxidative stress and inflammatory environment in the brain of T2D animals. Regular exercise has significant benefits on insulin sensitivity in adults with type 2 diabetes and may persist for more than 72 hours after the last exercise session. Long-term intense exercise can generally lead to higher levels of inflammatory mediators and thus may increase the risk of injury and chronic inflammation. In contrast, moderate exercise or vigorous exercise with adequate rest periods can achieve maximum benefit. Exercise can protect against age-related cognitive decline, Alzheimer's disease (AD), and vascular dementia. We provide evidence of swimming exercise in other animal models that assess cognitive functions and hippocampal inflammatory and Neurotrophic systems. In support of our data, studies are showing that swimming exercise can improve cognitive deficits in various animal models. Regular swimming exercise in mice significantly increases working, spatial and cognitive memory in Alzheimer's disease conditions or is effective in healthy conditions as well. Overall, this study shows that swimming exercise may be suggested as a complementary non-pharmacological strategy for the treatment of cognitive decline in affected individuals. However, further studies should focus on training protocols that can be used in humans.

Multiple sclerosis (MS) is an autoimmune disease and chronic inflammation of the central nervous system that is associated with inflammation, demyelination, and destruction of axons. These symptoms potentially harmed the quality of life and day-to-day activities in MS persons. Therefore, therapeutic interventions that modulate the immunity system can help to relieve these symptoms and prevent disease progression. Pro-inflammatory cytokines such as interleukine-17 (IL-17) and anti-inflammatory cytokines such as interleukine-10 (IL-10) have an important role in MS progression. Exercise training as non-pharmaceutical intervention seems to have a good potential for the treatment and control of neuroinflammation disease symptoms, especially MS via upregulation of cytokines. Fatigue one of the common symptoms in MS peoples that correlated with cytokines. However, the effectiveness of exercise training types on MS peoples not investigated obviously. Recently, the use of functional training has become common in patients and the elderly. Previous studies were reported efficiency of this functional training for rehabilitation, physical fitness, and wellness. Functional training are any exercises that tried to train the muscles in coordinated, multi-axis, multi-articulated movement patterns, with dynamic tasks and by constantly changing the support base of the movement to improve performance. TRX suspension training, elastic band training, and rhythmic aerobic are components of functional training.  To our knowledge, no study has investigated the effect of functional training with TRX suspension training, elastic band training, and rhythmic aerobic training on inflammatory factors, fatigue, and body composition in MS persons. Therefore, the purpose of the present study was to investigate of the effect of the combined functional training on serum levels of IL-17, IL-10, fatigue, and body composition in MS women.

Twenty relapsing-remitting MS women with expanded disability status scale (EDSS) ˂5.0. The participant EDSS evaluated by an experienced neurologist. Inclusion criteria were the lack of regular exercise, no relapse of the disease for the last six months, lack of pregnancy, non-smoking, non-addiction to drugs and alcohol, no history of cardiovascular, metabolic, mental, cancer, and orthopedic diseases. Exclusion criteria were relapse of disease, inability to performing training program, and had signs of any diseases. Participants were randomly divided into combined functional training and control group. Just 16 subjects could complete all stages of the present study. The combined functional training group participated in eight weeks with 3 days per week. After standard warm-up, subjects performed rhythmic aerobic training with an intensity of 55-70% of maximum heart rate. Session duration was 15 minutes (min) in the 1 and 2 weeks and 20 min from the 3-8 weeks. Afterwards, resistance training includes of elastic band training, TRX suspension training, and bodyweight training performed after 5-10 min resting break. Participants used one of the resistance training modes after aerobic training in each session. They performed 1 set in 1-4 weeks and 2 sets in 5-8 weeks. 1-2 min of resting breaks were considered between the exercises and sets. Elastic band exercises include of flexion of biceps, triceps, and thigh muscles. Training intensity was determined by color and elongation rate of the bands. Participants were used of blue color Theraband according to their condition and ability (25-100% elongation with a resistance of 1.3 to 2.3 kg).  TRX suspension exercises also include of rowing, squat, lung, and sit-ups. Bodyweight training was consisting of active and passive movements to strengthen and improve the balance of arms, legs, and trunk. After main training, standard cool-down was done. The training intensity was monitored every week by the Borg 6-20 category rate of perceived exertion (RPE) scale. The RPE for first 4 weeks was light to moderate (10-13), and the last 4 weeks intensity was moderate to hard (13-16). The control group had no regular physical activity during this period. Blood samples were taken 48 hours before and after the training intervention from all participants in pre and posttest to determine serum levels of IL-17 and IL-10 by electrochemiluminescence enzyme-linked immunosorbent assay method with commercial ELISA kits (Shanghai crystal day biotech co, China). Fatigue severity and body composition were evaluated using a fatigue severity scale (FSS) questionnaire and bioelectrical impedance analyses (BIA) method by Inbody-3 device made in Korea, respectively. For data analyses, two-way mixed ANOVA with independent and paired samples T-tests were used. A significant time X group interaction in the multivariate tests of the ANOVA was considered to indicate a significant training effect. Delta changes (posttest-pretest) were calculated and analyzed for variables that have significant differences in between-subjects factor. The significance level in all analyses was set at P≤0.05.

Mixed ANOVA analysis indicated significant differences in time x group interaction between IL-10, 1L-17, and fatigue. Between-group changes showed that combined functional training resulted in a significant reduction of IL-17, fatigue, and significant increase in IL-10 levels compared with the control group.  Time interaction demonstrated significant changes in IL-10, IL-17, fatigue and body-fat percentage. IL-17, fatigue, and body-fat percentage in the combined functional training group were significantly decreased compared with the pre-test. IL-10 in the combined functional training group was significantly increased compared with the pre-test. However, fat-free mass did not change significantly in multiple sclerosis women.

Today, aerobic, anaerobic, and resistance exercise has been considered as the most promising non-pharmacological treatment for MS patients with disabilities to reduce fatigue and depression and improve the quality of life of these people without aggravating symptoms. Previous studies have reported that exercise may have indirect anti-inflammatory effects and may be useful in the activity of the MS immune system. Exercise can mediate immune function through local and systemic production of cytokines. With the results obtained after eight weeks of combined functional training in the present study, it can be concluded that the selected functional training along with a benefiting variety of training and combination of applied exercises, could reduce and prevent the exacerbation of symptoms such as fatigue. It was also effective in reducing inflammatory markers and may be effective in reducing disease progression, nerve cell destruction and reducing disease relapsing. It also reduced body-fat percentage. Therefore, the combined functional training program which has a home-base nature, can be recommended to MS patients along with another medical intervention to control and treatment of the disease symptoms.

Autism Spectrum Disorders (ASD) refers to a group of neurodevelopmental abnormalities characterized by impairment in communication, social skills and eye contacts with restrictive interests and repetitive behaviors. Individuals with autism show variable reactions in sensitive situations. Some children have normal intelligence and some have intellectual disability, macrocephaly, microcephaly, developmental delay and/or epilepsy. The symptoms appear in infancy and early childhood and affect daily functioning. Recent studies suggest that approximately 1 in 54 children are affected by an autism spectrum disorder. Autism spectrum disorder is notably four times more common in boys than in girls. Many types of research have revealed that genetic and environmental factors are linked to ASD. Major susceptibility factors can play a critical role in the development of autistic behaviors. It is well accepted that ASD have a strong genetic predisposition; however, genes that cause neuropsychiatric disorders are unknown and more than 100 genes are involved in ASD patients. Several genetic factors, such as mitochondrial DNA (mtDNA) variations, have been linked to autistic behaviors. We searched the PubMed, Science Direct, Elsevier, SID, HGMD, SFARI and AUTDB databases for mitochondrial dysfunction associated with the development of autistic behaviors published between 2010 and 2020. The purpose of the search strategy was to obtain relevant studies that provided appropriate information. In 1985, Coleman and Blass made the first hypothesis associating ASD with high levels of lactate in the plasma of individuals with autistic behaviors. Studies showed that various biomarkers of mitochondrial disruption (alanine-to-lysine ratio, acylcarnitine) are altered in some cases with ASD. So far, a great deal of research has been carried out in the field of genetics, perinatal factors, immune and environmental factors affecting autistic behaviors, so that in the latest update of genes involved in human and animal models of autism (on AutDB and SFARI.GENE databases), about 2000 genes involved in the etiology of autism and autistic behaviors have been classified. This list contains many genes including mTOR, MECP2 and genes involved in mitochondrial function or responsible for mtDNA maintenance. Several pathogenic variations that cause defects in mitochondrial metabolic pathways can lead to alterations in neuronal circuits and neurotransmitter systems. Protein coding genes of the mitochondria are components of the respiratory oxidative phosphorylation chain. Oxidative phosphorylation is vital to the growing nerve cells. Studies show that the capacity of oxidative phosphorylation in granulocytes is significantly lower in autistic children, in comparison with normal children. There is evidence of modified immune function in neural systems. The antigen-antibody complexes can induce immune cell migration and stimulate neuro-inflammation. Several investigations revealed that an immune abnormality during pregnancy or postnatal environment results in psychiatric disorders. Immune system irregularities, including defects in T cell responses or Th1/Th2 cytokines, have been reported in individuals with psychiatric disorders, proposing that unusual immune functions in the brain may play an important role in a significant subset of children with autism. Furthermore, Interferons can also induce the expression of more than 300 genes, some of which are mitochondrial genes and some are nuclear genes involved in regulating mitochondrial function. Glucocorticoids can inhibit the production of certain cytokines, such as TNF-α, IL-2, IL-6, IL1β and IL-8, and also can alter the production of anti-inflammatory cytokines, such as IL-10, IL-4, and growth factor-β. Besides, nuclear- or mitochondrial-encoded oxidative phosphorylation subunits (OXPHOS) are regulated by glucocorticoids that their receptors have been identified in the mitochondria. In summary, immune system disorders can impair prenatal brain development or postnatal brain function, so that they can create causality with the ASD phenotype. Also, some maternal allergies during pregnancy, such as exposure to infections, can cause persistent and long-term changes in mitochondrial functions that can lead to autism-like behaviors. This study focused on some clinical aspects of mitochondrial dysfunction in ASD. Most children with autistic behaviors indicate mitochondrial dysfunction and enhanced oxidative stress. Published findings have revealed broad alterations in the immune and nervous systems of children with autistic behaviors. Detection of dependent factors related to ASD can help in the early intervention of these children to address psychological requirements. This article tries to give a useful summary of critical pathways involved in mitochondrial dysfunction in autistic behaviors. Data of this review will give a wide perspective to genetic factors in autism.