Parkinson's disease, the second most prevalent neurodegenerative disorder lacking a recognized etiology, is influenced by oxidative stress and alterations in inflammatory cytokine levels. This study aimed to investigate the expression levels of Interleukin(IL)1 receptor accessory protein (IL-1RAcP), IL1β, IL1α, IL33, and IL36 genes in blood cells and serum IL-1β levels in Parkinson's disease patients compared to healthy controls (HCs).I n this case-control study, 44 Parkinson's disease patients and 44 age- and sex-matched HCs were included. Gene expression levels were assessed using Quantitative Real-time PCR, and serum IL-1β levels were measured via enzyme-linked immunosorbent assay. Advanced statistical analyses using the Bayesian regression model in R software were employed. Parkinson's disease patients exhibited elevated expression levels of IL-1RAcP and IL1β genes  but decreased levels of IL1α, IL33, and IL36 compared to HCs. Age-based differences were not significant. Regarding gender, IL33 transcript levels were significantly higher in males, and serum IL-1β levels were increased in patients. Subgroup analysis by gender indicated alterations in IL1β and IL-1RAcP expression in both genders, while IL1α, IL33, and IL36 showed reduced expression only in males. Remarkably, only female patients displayed significantly higher serum IL-1β levels than female HCs. These findings suggest that dysregulation of immune-related factors plays a crucial role in Parkinson's disease.

Background: Inflammatory protein C3 and IL-1β are significantly involved in the pathophysiology of type 2 diabetes (T2D) and Alzheimer's disease. Moreover, examining the importance of aerobic exercise timing (light vs. dark phase) can provide a better understanding of how exercise timing affects inflammatory markers associated with neurological diseases in older adult women with T2D. Therefore, this study aimed to investigate the effect of aerobic exercise timing on C3 and IL-1β levels in older adults’ women with T2D. Methods: In this semi-experimental study, 45 women with T2D with an average age of 60 ± 5.07 years were divided into training groups (light and dark phase) and control (15 people in each group). Aerobic exercise was performed for 12 weeks at a moderate intensity (60-70% of heart rate reserve). Protein levels (C3 and IL-1β) were measured before and after the intervention using the ELISA method. Data were analyzed using SPSS27 software and ANOVA with a significance level of 0.05. Results: Complement C3 was significantly lower in the dark phase exercise group compared to the control group (P= 0.0083). Additionally, the results showed that dark phase aerobic exercise significantly decreased C3 (P= 0.0028) and IL-1β (P= 0.0045) levels compared to baseline. Conclusion: Aerobic exercise performed during the dark phase effectively reduced inflammatory protein levels of C3 and IL-1β in older adult women with T2D, suggesting it could be considered as a crucial strategy in managing this disease.

Introduction: As a chronic neurological disorder, epilepsy is affected by social stress, which is one of the numerous complications in societies. In addition to medication, enriched environment (EE) and exercise are among the complementary strategies in the treatment of epilepsy. Oxidative stress, which potentially can activate the inflammatory pathways, is one of the causes of this disorder. So, we tried to examine thoroughly the beneficial impacts of EE and exercise on neuroinflammation in epileptic rats. Methods: Male Wistar rats were divided into five groups of twelve rats each, including: a control group, a group induced with pilocarpine to simulate epilepsy, an epileptic group subjected to social stress, an epileptic group placed in an enriched environment, and an epileptic group subjected to an exercise regimen. The impact of social stress, enriched environment, and exercise on oxidative stress biomarkers was investigated through TBARS  spectrophotometric test   and the gene expression of NLRP3, Caspase-1, IL18, and IL1β were evaluated through real-time PCR method. Results: Epilepsy and social stress caused a reduction in superoxide dismutase (SOD) and glutathione peroxidase (GPx) (p<0.05). Moreover, they resulted in an enhancement of plasma malondialdehyde (MDA), NLRP3, Caspase-1, interleukin-18 (IL18), and IL1β gene expression (p<0.05). Exercise increased the GPx and diminished the expression of Caspase-1 and IL-18 inflammatory genes (p<0.05). Accordingly, EE enhanced the SOD and GPx antioxidant indicators and reduced proinflammatory gene expression. Conclusion: In this research, social stress resulted in elevated levels of oxidative markers and upregulation of inflammatory gene expression. EE and regular exercise improved the situation.

This study evaluated the beneficial effects of quercetin nano-phytosome on inflammatory parameters in multiple sclerosis. The animals were divided into five groups, including Control, 150 Quercetin, 300 Quercetin, 150 and 300 nano-phytosome of Quercetin. At the end of the study, serum levels of Granulocyte-macrophage colony stimulator (GMCSF), interleukin 1β (IL1β), interleukin 2 (IL2), interleukin 6 (IL6), interleukin 10 (IL10), interleukin 17 (IL17), Interleukin gamma (IFNγ) and tumor necrosis factor alpha (TNFα) were determined. The results showed that administration of Quercetin and its nano-phytsome significantly decreased the levels of IL-1β, IL-2, IL-6, IL-17, IFN-γ, TNF-α and GM-CSF and increased IL-10 in comparison to the control group. The treated animals with nano-phytsome significantly decreased IL-2, IL-1β, IL-17, IL-6, IFN-γ, TNF-α and GM-CSF and increased IL-10 compared with Quercetin group. Quercetin nanophytosomes can be used to effectively improve inflammation. We recommend using quercetin nanophytosomes to reduce inflammation in patients with multiple sclerosis.

This study was aimed to monitor water pullution of Uzuncayir Dam Lake using the changes of IL-6, IL1β and TNF-α levels in Capoeta umbla (Heckel, 1843) liver tissue at ten stations in March and September 2011. In this study C. umbla (Heckel, 1843) was used as the indicator organism. Tumor necrosis factor-a (TNF-a), interlekuin1b (IL-1b) and interleukin-6 (IL-6) levels were determined in samples of the liver tissue by ELISA kit. The lowest mean IL-1b levels were found at station 6. The mean IL-1b was reached its maximum level at station 2. The difference between the mean levels of IL-6 was found to be significant (p<0.05) amoung stations. The IL-6 levels were significantly increased in September at stations 1, 2, 7 and 8 (p<0.01) compared to the values in March. The mean levels of TNF-a were found to be significant (p<0.05) amoung stations. The TNF-a levels significantly decreased in September at stations 1 and 9 (p<0.01). TNF-a, IL-1b and IL-6 levels in C. umbla can be used as early diagnostic indicators against adverse environmental events and useful and reliable bioindicators in determining the pollution of the aquatic ecosystem.

Introduction: Type I diabetes is an autoimmune disease associated with T lymphocytes function in beta cells. This process can increase cytokine secretion, which can cause beta cell inflammation and death. Since GABA, (γ-aminobutyric acid) is a major inhibitory neurotransmitter, and low concentration of GABA can increase cytokine secretion, the aim of this study was demonstrate to the inhibitory effect of GABA administration on cytokine secretion and decrease in beta cell death and also to show the ability of beta cells in insulin secretion. Material and Methods: Seven week old CD1 mice were used. To induce diabetes, animals received 40 mg/kg of STZ five days continuously. Two months later, animals were divided into two groups, one receiving 200 micromole of GABA and the other (controls) the same volume of PBS for 10 weeks. Results: Serum glucagon levels, and alpha cells significantly decreased in the (IL12 IL1β, TNFa) mass and some cytokine levels in the GABA group. Plasma insulin level and beta cell mass significantly increased in comparison to the control group. Conclusion: From the results of this study we conclude that GABA administration causes inhibition in cytokine secretion, improves beta cell mass and increases insulin secretion. May be, in the future, if GABA shows no side effects we can use GABA for type one diabetes.

Introduction. Ischemia followed by reperfusion in organ transplantations can lead to ischemia-reperfusion (I-R) injury, which is associated with oxidative stress and inflammatory responses. Alpha-pinene is an organic terpene with well-known antioxidant, anti-inflammatory, and anti-apoptotic properties. This study examines the preventive effects of alpha-pinene against renal I-R-induced kidney dysfunction, oxidative and inflammatory status, apoptosis, and histopathology changes. Methods. Forty-two adult male Wistar rats weighting 200-250 gr were divided into six groups (n = 7): Control, Right Nephrectomy, Ischemia-Reperfusion (45 min ischemia and 24 h reperfusion), and I-R + three different doses of alpha-pinene (2.5, 5, and 10 mg/kg) 24 hours and just before induction of ischemia through gavage. After 24 hours, urine, serum, and the remaining kidney were collected for biochemical and tissue analysis. Results. Renal I-R caused kidney damage indicated by a significant decrease in creatinine clearance, induction of oxidative stress, increased inflammatory cytokines, and histopathological injuries. Alpha-pinene significantly improved the damage by restoring the changes toward the control group. Alpha-pinene, in the effective dose (2.5 mg/kg), reduced the levels of Bax, Bcl-2, TNF-α, and IL1β and contributed to regenerating tissue damage following renal I-R. Conclusions. Aalpha-pinene has been able to reduce the complications due to its antioxidant, anti-inflammatory, and anti-apoptotic properties. It is suggested that it can be used as a pretreatment in reducing renal complications in renal transplantation.

Now evidence is mounting that suggests people with periodontal disease a bacterial infection, may be more at risk for heart disease and have nearly twice the risk of having a fatal heart attack, than patients without periodontal disease. It is our central hypothesis that periodontal disease, which are chronic Gram-negative infections, represent a previously unrecognized risk factor for atherosclerosis and thromboembolic events. Previous studies have demonstrated an association between periodontal disease severity and risk of coronary heart disease-and stroke. We hypothesize that this association may be due to an underlying inflammatory response trait, which places an individual at high risk for developing both periodontal disease and atherosclerosis. We further suggest that periodontal disease, once established, provides a biological burden of endotocxin (Lipoplysaccharide) and inflammatory cytokines (especially TXA2, IL-1, PGE2, and TNF-a) which serve to initiate and exacerbate atherogenesis and thromboembolic events. While more research is needed to confirm how periodontal bacteria may affect your heart, one possibility is that periodontal bacteria enter the blood through inflamed gums and cause small blood clots that contribute to clogged arteries.Another possibility is that the inflammation caused by periodontal disease contributes to the buildup of fatty deposits inside heart arteries.