scholarly journals An Increase in TNF-α Levels in Fetus due to Prenatal Ischemic Hypoxia

2021 ◽  
Vol 9 (T5) ◽  
pp. 44-47
Author(s):  
Ratna Indriawati ◽  
Nurvita Risdiana ◽  
Tunjung Wibowo
Keyword(s):  
Neural Development ◽  
Sensitive Period ◽  
Control Group ◽  
Mortality And Morbidity ◽  
Cell Dysfunction ◽  
Ischemic Hypoxia ◽  
Tnf Α ◽  
Post Test ◽  
Elisa Technique ◽  
Factor Α

BACKGROUND: Prenatal ischemic hypoxia can increase mortality and morbidity and affect the immune system. One of the immune responses is tumor necrosis factor-α (TNF-α) levels. However, the cellular mechanism of immune response abnormalities due to prenatal hypoxia remains unclear. An 11–17-day-old fetus is a sensitive period of neural development. Brain ischemia will cause cell dysfunction and can even affect TNF-α levels. Thus, how prenatal ischemic hypoxia increases TNF-α levels in the fetus remains unclear. AIM: This study aims to examine the effect of the onset and duration of prenatal ischemic hypoxia on TNF-α levels. METHODOLOGY: An experimental study with a post-test control design was conducted. Thirty Rattus norvegicus were induced with prenatal ischemic hypoxia (embryos aged 7, 12, and 17 days). The independent variable was prenatal ischemic hypoxia, while the dependent variable was TNF-α levels. TNF-α was measured using the ELISA technique and was carried out when the fetus was 19 days old (E19). The TNF-α was analyzed using ANOVA, and the limit of significance was set at p < 0.05. RESULTS: The TNF-α levels in the prenatal ischemic hypoxia group were statistically higher than in the control group (p < 0.05). The more the onset and the longer the ischemic hypoxia is, the higher the TNF-level (p < 0.05). CONCLUSION: The prenatal ischemic hypoxia increased TNF-α levels in the fetus.

Synthesis of Novel 8-Hydroxyquinoline Derivatives through Mannich Reaction and their Biological Evaluation as Potential Immunomodulatory Agents

2020 ◽  
Vol 16 (4) ◽  
pp. 531-543
Author(s):  
Shaheen Faizi ◽  
Tahira Sarfaraz ◽  
Saima Sumbul ◽  
Almas Jabeen ◽  
Sobia A. Halim ◽  
...  
Keyword(s):  
Mannich Reaction ◽  
Aromatic Aldehydes ◽  
Mannich Bases ◽  
Biological Evaluation ◽  
Mechanism Of Inhibition ◽  
Potent Inhibition ◽  
Tnf Α ◽  
Elisa Technique ◽  
Factor Α ◽  
New Compounds

Background: In continuation of our work on Mannich reaction on 8-hydroxyquinoline, fifteen different combinations of aromatic aldehydes and aniline were subjected to Mannich reaction from which twelve products (eight Mannich bases, two imines and two intramolecularly cyclized products with benzofuranone skeleton) were obtained. Among them six compounds (1, 2, 6, 8, 9 and 12) are the new compounds. The structures of the compounds were characterized by UV, IR, MS and 1H NMR. Method: The compounds were tested for the inhibition of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and Interleukin-1β (IL-1β) at a concentration of 25 µg/mL. The cytokines were produced by THP-1 cells differentiated with PMA for 24hrs and stimulated with LPS for 4 hrs and supernatant were analyzed through ELISA technique. Results and Discussion: Compounds 1-5, 8 and 9 inhibited the production of TNF-α and IL-1β. Compounds 1, 3, and 8 exerted potent inhibitions of TNF-α with 71%, 71%, and 83% inhibition, respectively. Compounds 1 and 8 significantly inhibited the production of IL-1β with 64% and 78% inhibition, respectively. Conclusion: Compounds 1 and 8 significantly inhibited the production of IL-1β with 64% and 78% inhibition, respectively. Notably compound 8 showed the most potent inhibition of these cytokines. Additionally, the effect of compounds on viability of THP-1 cells was also evaluated. Moreover, molecular docking was carried out to study the mechanism of inhibition of TNF-α production.

scholarly journals The Effects of Rice Husk Liquid Smoke in Porphyromonas gingivalis-Induced Periodontitis

2021 ◽  
Author(s):  
Theresia Indah Budhy ◽  
Ira Arundina ◽  
Meircurius Dwi Condro Surboyo ◽  
Anisa Nur Halimah
Keyword(s):  
Growth Factor ◽  
Porphyromonas Gingivalis ◽  
Rice Husk ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Control Group ◽  
Proliferation Markers ◽  
Liquid Smoke ◽  
Tnf Α ◽  
Factor Α

Abstract Objectives The purpose of this study is to analyze the effects of rice husk liquid smoke in Porphyromonas gingivalis-induced periodontitis in the inflammatory and proliferation marker such as nuclear factor kappa β (NF-kB), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), transforming growth factor-β (TGF-β), fibroblast growth factor 2 (FGF2), collagen type 1 (COL-1) expression, and the number of macrophages, lymphocytes, and fibroblasts. Materials and Methods Rice husk liquid smoke is obtained by the pyrolysis process. Porphyromonas gingivalis-induced periodontitis in 20 μL phosphate-buffered saline containing 1 × 109 CFU was injected into the lower anterior gingival sulcus of Wistar rats. The periodontitis was then treated with 20 μL/20 g body weight of rice husk liquid smoke once a day for 2 and 7 days, respectively. After treatment, the bone and lower anterior gingival sulcus were analyzed with immunohistochemistry and hematoxylin–eosin staining. Results The treatment of periodontitis with rice husk liquid smoke showed a lower NF-kB, TNF-α, and IL-6 expression and a higher TGF-β, FGF2, and COL-1 expression than the control after treatment for 2 and 7 days (p < 0.05), respectively. The number of macrophages and fibroblasts was also higher when compared with the control group (p < 0.05), but the number of lymphocytes was lower than the control (p < 0.05). Conclusion Rice husk liquid smoke showed its effects on Porphyromonas gingivalis-induced periodontitis with a decrease in inflammatory markers and an increase in proliferation markers. The development of a rice husk liquid smoke periodontitis treatment is promising.

scholarly journals Association of Tumor Necrosis Factor-α -308G>A, -238G>A and -376G>A polymorphisms with recurrent pregnancy loss risk in the Greek population

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Sofoklis Stavros ◽  
Despoina Mavrogianni ◽  
Myrto Papamentzelopoulou ◽  
Evaggelos Basamakis ◽  
Hend Khudeir ◽  
...  
Keyword(s):  
Pregnancy Loss ◽  
Recurrent Pregnancy Loss ◽  
Pcr Amplification ◽  
Greek Population ◽  
Control Group ◽  
Increased Risk ◽  
Tnf Α ◽  
Caucasian Women ◽  
Factor Α ◽  
And Control

Abstract Background Promoter region SNPs in TNF-α have been studied in association with Recurrent Pregnancy Loss (RPL) occurrence in various populations. Among them, −238G > A, −308G > A and − 376G > A have been frequently investigated for their potential role in recurrent abortions. The aim of the present study is to evaluate the correlation among TNF-α 238, TNF-α 308 and TNF-α 376 polymorphisms and recurrent pregnancy loss risk in Greek women. Methods This study included 94 Caucasian women with at least two miscarriages of unexplained aetiology, before the 20th week of gestation. The control group consisted of 89 Caucasian women of proven fertility, with no history of pregnancy loss. DNA samples were subjected to PCR amplification using specific primers. Sanger sequencing was applied to investigate the presence of TNF-α 238, TNF-α 308, TNF-α 376 polymorphisms in all samples. Results The TNF-α 238 and TNF-α 308 variants were both detected in RPL and control groups (7.45% vs 4.49 and 45.16% vs 36.73%, respectively), but with no statistically significant association (p-value 0.396 and 0.374, respectively). The TNF-α 376 variant was not detected at all in both control and RPL groups. When TNF-α 238 and TNF-α 308 genotypes were combined no association with RPL was detected (p-value = 0.694). In subgroup analysis by parity, RPL patients carrying the A allele reported less previous births. Conclusions This is the first study demonstrating TNF-α 238 and TNF-α 308 gene expression and the absence of TNF-α 376 variant in Greek women with RPL. However, no association emerged between each polymorphism studied and the occurrence of recurrent pregnancy loss. Accordingly, TNF-α -308G > A, −238G > A and -376G > A variants are not considered genetic markers for identifying women at increased risk of recurrent pregnancy loss in the Greek population.

scholarly journals The Immuno modulatory Changes of Patients with Tuberculosis.

2018 ◽  
Vol 9 (SPL1) ◽  
Author(s):  
Rafal J Al-Saigh ◽  
Hussam Al-Humadi
Keyword(s):  
Rural Areas ◽  
Liver Function Tests ◽  
Pulmonary Diseases ◽  
Control Group ◽  
Chronic Obstructive ◽  
Descriptive Data ◽  
Tnf Α ◽  
Significant Difference ◽  
Level Versus ◽  
Factor Α

Tuberculosis(TB) is aninfectious disease caused by Mycobacterium tuberculosis. The aim was to investigate the levels of immunomodulatory markers like interluekin-6 (IL-6), tumor necrotizing factor-α (TNF- α),cell differentiation-4 (CD4) and CD8 levels in those patients with active tuberculosis (TB) disease in comparison with control group. 41 Adults diagnosed with TB were included in comparison to 32 healthy individuals at Babylon health center for pulmonary diseases and TB. Descriptive data for patients and control group werecollected by well-trained researcher following a structured questionnaire. In parallel, peripheral blood collected to determine IL-6, TNF- α,CD4 and CD8. Then the assessment for the association between clinical and descriptive data and immunomodulatory markers levels was investigated statistically. The majority of TB patients were males (56%) and 71% were resident in rural areas; 47% of them were living in middle socioeconomic state,moreover,47% of TB cases had diabetes,furthermore,51% had chronic obstructive pulmonary diseases,12% had hypertension and 39% of them had chronic anemia with 47% smokers with no significant difference versus control. Following to that,there was highly increased in IL-6 and TNF-α levels in TB patients versus control (P<0.001),with low CD4 level versus control (P<0.001). While there was no significant change shown in CD8 levels versus control and this might highly be correlated with 30% of abnormal liver function tests among TB patients. A high proportion of TB patients have low CD4 level mostly associated with active disease. Moreover,the increase of IL-6 and TNF-α levels suggests a inverse impact on CD4 level which closely associated with the outcome of the disease.

scholarly journals Analysis on the Expression and Prognostic Value of LncRNA FAF in Patients with Coronary Heart Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Hai Xu ◽  
Xiwen Zhang ◽  
Kun Yu ◽  
Gang Zhang ◽  
Yafei Shi ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Poor Prognosis ◽  
Prognostic Value ◽  
High Sensitivity ◽  
Control Group ◽  
Coronary Lesion ◽  
Tnf Α ◽  
Factor Α

Objective. To investigate the expression and prognostic value of LncRNA FAF in patients with coronary heart disease. Patients and Methods. 97 patients with coronary heart disease who came to our hospital were selected as the research group (RG), and 97 healthy people who came to our hospital for physical examination during the same period were selected as the control group (CG). The serum LncRNA FAF, plasma homocysteine (HCY), lipoprotein A (Lp-a), serum tumor necrosis factor α (TNF-α), and high-sensitivity C-reactive protein (hsCRP) in the two groups of patients were detected, and their correlations were analyzed. Then, the predictive value and risk factors of FAF for poor prognosis of patients with coronary heart disease were analyzed. Results. The expression of LncRNA FAF in the serum of patients in the RG was significantly lower than that in the CG, and the expressions of HCY, Lp-a, TNF-α, and hsCRP were significantly higher than those in the CG (p <0.05). The AUC of FAF in the diagnosis of coronary heart disease was more than 0.9. FAF was negatively correlated with the coronary lesion vessels, HCY, Lp-a, TNF-α, and hsCRP expressions in patients with coronary heart disease ( p < 0.05 ). The ROC of FAF for predicting poor prognosis in patients with coronary heart disease was greater than 0.9. Low expression of FAF; high expressions of HCY, Lp-a, and hsCRP; and increase of coronary lesion vessels were independent risk factors for poor prognosis in patients with coronary heart disease. Conclusions. LncRNA FAF was lowly expressed in the serum of patients with coronary heart disease, and it was of high value in the diagnosis and prediction of poor prognosis of coronary heart disease. It was also an independent risk factor for poor prognosis of patients with coronary heart disease and may be a potential target for diagnosis and treatment of coronary heart disease.

The change of proinflammatory cytokine tumor necrosis factor α level in the use of meloxicam in rat model of osteoarthritis

2019 ◽  
Vol 30 (6) ◽  
Author(s):  
Junaidi Khotib ◽  
Naning Windi Utami ◽  
Maria Apriliani Gani ◽  
Chrismawan Ardianto
Keyword(s):  
Tumor Necrosis Factor ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Treatment Groups ◽  
Tnf Α ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background Osteoarthritis (OA) is a chronic disease in the joints. One of the proinflammatory cytokines that is thought to have a major role in the inflammatory process, the emergence of pain, and cartilage damage in OA is tumor necrosis factor α (TNF-α). Meloxicam is a nonsteroidal anti-inflammatory drug class of drugs that is relatively selective in inhibiting the activity of cyclooxygenase 2 (COX-2) formation. This study is conducted to prove the change in TNF-α level in the use of meloxicam with model in animals suffering from OA. Methods The OA rat model was induced with sodium monoiodoacetate intra-articularly. Rats were divided into 5 groups: negative control group, positive control group, and treatment groups with various doses of meloxicam. Hyperalgesia effect was evaluated using a warm plate test, and TNF-α level was determined using enzyme-linked immunosorbent assay. Results The treatment groups that received meloxicam at a dose of 1.0, 3.0, or 10.0 mg/kg body weight (BW) did not show significant differences in rat knee joint diameter (p = 0.99), but showed a significant difference in sensitivity to heat stimulation (p = 0.02) compared to the control group. Osteoarthritis rats experienced a significant reduction in TNF-α level after being given meloxicam at a dose of 10 mg/kg BW compared with the control group. This shows that the 10 mg/kg BW of meloxicam is a potential dose in reducing the TNF-α level in OA rat models. Conclusions Based on these data, it can be concluded that the inhibition of pain and the development of OA by meloxicam in animal models may be assigned to a decreased level of TNF-α.

T-614 inhibits human aortic adventitial fibroblast proliferation and promotes interleukin-8 production in vitro

Vascular ◽  
2019 ◽  
Vol 28 (3) ◽  
pp. 314-320
Author(s):  
Weiping Ci ◽  
Tian Wang ◽  
Taotao Li ◽  
Jin Wan
Keyword(s):  
Cell Viability ◽  
Vascular Wall ◽  
Underlying Mechanism ◽  
Interleukin 8 ◽  
Control Group ◽  
Survival Fraction ◽  
Tnf Α ◽  
Significant Difference ◽  
Factor Α

Objectives The effect and underlying mechanism of T-614 (iguratimod) on Takayasu’s arteritis (TA) are unknown. Here, we report the effects of T-614 on cell proliferation and interleukin-8 (IL-8) production in human aortic adventitial fibroblasts (HAAFs) in vitro and explore its initial benefit in terms of vascular wall inflammation and remodeling for patients with TA. Methods HAAFs were cultured with 0, 5, 50, 100, or 250 μg/ml T-614 in the absence or presence of tumor necrosis factor-α (TNF-α) in vitro. Cell viability was determined by a modified MTT assay. Supernatant IL-8 levels were measured by enzyme-linked immunosorbent assays. Results In the presence of TNF-α, compared to that in the control group, cell viability of HAAFs significantly decreased in the 50, 100, and 250 μg/ml T-614 treatment groups (OD value: P <  0.01, P <  0.001, P <  0.001, respectively; survival fraction (SF): P <  0.05, P <  0.001, P <  0.001, respectively). However, there was no significant difference in cell viability between TNF-α-stimulated and unstimulated groups at the same concentration of T-614. In the absence or presence of TNF-α, T-614 suppressed HAAF cell viability dose-dependently (OD value: r = −0.915, P =  0.000; r = −0.926, P =  0.000, respectively; SF: r = −0.897, P =  0.000; r = −0.885, P =  0.000, respectively). Compared to that in the control group, in the absence of TNF-α, IL-8 levels in the 5 and 100 μg/ml T-614-treated groups were significantly higher ( P <  0.05); in the presence of TNF-α, IL-8 levels in the 5, 50, and 100 μg/ml T-614-treated groups were significantly higher ( P <  0.001, P <  0.001, P <  0.01, respectively). Further, there was a negative correlation between supernatant IL-8 levels and T-614 concentration in groups stimulated with TNF-α ( r = −0.670, P =  0.000), but there was no significant correlation between these parameters in groups that were not stimulated with TNF-α. Conclusions In the absence or presence of TNF-α, T-614 can inhibit HAAF proliferation and promote IL-8 production in vitro; therefore, it could be used to prevent adventitial thickening of the aorta and improve vascular remodeling in inflammatory environments in vitro and might provide a new immunotherapeutic intervention for TA.

scholarly journals Application of Dexmedetomidine in Cardiopulmonary Bypass Prefilling

Dose-Response ◽  
2020 ◽  
Vol 18 (3) ◽  
pp. 155932582093976 ◽  
Author(s):  
Li Wang ◽  
Shaowei Wang ◽  
Zhen Xing ◽  
Fulong Li ◽  
Jinliang Teng ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Anesthesia Induction ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective: The purpose of this study was to explore the application of dexmedetomidine (Dex) in cardiopulmonary bypass. Methods: A total of 60 patients undergoing elective cardiopulmonary bypass were divided into control (C) group and Dex group. In the Dex group, appropriate amount of Dex was added into the membrane lung prefilling solution before anesthesia induction, while those in control group were given normal saline. The levels of mean arterial pressure (MAP) and heart rate (HR) at different times were measured. The levels of cardiac troponin I (CTNI), malondialdehyde (MDA), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) at different points (T0/T1/T2/T3/T4) in both groups were measured by enzyme-linked immunosorbent assay kits. Results: The intraoperative and postoperative levels of MAP and HR in the 2 groups were significantly lower than those preoperatively ( P < .05). The levels of MAP and HR in the Dex group were significantly lower than those of the C group ( P < .05). The levels of CTNI/MDA/IL-6/TNF-α at different points in both groups were significantly higher than those at T0 ( P < .05). The serum levels of CTNI, MDA, IL-6, and TNF-α in the Dex group at T1/T2/T3/T4 were significantly lower than those in the C group ( P < .05). The rate of arrhythmia in the Dex group was significantly lower than that in the C group ( P < .05). Conclusion: Dexmedetomidine has a stable effect in cardiopulmonary priming solution.

Serum and BAL cytokine and antioxidant enzyme levels at different stages of pneumoconiosis in coal workers

2008 ◽  
Vol 27 (12) ◽  
pp. 871-877 ◽  
Author(s):  
OC Ulker ◽  
B Yucesoy ◽  
O Demir ◽  
IO Tekin ◽  
A Karakaya
Keyword(s):  
Antioxidant Enzymes ◽  
Transforming Growth Factor ◽  
Coal Dust ◽  
Transforming Growth Factor Β ◽  
Control Group ◽  
Tnf Α ◽  
Patient Groups ◽  
Coal Workers Pneumoconiosis ◽  
Factor Α ◽  
Coal Workers

Coal workers’ pneumoconiosis (CWP) is an occupational pulmonary disease that occurs by chronic inhalation of coal dust. CWP is divided into two stages depending on the extent of the disease, as simple pneumoconiosis (SP) and progressive massive fibrosis (PMF). In the present study, serum and bronchoalveolar lavage (BAL) cytokine (interleukin-1β [IL-1β], IL-6, tumor necrosis factor-α [TNF-α], transforming growth factor-β [TGF-β]) and antioxidant enzymes levels, their relation with the disease severity, and whether they can be considered as biological markers were investigated. Serum and BAL levels of IL-1β, IL-6, and TNF-α were higher in SP and PMF patient groups compared with that in active and retired miner groups. Serum and BAL IL-1β, IL-6, and TNF-α levels were also found to be higher in patients with PMF compared with the SP group. BAL superoxide dismutase (SOD), glutathione peroxidase, and catalase levels and serum SOD level were increased in both patient groups compared with the control group. In addition, mean serum and BAL TGF-β levels were found to be increased in patients with SP compared with PMF group. Based on these results, BAL and serum cytokine and antioxidant enzymes levels were evaluated and discussed as potential biomarkers for different stages of CWP.

scholarly journals Glucagon-like peptide-1 attenuates tumour necrosis factor-α-mediated induction of plasmogen activator inhibitor-1 expression

2007 ◽  
Vol 196 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Hongbin Liu ◽  
Yunshan Hu ◽  
Richard W Simpson ◽  
Anthony E Dear
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Cell Dysfunction ◽  
Tnf Α ◽  
Glucagon Like Peptide 1 ◽  
Factor Α ◽  
Activator Inhibitor ◽  
Necrosis Factor ◽  
Pai 1

Glucagon-like peptide-1 (GLP-1) has been proposed as a target for treatment of type 2 diabetes. GLP-1 has also been demonstrated to improve endothelial cell dysfunction in diabetic patients. Elevated plasmogen activator inhibitor-1 (PAI-1) levels have been implicated in endothelial cell dysfunction. The effect of GLP-1 on PAI-1 expression in vascular endothelial cells has not been explored. In a spontaneously transformed human umbilical vein endothelial cell (HUVEC) line, C11-spontaneously transformed HUVEC (STH) and primary HUVEC cells, GLP-1 treatment, in the presence of a dipeptidyl peptidase IV inhibitor, attenuated induction of PAI-1 protein and mRNA expression by tumour necrosis factor-α (TNF-α). GLP-1 also inhibited the effect of TNF-α on a reporter gene construct harbouring the proximal PAI-1 promoter. In addition, GLP-1 attenuated TNF-α-mediated induction of Nur77 mRNA and TNF-α-mediated binding of nuclear proteins (NPs) to the PAI-1, Nur77, cis-acting response element nerve growth factor induced clone B response element (NBRE). GLP-1 treatment also inhibited TNF-α-mediated induction of Akt phosphorylation. Taken together, these observations suggest that GLP-1 inhibits TNF-α-mediated PAI-1 induction in vascular endothelial cells, and this effect may involve Akt-mediated signalling events and the modulation of Nur77 expression and NP binding to the PAI-1 NBRE.

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