The cardiotoxic effects of acute and chronic grayanotoxin-III in rats

The purpose of this study is to histologically and immunohistochemically determine the changes created by grayanotoxin-III (GTX-III), which is a sodium channel neurotoxin, on heart tissues in different dosages. Rats were randomly divided into 10 groups to determine the acute and chronic effects of GTX-III. While the rats in groups 1 and 6 were control rats, the rats in groups 2–5 (1, 2, 4, and 8 μg/kg bw GTX-III) received a single dose of intraperitoneal GTX-III, and the rats in groups 7–10 received GTX-III every day for 3 weeks. As a result of the trial, in the heart tissues, histopathological changes were determined by hematoxylin–eosin staining, interleukin-1 (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and brain natriuretic peptide (BNP) were determined by the avidin–biotin peroxidase method, and apoptosis was examined by immunohistochemistry (IHC) analysis and the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining method. In the immunohistochemistry sense, while the BNP level in the AGTX-III groups did not vary significantly, an increase in dosage significantly increased the IL-6, IL-1β, and TNF-α levels in comparison to the control groups. In their comparison to the control groups, the BNP levels increase and the IL-6 and IL-1β levels decreased in the CGTX-III groups. TUNEL analysis revealed that apoptosis increased in both the acute and chronic groups.

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The anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on acrylamide-induced neurotoxicity in rats

10.21203/rs.2.16758/v3 ◽

2020 ◽

Author(s):

Jie Guo ◽

Xiaolu Cao ◽

Xianmin Hu ◽

Shulan Li ◽

Jun Wang

Keyword(s):

Oxidative Stress ◽

Terminal Deoxynucleotidyl Transferase ◽

Tunel Staining ◽

Apoptotic Cells ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

Tnf Α ◽

Anti Inflammatory ◽

Factor Α ◽

Necrosis Factor

Abstract Background: Acrylamide (ACR) formed during heating of tobacco and carbohydrate-rich food as well as widely applied in industries has been known as a well-established neurotoxic pollutant. Although the precise mechanism is unclear, enhanced apoptosis, oxidative stress and inflammation have been demonstrated to contribute to the ACR-induced neurotoxicity. In this study, we assessed the possible anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin, the most active component in a popular spice known as turmeric, on the neurotoxicity caused by ACR in rats.Methods: Curcumin at the dose of 50 and 100 mg/kg was orally given to ACR- intoxicated Sprague-Dawley rats exposed by ACR at 40mg/kg for 4 weeks. All rats were subjected to behavioral analysis. The HE staining and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) staining were used to detect histopathological changes and apoptotic cells, respectively. The mRNA and protein expressions of apoptosis-related molecule telomerase reverse transcriptase (TERT) were detected using real-time PCR and immunohistochemistry, respectively. The contents of malondialdehyde (MDA) and glutathione (GSH) as well as the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured as the indicators for evaluating the level of oxidative stress in brain. The levels of pro-inflammatory cytokinestumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the cerebral homogenates were detected using ELISA assay.Results: ACR-induced weigh loss, deficits in motor function as well as pathological alterations in brains were significantly improved in rats administrated with 50 and 100 mg/kg curcumin. TUNEL-positive apoptotic cells in curcumin-treated ACR intoxicated brains were less than those in the ACR model group. Curcumin administration especially at the dose of 100 mg/kg upregulated the TERT mRNA expression and enhanced the number of TERT-positive cells in ACR-intoxicated cortex tissues. Moreover, curcumin treatment reduced the concentrations of TNF-α, IL-1β and MDA, while increased the GSH contents as well as the SOD and GSH-Px activities in the cerebral homogenates, in comparison to ACR control group.Conclusions: These data suggested the anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on ACR-induced neurotoxicity in rats. Maintaining TERT-related anti-apoptotic function might be one mechanism underlying the protective effect of curcumin on ACR-intoxicated brains.

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Tumor necrosis factor-α and interleukin-1 β levels in recurrent and persistent otitis media with effusion

Otolaryngology ◽

10.1067/mhn.2002.124188 ◽

2002 ◽

Vol 126 (4) ◽

pp. 417-422 ◽

Cited By ~ 7

Author(s):

Sertac Yetiser ◽

Bulent Satar ◽

Atilla Gumusgun ◽

Faruk Unal ◽

Yalcin Ozkaptan

Keyword(s):

Tumor Necrosis Factor ◽

Otitis Media ◽

Tumor Necrosis ◽

Otitis Media With Effusion ◽

Interleukin 1 ◽

Tertiary Referral Center ◽

Adenoid Tissue ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor

OBJECTIVE: Based on interleukin (IL)-1β and tumor necrosis factor (TNF)-α levels in effusions, our goals were to specify either recurrent or persistent otitis media with effusion (OME) is a mid stage in the development of chronic disease and to identify the factors that have an influence on cytokine levels. STUDY DESIGN: Samples from groups with recurrent (n = 15) and persistent (n = 39) OME were essayed for IL-1 β and TNF-α. Children were also grouped with respect to age, sex, quality of effusion, and the presence of pharyngeal adenoid tissue. SETTING: Tertiary referral center. RESULTS: In recurrent and persistent OME groups, IL-1β was higher than TNF-α ( P < 0.01). IL-β was higher in recurrent OME than in persistent OME ( P < 0.05). CONCLUSION: Recurrent OME seems to be closer to the chronic stage of the disease relative to persistent OME in terms of higher IL-1 β levels. Each exacerbation of acute disease in recurrent otitis media is likely to be mediated by IL-1 β. SIGNIFICANCE: We were able to clarify that recurrent OME is a stage that occurs before chronic OME. Therefore, the prevention of acute attacks in recurrent disease would also impede long-term damage to the middle ear.

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Predisposition to Hyperthyroidism May Be Influenced by Functional TNF-α, IL-1, IL-6, and IL-10 Polymorphisms: A Meta-Analysis

International Archives of Allergy and Immunology ◽

10.1159/000508284 ◽

2020 ◽

Vol 181 (12) ◽

pp. 956-965

Author(s):

Hong Ma ◽

Ting Tan ◽

Jie Wu ◽

Juan Chen ◽

Xiaohong Zhang

Keyword(s):

Meta Analysis ◽

Interleukin 1 ◽

Interleukin 10 ◽

Interleukin 4 ◽

Asian Origin ◽

Tnf Α ◽

Caucasian Origin ◽

Meta Analyses ◽

Factor Α ◽

Necrosis Factor

Background: Predisposition to hyperthyroidism may be influenced by functional gene polymorphisms in tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-4 (IL-4), interleukin-6 (IL-6), and interleukin-10 (IL-10). However, the results of the studies published so far remain discrepant, so we conducted a meta-analysis to more robustly investigate relationships between TNF-α/IL-1/IL-4/IL-6/IL-10 polymorphisms and predisposition to hyperthyroidism. Methods: A comprehensive literature retrieval from PubMed, Embase, Web of Science, WanFang, VIP, and CNKI was endorsed by the authors, and 38 studies were found to be eligible for pooled meta-analyses. Results: We found that genotypic frequencies of TNF-α −308 G/A, IL-1A −889 C/T, IL-6 −174 G/C, IL-6 −572 G/C, IL-10 −819 C/T, and IL-10 −1082 A/G polymorphisms among cases were significantly different from those among controls. Moreover, we also found that genotypic frequencies of TNF-α −308 G/A and IL-6 −174 G/C polymorphisms among cases of Caucasian origin were significantly different from those among Caucasian controls, and genotypic frequencies of IL-1A −889 C/T, IL-1B −511 C/T, IL-6 −174 G/C, IL-6 −572 G/C, and IL-10 −1,082 A/G polymorphisms among cases of Asian origin were also significantly different from those among Asian controls. Conclusions: This meta-analysis suggests that TNF-α −308 G/A, IL-1A −889 C/T, IL-1B −511 C/T, IL-6 −174 G/C, IL-6 −572 G/C, IL-10 −819 C/T, and IL-10 −1,082 A/G polymorphisms may influence predisposition to hyperthyroidism in certain ethnic groups.

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The Augmented Productions of Neopterin and Cytokines from Macrophages/monocytes in vitro

Pteridines ◽

10.1515/pteridines.1996.7.3.72 ◽

1996 ◽

Vol 7 (3) ◽

pp. 72-76

Author(s):

Tadashi Lizuka ◽

Mitsuyo Sasaki ◽

Hitomi Kamisako ◽

Ko Oishi ◽

Shigeru Uemura ◽

...

Keyword(s):

Kawasaki Disease ◽

Interleukin 1 ◽

Poly I:C ◽

Recombinant Interferon ◽

Preliminary Examination ◽

Tnf Α ◽

Ifn Γ ◽

Factor Α ◽

Necrosis Factor

Summary In Kawasaki disease patients, increases in excretion of urinary neopterin coincided with fever and monocytosis in peripheral blood. We examined the products of neopterin, tumor necrosis factor-α (TNFα) and Interleukin-1 β (1L-1β) from healthy adult macrophages/monocytes (Mφ>/M), after stimulation with several activators to obtain some understanding of Kawasaki disease. Upon stimulation with either lipopolysaccharide (LPS) or polyinosinate-polycytidylate (Poly I:C), the Mφ/M released neopterin and pyogenic products (TNF-α or 1L-1β). The release of neopterin was eliminated by the addition of the anti-interferon-y antibody. The production of both TNF-α, 1L-1β and neopterin from Mφ/M upon stimulation of LPS was augmented in a co-culture with low dose recombinant interferon-y (rIFN-γ). Upon stimulation with rIFN-γ alone, however, the Mφ/M released neopterin but not the pyogenic products. A preliminary examination failed to detect. any difference in the response of the Mφ/M in adults annd children after stimulation with LPS. We concluded that some endotoxins could trigger the onset of Kawasaki disease and that endogenous IFN-γ can play an important role in the abnormality of Kawasaki disease patients

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BNIP3 decreases the LPS-induced inflammation and apoptosis of chondrocytes by promoting the development of autophagy

10.21203/rs.3.rs-29090/v2 ◽

2020 ◽

Author(s):

Zetao Ma ◽

Deli Wang ◽

Jian Weng ◽

Sheng Zhang ◽

Yuanshi Zhang

Keyword(s):

Interleukin 1 ◽

Interleukin 1 Beta ◽

Related Protein ◽

Interacting Protein ◽

Tnf Α ◽

Adenovirus E1b ◽

Factor Α ◽

Related Proteins ◽

Necrosis Factor ◽

Proinflammatory Factors

Abstract Background: Inflammation and apoptosis of chondrocytes are the pathological basis of osteoarthritis. Autophagy could alleviate the symptoms of inflammation and apoptosis. Previous study has shown that BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) can induce the occurrence and development of autophagy. However, it is unknown whether autophagy induced by BNIP3 can alleviate the inflammation and apoptosis of chondrocytes. Methods: We used the lentivirus to construct the overexpression BNIP3 chondrocytes. Next, the lipopolysaccharide (LPS) was used to stimulate these cells to simulate the physiological environment of osteoarthritis. After that, the enzyme-linked immunosorbent assays (ELISA) were performed to determine the levels of tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) and the flow cytometry was performed to detect the apoptosis rates of chondrocytes. At last, the expression of autophagy related proteins was detected with the western blotting. Results: The expression of BNIP3 was suppressed after treatment with LPS. However, overexpression of BNIP3 inhibited the secretion of proinflammatory factors (TNF-α, IL-1β and IL-6) and decreased the apoptosis of chondrocytes. Furthermore, overexpression of BNIP3 led to the upregulation of autophagy related proteins expression including little computer 3 (LC3), autophagy-related protein 7 (ATG7) and Beclin-1. Application of autophagy inhibitor recovered the expression of proinflammatory factors and apoptosis rates of chondrocytes. Conclusions: BNIP3 decreased the LPS induced inflammation and apoptosis of chondrocytes by activating the autophagy.

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Regulation of Murine Protein C Gene Expression In Vivo: Effects of Tumor Necrosis Factor-α, Interleukin-1, and Transforming Growth Factor-β

Thrombosis and Haemostasis ◽

10.1055/s-0037-1614379 ◽

1999 ◽

Vol 82 (10) ◽

pp. 1297-1301 ◽

Cited By ~ 21

Author(s):

Takayoshi Shimokawa ◽

Tetsuhito Kojima ◽

David Loskutoff ◽

Hidehiko Saito ◽

Koji Yamamoto

Keyword(s):

Growth Factor ◽

Protein C ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Transforming Growth Factor ◽

Interleukin 1 ◽

Transforming Growth Factor Β ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor

SummaryProtein C is a precursor of the anticoagulant serine protease, activated protein C, which inhibits coagulation factors Va and VIIIa. Although the liver appears to be the primary site of protein C synthesis, we previously demonstrated that the kidney and male reproductive organs also expressed abundant protein C mRNA in the mouse. In the present study, we further investigated the effects of tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and transforming growth factor-β (TGF-β) on the expression of protein C mRNA in the principal producing organs, i.e., the liver, kidney, and testis. Both quantitative reverse transcription-PCR assay and in situ hybridization analysis revealed that TNF-α decreased protein C mRNA expression in the liver, kidney, and testis. IL-1 also down-regulated protein C mRNA expression in the liver and testis, but not in the kidney. In contrast, TGF-β unchanged the expression level of protein C mRNA in these three organs. These observations suggest that TNF-α and IL-1 may contribute to an increase in the procoagulant potential by down-regulation of protein C synthesis in the tissues during inflammatory processes.

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Release of tumour necrosis factor alpha into bronchial alveolar lavage fluid following antigen challenge in passively sensitized guinea-pigs

Mediators of Inflammation ◽

10.1155/s0962935192000644 ◽

1992 ◽

Vol 1 (6) ◽

pp. 425-428 ◽

Cited By ~ 2

Author(s):

D. E. Kelly ◽

M. Denis ◽

D. F. Biggs

Keyword(s):

Tumour Necrosis Factor ◽

Guinea Pigs ◽

Tumour Necrosis ◽

Interleukin 1 ◽

Lavage Fluid ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Factor Α ◽

Bronchial Alveolar Lavage ◽

Necrosis Factor

Five groups of ten female guinea-pigs were passively sensitized against ovalbumin (OA) (n = 9) or control guinea-pig serum (n = 1). 24 h later, they received mepyramine (0.5 mg/kg, i.p.) and 30 min later inhaled aerosols of: (A) OA (2 in 0.9% saline, 8 min, n = 4/9); (B) saline (40 min, n = 4/9); (C) LPS (40 min, Escherichia coli 0111:B4, 150 ng/kg in PBS, n = 1/9); and (D) the control animal was treated as in (C) (n = 1). Their tracheas were cannulated under pentobarbital anaesthesia and bronchial alveolar lavage (BAL) was performed with 2 × 5 ml PBS containing BSA (1%) (n = 1 group), or BSA (1%) and aprotinin (1000 KIU/ml) (n = 4 groups), at 30, 60, 90 or 120 min post-inhalations. BAL fluids recovered were centrifuged, the supernatants recovered and frozen until assayed for tumour necrosis factor-α (TNF-α), interleukin-1 (IL-1) and interleukin-6 (IL-6). No TNF-α could be detected unless aprotinin was present in the lavaging solution. BAL fluid from OA-sensitized and control animals that had inhaled LPS contained high levels of TNF-α that peaked at 90 min. BAL fluid from OA sensitized animals that inhaled OA aerosols contained no detectable TNF-α at 30 min, but it was found in increasing amounts at 60, 90 and 120 min; TNF-α was not detected in fluid from any of the animals that inhaled saline. As BAL fluids were toxic to the cells used in the assays, neither IL-1 nor IL-6 could be measured. We conclude that the monokine TNF-α is released into BAL fluid following anaphylactic challenge of passively sensitized guinea-pigs. The presence of the antiprotease, aprotinin, in the lavaging solution is essential for the detection and measurement of TNF-α in BAL fluid.

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Differential Effects of Interleukin 1-α (IL-1α) or Tumor Necrosis Factor-α (TNF-α) on Motility of Human Melanoma Cell Lines on Fibronectin

Journal of Investigative Dermatology ◽

10.1111/1523-1747.ep12383385 ◽

1994 ◽

Vol 102 (6) ◽

pp. 898-905 ◽

Cited By ~ 13

Author(s):

Sybren K Dekker ◽

Jacqueline Vink ◽

Bert Jan Vermeer ◽

Jan A Bruijn ◽

Martin C Mihm ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Cell Lines ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Interleukin 1 ◽

Human Melanoma ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor ◽

Melanoma Cell Lines

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Differences of plasma IL-1 and TNF-α in healthy Chinese Population

Open Medicine ◽

10.1515/med-2015-0044 ◽

2015 ◽

Vol 10 (1) ◽

Author(s):

Jintao Yuan ◽

Lan Wang ◽

Yijin Lin ◽

Jianhong Chen ◽

Jianghong Hu

Keyword(s):

Immune Responses ◽

Opportunistic Infections ◽

Inflammatory Diseases ◽

Interleukin 1 ◽

Predictive Biomarkers ◽

Enzyme Linked Immunosorbent Assay ◽

Tnf Α ◽

Inflammatory Processes ◽

Factor Α ◽

Necrosis Factor

AbstractPle iotropic proinflammatory cytokines, interleukin- 1 (IL-1) and tumor necrosis factor-α (TNF-α), involved in the regulations of various immune responses, inflammatory processes and hematopoiesis. In the present study, the expression levels of IL-1 and TNF-α were detected by enzyme-linked immunosorbent assay (ELISA). Following the cytokine blockade as a successful clinical therapy for autoimm une diseases such as rheumatoid arthritis, the patients are more susceptible to a variety of opportunistic infections. IL-1 and TNF-α may be useful predictive biomarkers of diseases and offer potential targets for therapeutic intervention of inflammatory diseases. However, our results showed that the plasma IL-1 level was significantly higher in women compared to men (69.5 ± 19.8 pg/ ml in men and 80.1 ± 19.5 pg/ml in women, respectively); the plasma levels of TNF-α were higher in men than women (20.8 ± 4.9 pg/ml and 18.7 ± 7.1 pg/ml, respectively). The significant gender difference of plasma interleukin-1 (IL-1) and TNF-α levels present in healthy adults in Jiangsu Province, China (P=0.002 and P=0.015, respectively), and may be as a hint for sex differences of susceptibility to many diseases and elementary immune response.

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