Exercise pretraining attenuates endotoxin-induced hemodynamic alteration in type I diabetic rats

2008 ◽  
Vol 33 (5) ◽  
pp. 976-983 ◽  
Author(s):  
Ching-Hsia Hung ◽  
Yu-Wen Chen ◽  
Dong-Zi Shao ◽  
Che-Ning Chang ◽  
Yung-Yuh Tsai ◽  
...  
Keyword(s):  
Exercise Training ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Diabetic Rats ◽  
Type I ◽  
Cardiovascular Dysfunction ◽  
Factor Α ◽  
Hsp72 Expression ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis

Higher expression of heat shock protein 72 (HSP72) reduces the mortality rate and organ damage in septic shock and prevents cardiac mitochondrial dysfunction due to lipopolysaccharide (LPS). Our hypothesis is that exercise preconditioning may increase the expression of HSP72 in heart and the nucleus tractus solitarii (NTS) of the brain to alleviate the cardiovascular dysfunction in type I diabetic rats receiving endotoxin. Wistar rats were randomly assigned to the following groups: sedentary normal, sedentary type I diabetic rats, and type I diabetic rats with exercise training. The trained rats ran on a treadmill 5 d·week–1, 30–60 min·d–1, at an intensity of 1.0 mile·h–1 (1 mile = 1.6 km) over a 3 week period. Twenty-four hours after the last training session, we compared the temporal profiles of mean arterial pressure, heart rate, cardiac output, stroke volume, and serum tumor necrosis factor α level in rats receiving an injection of LPS. In addition, HSP72 expression in heart and NTS from each group was determined. We found that HSP72 expression in the heart and NTS was significantly increased in diabetic rats with exercise training. After administration of LPS, the survival time was significantly longer in diabetic rats with exercise training. Additionaly, serum tumor necrosis factor α levels decreased as compared with those rats not receiving exercise training. Exercise training also diminished cardiovascular dysfunction in diabetic rats during endotoxemia. These data suggest that exercise may increase the expression of HSP72 in the heart and NTS to protect against the high mortality rate and attenuate cardiovascular dysfunction in diabetic rats during endotoxemia.

Mo1860 - High Fecal and Serum Tumor Necrosis Factor-α Levels are Associated with Non-Response to Infliximab in Patients with Ulcerative Colitis

2018 ◽  
Vol 154 (6) ◽  
pp. S-829
Author(s):  
Hadar Meringer-Milwidsky ◽  
Nitsan Maharshak ◽  
Yulia Ron ◽  
Henit A. Yanai ◽  
Sarit Cohen-Kedar ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis

scholarly journals Tumor Necrosis Factor-α-Induced Protein 8-Like 2 Negatively Regulates Innate Immunity Against RNA Virus by Targeting RIG-I in Macrophages

2021 ◽  
Vol 12 ◽  
Author(s):  
Ziqi Zou ◽  
Mengyao Li ◽  
Yunlian Zhou ◽  
Jiaying Li ◽  
Ting Pan ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Retinoic Acid ◽  
Viral Infection ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Rna Virus ◽  
Type I ◽  
Factor Α ◽  
Necrosis Factor ◽  
Inducible Gene

A systematic and flexible immunoregulatory network is required to ensure the proper outcome of antiviral immune signaling and maintain homeostasis during viral infection. Tumor necrosis factor-α-induced protein 8-like 2 (TIPE2), a novel immunoregulatory protein, has been extensively studied in inflammatory response, apoptosis, and cancer. However, the function of TIPE2 in antiviral innate immunity is poorly clarified. In this study, we reported that the expression of TIPE2 declined at the early period and then climbed up in macrophages under RNA virus stimulation. Knockout of TIPE2 in the macrophages enhanced the antiviral capacity and facilitated type I interferon (IFN) signaling after RNA viral infection both in vitro and in vivo. Consistently, overexpression of TIPE2 inhibited the production of type I IFNs and pro-inflammatory cytokines, and thus promoted the viral infection. Moreover, TIPE2 restrained the activation of TBK1 and IRF3 in the retinoic acid inducible gene-I (RIG-I)-like receptors (RLR) signaling pathway by directly interacting with retinoic acid inducible gene-I (RIG-I). Taken together, our results suggested that TIPE2 suppresses the type I IFN response induced by RNA virus by targeting RIG-I and blocking the activation of downstream signaling. These findings will provide new insights to reveal the immunological function of TIPE2 and may help to develop new strategies for the clinical treatment of RNA viral infections.

scholarly journals Cannabinoid Reduces Inflammatory Cytokines, Tumor Necrosis Factor-α, and Type I Interferons in Dermatomyositis In Vitro

2017 ◽  
Vol 137 (11) ◽  
pp. 2445-2447 ◽  
Author(s):  
Elizabeth S. Robinson ◽  
Paul Alves ◽  
Muhammad M. Bashir ◽  
Majid Zeidi ◽  
Rui Feng ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Cytokines ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Type I Interferons ◽  
Type I ◽  
Factor Α ◽  
Necrosis Factor

Study of serum tumor necrosis factor-α in patients with liver cirrhosis

2015 ◽  
Vol 28 (2) ◽  
pp. 525
Author(s):  
AhmedSalah Abdel-Aziz ◽  
HanySaied Sabry ◽  
AmiraAbdel-Kader El-Hendy ◽  
HosamIbrahim Mohammed ◽  
AbdallahSaid Essa
Keyword(s):  
Liver Cirrhosis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis

scholarly journals PSIX-9 Dietary β-sitosterol improves immunity and antioxidant status in broilers

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 346-346
Author(s):  
Yefei Cheng ◽  
Yueping Chen ◽  
Chao Wen ◽  
Yanmin Zhou
Keyword(s):  
Superoxide Dismutase ◽  
Tumor Necrosis Factor ◽  
Immunoglobulin G ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Hepatic Glutathione ◽  
Factor Α ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis

Abstract The application effects of phytosterols on poultry production have been reported. However, due to the mixed compositions, it is difficult to explain their action mode and physiological functions. β-sitosterol, the most abundant phytosterol, is naturally widespread in plant products. Information, however, is scarce in terms of effects of β-sitosterol on broilers. This research therefore investigated effects of dietary β-sitosterol with different levels on immunity and antioxidant capacity in broilers. Two hundred and forty one-day-old chicks were randomly allocated into five treatments of six replicates. Chickens in the five groups were fed a basal diet supplemented with 0 (control group), 40, 60, 80, and 100 mg/kg β-sitesterol for 42 days, respectively. Data were analyzed by one-way analysis of variance. Polynomial contrasts were used to test the linear and quadratic response to β-sitosterol levels. Difference among groups was evaluated using Tukey’s test, which was considered significant if P < 0.05. Dietary β-sitosterol linearly increased (P < 0.05) contents of serum immunoglobulin G and hepatic glutathione, activities of serum superoxide dismutase and catalase, whereas linearly decreased (P < 0.05) concentrations of serum tumor necrosis factor α and hepatic malondialdehyde. Serum interleukin 1β level was linearly and quadratically reduced by β-sitosterol inclusion (P < 0.05). Compared with the control group, dietary β-sitosterol with higher levels than 60 mg/kg increased concentrations of serum immunoglobulin G and hepatic glutathione, activities of serum superoxide dismutase and catalase (P < 0.05), whereas decreased serum tumor necrosis factor α content (P < 0.05). Its dosages higher than 40 mg/kg reduced serum interleukin 1β content (P < 0.05), and 100 mg/kg of which lowered hepatic malondialdehyde concentration (P < 0.05). The results indicated that dietary β-sitosterol could improve immunity and antioxidant ability in broilers. Also, a level of 80 mg/kg β-sitosterol supplementation was recommended into broiler diet.

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