scholarly journals Sparassis crispa Intake Improves the Reduced Lipopolysaccharide-Induced TNF-α Production That Occurs upon Exhaustive Exercise in Mice

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2049 ◽  
Author(s):  
Masataka Uchida ◽  
Naoki Horii ◽  
Natsuki Hasegawa ◽  
Eri Oyanagi ◽  
Hiromi Yano ◽  
...  
Keyword(s):  
Small Intestine ◽  
Edible Mushroom ◽  
Treadmill Running ◽  
Exhaustive Exercise ◽  
Tnf Α ◽  
Normal Chow ◽  
Sparassis Crispa ◽  
Exercise Induced ◽  
Α Level ◽  
Myd88 Protein

Our previous study showed that lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-α production is inhibited by acute exhaustive exercise in mice, leading to transient immunodepression after exercise. Sparassis crispa (SC), an edible mushroom, has immunopotentiative properties. This study aimed to clarify the effects of SC intake on reduced LPS-induced TNF-α production upon exhaustive exercise in mice. Male C3H/HeN mice were randomly divided into three groups: normal chow intake + resting sedentary, normal chow intake + acute exhaustive treadmill running exercise, and SC intake (chow containing 5% SC powder for 8 weeks) + the exhaustive exercise groups. Each group was injected with LPS immediately after the exhaustive exercise or rest. Plasma and tissue TNF-α levels were significantly decreased by exhaustive exercise. However, this reduction of the TNF-α level was partially attenuated in the plasma and small intestine by SC intake. Although levels of TLR4 and MyD88 protein expression were significantly decreased in tissues by exhaustive exercise, the reduction of TLR4 and MyD88 levels in the small intestine was partially attenuated by SC intake. These results suggest that SC intake attenuates exhaustive exercise-induced reduction of TNF-α production via the retention of TLR4 and MyD88 expression in the small intestine.

Exercise-induced oxidative stress affects erythrocytes in sedentary rats but not exercise-trained rats

2001 ◽  
Vol 91 (5) ◽  
pp. 1999-2004 ◽  
Author(s):  
Ümit Kemal Şentürk ◽  
Filiz Gündüz ◽  
Oktay Kuru ◽  
Mehmet R. Aktekin ◽  
Dijle Kipmen ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Oxidant Stress ◽  
Osmotic Fragility ◽  
Treadmill Running ◽  
Exhaustive Exercise ◽  
Antioxidant Vitamin ◽  
Structural Alterations ◽  
Plasma Hemoglobin ◽  
Exercise Induced ◽  
Erythrocyte Lipid

Oxidant stress is one of the factors proposed to be responsible for damaged erythrocytes observed during and after exercise. The impact of exertional oxidant stress after acute exhaustive treadmill running on erythrocyte damage was investigated in sedentary (Sed) and exercise-trained (ET) rats treated with or without antioxidant vitamins C and E. Exhaustive exercise led to statistically significant increments in the levels of thiobarbituric acid-reactive substance (TBARS) and H2O2-induced TBARS in Sed rats and resulted in functional and structural alterations in erythrocytes (plasma hemoglobin concentrations, methemoglobin levels, and rise in osmotic fragility of erythrocytes with decrease in erythrocyte deformability). Administration of antioxidant vitamin for 1 mo before exhaustive exercises prevented lipid peroxidation (TBARS, H2O2-induced TBARS) in Sed rats without any functional or structural alterations in erythrocytes. Parameters indicating erythrocyte lipid peroxidation and deterioration after exhaustive exercise in rats trained regularly with treadmill running for 1 mo were not different from those in Sed controls. Erythrocyte lipid peroxidation (TBARS) increased in exhausted-ET rats compared with ET controls; however, the plasma hemoglobin, methemoglobin levels, and erythrocyte osmotic fragility and deformability did not differ. Exhaustive exercise-induced lipid peroxidation in ET rats on antioxidant vitamin treatment was prevented, whereas functional and structural parameters of erythrocytes were not different from those of the ET controls. We conclude that exertional oxidant stress contributed to erythrocyte deterioration due to exercise in Sed but not in ET rats.

Superoxide dismutase derivative reduces oxidative damage in skeletal muscle of rats during exhaustive exercise

1995 ◽  
Vol 79 (1) ◽  
pp. 129-135 ◽  
Author(s):  
Z. Radak ◽  
K. Asano ◽  
M. Inoue ◽  
T. Kizaki ◽  
S. Oh-Ishi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Superoxide Dismutase ◽  
Xanthine Oxidase ◽  
Thiobarbituric Acid ◽  
Experimental Period ◽  
Treadmill Running ◽  
Exhaustive Exercise ◽  
Thiobarbituric Acid Reactive Substances ◽  
Exercise Induced

A superoxide dismutase derivative (SM-SOD) that circulates and is bound to albumin with a half-life of 6 h was injected intraperitoneally into rats before exhaustive treadmill running to study its antioxidant scavenging capacity in the plasma and soleus and tibialis muscles. The exercise induced a marked increase in xanthine oxidase activity in plasma and an increase in thiobarbituric acid-reactive substances in the plasma as well as in the soleus and tibialis muscles of nonadministered rats immediately after the exercise. The immunoreactive content and activity of both SOD isoenzymes (Cu,Zn-SOD and Mn-SOD) of the nonadministered rats increased in the soleus and tibialis muscles immediately after running. SM-SOD treatment definitely attenuated the degree of the increase in thiobarbituric acid-reactive substances and xanthine oxidase in all samples examined immediately after exercise. Glutathione peroxidase activity significantly increased in the soleus muscle of nonadministered rats 1 day after running, whereas catalase activity remained unchanged throughout the experimental period. These results suggest that a single bout of exhaustive exercise induces oxidative stress in skeletal muscle of rats and that this oxidative stress can be attenuated by exogenous SM-SOD.

scholarly journals The Effect of High-Fat Diet and Exercise Intervention on the TNF-α Level in Rat Spleen

2021 ◽  
Vol 12 ◽  
Author(s):  
Lin Feng ◽  
Yinan Ma
Keyword(s):  
Chronic Inflammation ◽  
High Fat Diet ◽  
Exercise Intervention ◽  
Total Cell ◽  
Treadmill Running ◽  
High Fat ◽  
Cell Numbers ◽  
Abnormal Expression ◽  
Tnf Α ◽  
Α Level

High-fat diet (HFD) consumption can trigger chronic inflammation in some tissues. However, it remains unclear if HFD induces chronic inflammation in the spleen. This investigation aims to address the effect of HFD consumption and exercise intervention on the level of tumor necrosis factor alpha (TNF-α) in the spleen. Rats were subjected to HFD feeding and/or moderate-intensity treadmill running. The TNF-α levels in plasma and spleen were detected by ELISA. The mass and total cell numbers of the spleen were measured. In addition, the expression of TNF-α and its relevant gene mRNAs in macrophages from the spleen were analyzed by qRT-PCR. We found that HFD consumption did not significantly affect the mass and total cell numbers of the spleen. However, HFD consumption significantly increased splenic TNF-α level, the expression of TNF-α, toll-like receptor 4, and nuclear factor κB p65 mRNAs. In contrast, the expression of nicotinic acetylcholine receptor alpha 7 subunit (α7nAChR) mRNA in macrophages was downregulated. Additionally, exercise abolished the increase in splenic TNF-α level as well as the abnormal expression of TNF-α and related gene mRNAs in macrophages in HFD-fed rats. In conclusion, our results reveal that HFD consumption increases TNF-α level in the spleen, which is along with upregulation of the expression of TLR4 and NF-κB mRNAs as well as downregulation of the expression of α7nAChR mRNA in splenic macrophages in rats. Exercise abolished detrimental effects of HFD on TNF-α level in the spleen and prevented abnormal expression of these genes in the macrophages from rat spleen.

Eccentric Overload Muscle Damage is Attenuated By a Novel Angiotensin- (1-7) Treatment

2018 ◽  
Vol 39 (10) ◽  
pp. 743-748 ◽  
Author(s):  
Lenice Becker ◽  
Nádia Totou ◽  
Samara Moura ◽  
Lucas Kangussu ◽  
Ruben Millán ◽  
...  
Keyword(s):  
Muscle Damage ◽  
Oral Formulation ◽  
Treated Group ◽  
Post Exercise ◽  
Tnf Α ◽  
Exercise Induced ◽  
Α Level ◽  
Eccentric Overload ◽  
Muscle Damage Markers ◽  
New Strategies

AbstractThe development of new strategies to attenuate exercise-induced muscle damage may be helpful for training regimens. The aim of this study was to determine whether a oral formulation of angiotensin Ang-(1-7)[HPβCD/Ang-(1-7)] is effective to reduce pain, and muscle damage markers after eccentric-overload exercise. HPβCD (Placebo) and HPβCD/Ang-(1-7) (Ang-(1-7) group were treated for 7 days (one capsule/day). The pain was measured by visual analogue scale, maximal strength (MS) using force platform. Blood samples were collected for cytokines and creatine kinase (CK) analysis. The Ang-(1-7)-treated group reported less pain immediately (3.46±0.64 vs. placebo 3.80±0.77 cm) and 24 h after exercise (3.07±0.71 vs. 3.73±0.58 cm placebo) and higher MS at 24 h (24±12 N) and 48 h (30±15 N) vs. placebo (-8±9 N and -10±9 N). The CK for Ang-(1-7) (0.5±0.1 and 0.9±0.2 U/L) were lower at 48 and 72 h vs. placebo (fold changes of 1.7±0.5 and 1.5±0.3 U/L). The TNF-α level was lower in the treated group post-exercise (38±2.5 pg/ml) vs. placebo (45±2.9 pg/ml) but no significant changes were observed for IL-6 and IL-10. Our data indicate that treatment with Ang-(1-7) may attenuate pain, some of the muscle damage markers and improves performance following eccentric exercise.

scholarly journals The Protect Effects of Chitosan Oligosaccharides on Intestinal Integrity by Regulating Oxidative Status and Inflammation under Oxidative Stress

Marine Drugs ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 57
Author(s):  
Ruixia Lan ◽  
Qingqing Chang ◽  
Linlin Wei ◽  
Zhihui Zhao
Keyword(s):  
Oxidative Stress ◽  
Drinking Water ◽  
Small Intestine ◽  
Mrna Expression ◽  
Basal Diet ◽  
Oxidative Status ◽  
Intestinal Integrity ◽  
Chitosan Oligosaccharides ◽  
Tnf Α ◽  
Α Level

The aim of this study was to evaluate the effects of the dietary supplementation of chitosan oligosaccharides (COS) on intestinal integrity, oxidative status, and the inflammation response with hydrogen peroxide (H2O2) challenge. In total, 30 rats were randomly assigned to three groups with 10 replications: CON group, basal diet; AS group, basal diet + 0.1% H2O2 in drinking water; ASC group, basal diet + 200 mg/kg COS + 0.1% H2O2 in drinking water. The results indicated that COS upregulated (p < 0.05) villus height (VH) of the small intestine, duodenum, and ileum; mucosal glutathione peroxidase activity; jejunum and ileum mucosal total antioxidant capacity; duodenum and ileum mucosal interleukin (IL)-6 level; jejunum mucosal tumor necrosis factor (TNF)-α level; duodenum and ileum mucosal IL-10 level; the mRNA expression level of zonula occludens (ZO)-1 in the jejunum and ileum, claudin in the duodenum, nuclear factor-erythroid 2-like 2 in the jejunum, and heme oxygenase-1 in the duodenum and ileum; and the protein expression of ZO-1 and claudin in jejunum; however, it downregulated (p < 0.05) serum diamine oxidase activity and D-lactate level; small intestine mucosal malondialdehyde content; duodenum and ileum mucosal IL-6 level; jejunum mucosal TNF-α level; and the mRNA expression of IL-6 in the duodenum and jejunum, and TNF-α in the jejunum and ileum. These results suggested COS could maintain intestinal integrity under oxidative stress by modulating the intestinal oxidative status and release of inflammatory cytokines.

The TNF-α level variation in the aqueous humour of the anterior chamber inindividuals with cataract

2020 ◽  
pp. 86-87
Author(s):  
V.S. Shevchenko ◽  
◽  
A.S. Prilutskii ◽  
K.Y. Tkachenko ◽  
◽  
...  
Keyword(s):  
Anterior Chamber ◽  
Aqueous Humour ◽  
Level Variation ◽  
Tnf Α ◽  
Α Level

Актуальность. Фактор некроза опухоли(TNF-α) является провоспалительным цитокином, продуцирующимся макрофагами и многими другими клетками. Данные о вариации концентрацииTNF-α во влаге передней камеры глаза у лиц, не имеющих выраженных воспалительных и аутоиммунных процессов практически единичны. Цель. Исследование диапазона вариации фактора некроза опухоли альфа во влаге передней камеры глаза у пациентов с возрастной катарактой. Материал и методы. Отобраны и обследованы 33 пациента, в возрасте от 47 до 82 лет, госпитализированных для плановой экстракции катаракты не имеющих выраженных сопутствующих воспалительных заболеваний (аутоиммунных, острых инфекционных болезней, обострением хронических заболеваний, глаукомы, перенесенного увеита и др.). Влага передней камеры забиралась при вскрытии передней камеры глаза во время факоэмульсификации катаракты. Исследование TNF-αпроводилось с помощью иммуноферментны хтест-систем, разработанных при участии сотрудников кафедры клинической иммунологии, аллергологии и эндокринологии ГОО ВПО «ДонНМУ им.М. Горького». Вышеуказанные тест-системы характеризует высокая чувствительность (0,5 пикограмм в миллилитре) и хорошая воспроизводимость. Результаты. При исследовании уровня TNF-αво влаге передней камеры глаза у пациентов с возрастной катарактой, мы выявили колебания данного показателя от 0 до 2,49 пкг/мл. Следует отметить, что полученные нами результаты показывают небольшую вариацию (в пределах низких значений) данного провоспалительного цитокина в исследованной жидкости у пациентов в возрасте от 47 до80 лет, не имеющих выраженной воспалительной(аутоиммунной и др.) патологии. Выводы. Показана низкая вариация TNF-α во влаге передней камеры глаза у пациентов с возрастной катарактой (у обследуемых исключена сопутствующая выраженная воспалительная патология). Результаты можно также использовать как контрольные при проведении сравнительныхисследований этого цитокина в данной среде у лицс различными заболеваниями глаза.

TNF-α Suppresses Autophagic Flux in Acinar Cells in IgG4-Related Sialadenitis

2019 ◽  
Vol 98 (12) ◽  
pp. 1386-1396 ◽  
Author(s):  
X. Hong ◽  
S.N. Min ◽  
Y.Y. Zhang ◽  
Y.T. Lin ◽  
F. Wang ◽  
...  
Keyword(s):  
Acinar Cell ◽  
Cell Injury ◽  
Ex Vivo ◽  
Secretory Granules ◽  
Acinar Cells ◽  
Autophagic Flux ◽  
C6 Cells ◽  
Tnf Α ◽  
Α Level

IgG4-related sialadenitis (IgG4-RS) is a newly recognized immune-mediated systemic fibroinflammatory disease that affects salivary glands and leads to hyposalivation. Tumor necrosis factor–α (TNF-α) is a critical proinflammatory cytokine involved in several salivary gland disorders, but its role and mechanism regarding acinar cell injury in IgG4-RS are unknown. Here, we found that TNF-α level was significantly increased in serum and submandibular gland (SMG) of patients and that serum TNF-α level was negatively correlated with saliva flow rate. Ultrastructural observations of IgG4-RS SMGs revealed accumulation of large autophagic vacuoles, as well as dense fibrous bundles, decreased secretory granules, widened intercellular spaces, swollen mitochondria, and expanded endoplasmic reticulum. Expression levels of LC3 and p62 were both increased in patients’ SMGs. TNF-α treatment led to elevated levels of LC3II and p62 in both SMG-C6 cells and cultured human SMG tissues but did not further increase their levels when combined with bafilomycin A1 treatment. Moreover, transfection of Ad-mCherry-GFP-LC3B in SMG-C6 cells confirmed the suppression of autophagic flux after TNF-α treatment. Immunofluorescence imaging revealed that costaining of LC3 and the lysosomal marker LAMP2 was significantly decreased in patients, TNF-α–treated SMG-C6 cells, and cultured human SMGs, indicating a reduction in autophagosome-lysosome fusion. Furthermore, the ratio of pro/mature cathepsin D was elevated in vivo, ex vivo, and in vitro. TNF-α also appeared to induce abnormal acidification of lysosomes in acinar cells, as assessed by lysosomal pH and LysoTracker DND-26 fluorescence intensity. In addition, TNF-α treatment induced transcription factor EB (TFEB) redistribution in SMG-C6 cells, which was consistent with the changes observed in IgG4-RS patients. TNF-α increased the phosphorylation of extracellular signal–regulated kinase (ERK) 1/2, and inhibition of ERK1/2 by U0126 reversed TNF-α–induced TFEB redistribution, lysosomal dysfunction, and autophagic flux suppression. These findings suggest that TNF-α is a key cytokine related to acinar cell injury in IgG4-RS through ERK1/2-mediated autophagic flux suppression.

scholarly journals High Levels of TNF-α and TIM-3 as a Biomarker of Immune Reconstitution Inflammatory Syndrome in People with HIV Infection

Life ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 527
Author(s):  
Lucero A. Ramon-Luing ◽  
Ranferi Ocaña-Guzman ◽  
Norma A. Téllez-Navarrete ◽  
Mario Preciado-García ◽  
Dámaris P. Romero-Rodríguez ◽  
...  
Keyword(s):  
Immune Reconstitution Inflammatory Syndrome ◽  
Immune Reconstitution ◽  
Control Group ◽  
Hiv Patients ◽  
Art Initiation ◽  
Tnf Α ◽  
Ifn Γ ◽  
Α Level ◽  
Inflammatory Syndrome

Immune reconstitution inflammatory syndrome (IRIS) is an exacerbated immune response that can occur to HIV+ patients after initiating antiretroviral therapy (ART). IRIS pathogenesis is unclear, but dysfunctional and exhausted cells have been reported in IRIS patients, and the TIM-3/Gal-9 axis has been associated with chronic phases of viral infection. This study aimed to evaluate the soluble levels of TIM-3 and Gal-9 and their relationship with IRIS development. TIM-3, Gal-9, TNF-α, IFN-γ, IL-6, TNFR1, TNFR2, E-cadherin, ADAM10, and ADAM17 were measured to search for IRIS-associated biomarkers in plasma samples from 0-, 4-, 8-, 12-, and 24-weeks after ART initiation of 61 HIV+ patients (15 patients developed IRIS, and 46 did not). We found that patients who developed IRIS had higher levels of TIM-3 [median 4806, IQR: 3206–6182] at the time of the IRIS events, compared to any other follow-up time evaluated in these patients or compared with a control group of patients who did not develop IRIS. Similarly, IRIS patients had a higher TNF-α level [median 10.89, IQR: 8.36–12.34] at IRIS events than any other follow-up time evaluated. Other molecules related to the TIM-3 and TNF-α pathway (Gal-9, IL-6, IFN-γ, TNFR1, TNFR2, ADAM-10, and ADAM-17) did not change during the IRIS events. In conclusion, our data suggest that a high level of soluble TIM-3 and TNF-α could be used as an IRIS biomarker.

scholarly journals Acute Low-Intensity Treadmill Running Upregulates the Expression of Intestinal Glucose Transporters via GLP-2 in Mice

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1735
Author(s):  
Kai Aoki ◽  
Takuji Suzuki ◽  
Fang Hui ◽  
Takuro Nakano ◽  
Koki Yanazawa ◽  
...  
Keyword(s):  
Small Intestine ◽  
Intestinal Tract ◽  
Glucose Transporter ◽  
Treadmill Running ◽  
Low Intensity ◽  
Glucose Transporter 2 ◽  
Intestinal Digestion ◽  
Glucagon Like Peptide ◽  
Low Intensity Exercise ◽  
Carbohydrate Digestion

The effects of exercise on nutrient digestion and absorption in the intestinal tract are not well understood. A few studies have reported that exercise training increases the expression of molecules involved in carbohydrate digestion and absorption. Exercise was also shown to increase the blood concentration of glucagon-like peptide-2 (GLP-2), which regulates carbohydrate digestion and absorption in the small intestine. Therefore, we investigated the effects of exercise on the expression of molecules involved in intestinal digestion and absorption, including GLP-2. Six-week-old male mice were divided into a sedentary (SED) and low-intensity exercise (LEx) group. LEx mice were required to run on a treadmill (12.5 m/min, 1 h), whereas SED mice rested. All mice were euthanized 1 h after exercise or rest, and plasma, jejunum, ileum, and colon samples were collected, followed by analysis via IHC, EIA, and immunoblotting. The levels of plasma GLP-2 and the jejunum expression of the GLP-2 receptor, sucrase-isomaltase (SI), and glucose transporter 2 (GLUT2) were higher in LEx mice. Thus, we showed that acute low-intensity exercise affects the expression of molecules involved in intestinal carbohydrate digestion and absorption via GLP-2. Our results suggest that exercise might be beneficial for small intestine function in individuals with intestinal frailty.

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