Leukocyte apoptosis, TNF-α concentration and oxidative damage in lead-exposed workers

Ischemia–reperfusion is defined as cellular damage after the reperfusion of ischemic tissue, and it is likely to occur in relation to various diseases and surgical procedures. The purpose of this study was to evaluate the capability of atorvastatin to prevent oxidative damage and modulate the release of proinflammatory cytokines in rat hindlimb during ischemia–reperfusion injury. The animals were divided into 4 groups (ischemia–reperfusion + vehicle, ischemia–reperfusion + atorvastatin, sham, and healthy controls) with 15 rats per group. The animals were exposed to ischemia for 6 h, followed by 24 h, 7 days, and 14 days of reperfusion. Atorvastatin was administered by gavage 14 days before ischemia–reperfusion induction. We then measured the serum concentrations and mRNA transcript levels of TNF-α, IL-1β, IL-6, IL-10, SOD2, and CAT. Hematoxylin and eosin stain were performed for histological analyses. Animals subjected to ischemia–reperfusion showed increased serum and transcript levels of TNF-α, IL-1β, IL-6, and IL-10 expressions with a concurrent increase in mRNA transcripts levels compared with sham and healthy controls. Groups treated with atorvastatin showed a significant CAT increase in the first 24 h, but CAT levels decreased at 7 and 14 days. SOD2 enzyme increased in serum without significant changes in mRNA expression. Histological analysis showed inflammatory infiltrate, microhemorrhages, and distortion of the tissue architecture in the first 7 days. At 14 days, the tissue showed loss and damage to myocytes. However, animals treated with atorvastatin showed few histological changes and a decrease in inflammatory cytokines. No significant changes in NO2, NO3, or 8-OHdG were observed. Atorvastatin showed a protective effect on the inflammation and tissue damage induced by ischemia–reperfusion in the hindlimb. The antioxidant effect of atorvastatin in the hindlimb is already unclear, and further research is needed to elucidate the molecular mechanism of this drug in the extremities.

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Does rosmarinic acid treatment have protective role against sepsis-induced oxidative damage in Wistar Albino rats?

Human & Experimental Toxicology ◽

10.1177/0960327115607971 ◽

2016 ◽

Vol 35 (8) ◽

pp. 877-886 ◽

Cited By ~ 21

Author(s):

M Bacanlı ◽

S Aydın ◽

G Taner ◽

HG Göktaş ◽

T Şahin ◽

...

Keyword(s):

Dna Damage ◽

Oxidative Damage ◽

Rosmarinic Acid ◽

Biological Activities ◽

Albino Rats ◽

Repair Capacity ◽

Tnf Α ◽

Liver And Kidney ◽

Wistar Albino Rats ◽

Α Level

Reactive oxygen species are believed to be involved in the development of sepsis. Plant-derived phenolic compounds are thought to be possible therapeutic agents against sepsis because of their antioxidant properties. Rosmarinic acid (RA) is a phenolic compound commonly found in various plants, which has many biological activities including antioxidant activity. The aim of this study was to investigate the effects of RA on sepsis-induced DNA damage in the lymphocytes and liver and kidney cells of Wistar albino rats by alkaline comet assay with and without formamidopyrimidine DNA glycosylase protein. The oxidative stress parameters such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and total glutathione (GSH) and malondialdehyde (MDA) levels in the liver and kidney tissues and an inflammatory cytokine, tumor necrosis factor α (TNF-α) level in plasma were also evaluated. It is found that DNA damage in the lymphocytes, livers, and kidneys of the RA-treated rats was significantly lower than that in the sepsis-induced rats. RA treatment also decreased the MDA levels and increased the GSH levels and SOD and GSH-Px activities in the livers and kidneys of the sepsis-induced rats. Plasma TNF-α level was found to be decreased in the RA-treated rats. It seems that RA might have a role in the attenuation of sepsis-induced oxidative damage not only by decreasing the DNA damage but also by increasing the antioxidant status and DNA repair capacity of the animals.

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Dietary quercetin ameliorates TPT-induced hepatic oxidative damage and apoptosis in zebrafish

10.21203/rs.3.rs-339016/v1 ◽

2021 ◽

Author(s):

Chunnuan Zhang ◽

Yuheng Wang ◽

Hongtao Ren ◽

Junhui Wang ◽

Dongxue Jiang ◽

...

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Basal Diet ◽

Control Group ◽

Antioxidant Enzyme Activities ◽

Mrna Levels ◽

Gene Expressions ◽

Apoptotic Gene ◽

Tnf Α ◽

Quercetin Treatment

Abstract The objective of this study was to determine the effects of quercetin on oxidative stress and apoptosis induced by TPT in zebrafish. 240 fish were divided into 4 groups with three repeats. D1: fish fed with the basal diet as the control group. D2: fish fed with basal diet and exposed in 10 ng/L TPT. D3: fish fed diets containing 100 mg/Kg quercetin and exposed in 10ng/L TPT. D4: fish fed diets containing 100 mg/Kg quercetin. The results showed that quercetin could ameliorate oxidative stress, which decreased MDA, NO levels and improved antioxidant enzyme activities. The key apoptotic gene expressions, including caspase3, Bax and caspase9 mRNA expression were significantly induced by TPT exposure as compared with the control group, while notably decreased the Bcl-2 gene. However, dietary quercetin prevented a significant increase in Bax, caspase3 and caspase9 mRNA levels induced by TPT exposure, but increased Bcl-2 mRNA levels. The results of our study also demonstrated that 10 ng/L TPT significantly up-regulated TNF-α, IL-1β, IL-8, and NF-kB p65 gene expression and down-regulated IL-10 and IkB expression compared to the control group. However, TPT-induced inflammation was significantly mitigated in the quercetin treatment group. In conclusion, our findings suggested that quercetin might alleviate hepatic oxidative damage and apoptosis induced by TPT.

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Antioxidant and Inflammatory Effects of Nelumbo nucifera Gaertn. Leaves

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/8375961 ◽

2021 ◽

Vol 2021 ◽

pp. 1-14

Author(s):

Chong Li ◽

Yongpeng He ◽

Yue Yang ◽

Yuting Gou ◽

Shuting Li ◽

...

Keyword(s):

Oxidative Damage ◽

Animal Studies ◽

Organ Index ◽

Tnf Α ◽

Ifn Γ ◽

Anti Inflammatory ◽

Kidney Liver ◽

Lung And Kidney

This study is aimed at identifying the bioactive components in lotus leaf flavonoid extract (LLFE) and analyzing the antioxidant and anti-inflammatory activities of LLFE in vitro and in vivo. The flavonoids in LLFE were determined by UHPLC-MS/MS. The effect of LLFE on damaged 293T cells (H2O2, 0.3 mmol/L) was determined by MTT assay, and the activity of antioxidant enzymes was measured by kits. We studied the antioxidant and anti-inflammatory effects of LLFE on D-Gal/LPS (30 mg/kg·bw and 3 μg/kg·bw)-induced aging mice. We also evaluated the main organ index, pathological changes in the liver, lung, and kidney, liver function index, biochemical index, cytokine level, and mRNA expression level in serum and liver. The results showed that LLFE contains baicalein, kaempferol, kaempferid, quercetin, isorhamnetin, hyperoside, lespenephryl, and rutin. LLFE reduced the oxidative damage sustained by 293T cells, increased the levels of SOD, CAT, GSH, and GSH-Px, and decreased the level of MDA. The animal studies revealed that LLFE reduced oxidative damage and inflammation in injured mice, inhibited increases in AST, ALT, MDA, and NO, increased SOD, CAT, GSH, and GSH-Px levels, upregulated anti-inflammatory cytokines IL-10 and IL-12, and downregulated proinflammatory cytokines IL-6, IL-1β, TNF-α, and IFN-γ. Furthermore, the expression of antioxidant- and anti-inflammatory-related mRNA was consistent with the above results.

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Life Quality and Cytokines Profile in Patients with Asthma and Osteoarthritis

International Journal of Biomedicine ◽

10.21103/article11(2)_oa2 ◽

2021 ◽

Vol 11 (2) ◽

pp. 137-140

Author(s):

Yuliya Ivanchuk ◽

Ludmila Tribuntceva ◽

Andrey Budnevsky ◽

Yanina Shkatova ◽

Evgeniy Ovsyannikov ◽

...

Keyword(s):

Quality Of Life ◽

Oxidative Damage ◽

Asthma Control ◽

Antioxidant Status ◽

Life Questionnaire ◽

Asthma Control Test ◽

Tnf Α ◽

Group 2 ◽

Group 1

The objective of this study was to evaluate levels of leptin, adiponectin, IL-4, IL-6, TNF-α, oxidative damage, and antioxidant status in patients with bronchial asthma (BA), compared to patients who suffer from both BA and osteoarthritis (OA), and analyze the quality of life in such patients. Methods and Results: The study included 103 patients (34 men and 69 women) diagnosed with moderate asthma aged from 30 to 70 years (mean age of 58.52±7.14 years). The levels of IL-4, IL-6, TNF-α, adiponectin, leptin, total antioxidant status (TAS), and total oxidative damage (TOD) were measured. Two questionnaires were used in this study: Asthma Quality of Life Questionnaire (AQLQ) and Asthma Control Test (АСТ). The levels of leptin, TNF-α, and Il-6 were significantly higher in Group 2 than in Group 1. On the contrary, the IL-4 level was higher in Group 1 than in Group 2. The TAS value was significantly higher in Group 1 than in Group 2 (P=0.0001). The TOD value was significantly higher in Group 2 than in Group 1 (P=0.0000). The domains of AQLQ(S) activity, symptoms, and emotions were decreased in patients of Group 2. The values of the ACT test were 18.0±2.61 points and 16.78±1.92 points in Group 1 and Group 2, respectively (P=0.0077). Conclusion: In patients with both asthma and osteoarthritis, levels of inflammatory cytokines, such as leptin, IL-6, and TNF-α, are significantly elevated as well as values of total oxidative status, which correlate with poorer asthma control and quality of life.

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Neuroprotective effect of hydroxy safflor yellow A against cerebral ischemia-reperfusion injury in rats: putative role of mPTP

Journal of Basic and Clinical Physiology and Pharmacology ◽

10.1515/jbcpp-2015-0021 ◽

2016 ◽

Vol 27 (1) ◽

pp. 1-8 ◽

Cited By ~ 14

Author(s):

Sruthi Ramagiri ◽

Rajeev Taliyan

Keyword(s):

Oxidative Damage ◽

Protective Effect ◽

Mitochondrial Permeability Transition ◽

Ischemia Reperfusion Injury ◽

Neuroprotective Effect ◽

Ischemia Reperfusion ◽

Radical Scavenger ◽

Neuroprotective Effects ◽

Y Maze ◽

Tnf Α

AbstractHydroxy safflor yellow A (HSYA) has been translated clinically for cardiovascular diseases. HSYA is also greatly acknowledged for its protective effects against cerebral ischemic-reperfusion (I/R) injury. Although the precise mechanism of cerebral I/R injury is not fully understood, oxygen-derived free radicals and mitochondrial permeability transition pore (mPTP) opening during I/R injury are widely recognized as an important contributor to neuronal injury. Thus, we speculated that the neuroprotective effects of HSYA against cerebral I/R injury may be associated with mPTP modulation.Induction of I/R injury was achieved by 60 min of middle cerebral artery occlusion, followed by reperfusion for 24 h. For behavior and cognitive assessment, neurological scoring (NSS), rotarod, and Y-maze task were performed. Oxidative damage was measured in terms of markers such as malondialdehyde, reduced glutathione, and catalase levels and cerebral infarct volumes were quantified using 2,3,5-triphenyl tetrazolinium chloride staining. I/R injury-induced inflammation was determined using tumor necrosis factor-α (TNF-α) levels.Animals exposed to I/R injury showed neurological severity, functional and cognitive disability, elevated oxidative markers, and TNF-α levels along with large infarct volumes. HSYA treatment during onset of reperfusion ameliorated performance in NSS, rotarod and Y-maze attenuated oxidative damage, TNF-α levels, and infarction rate. However, treatment with carboxyatractyloside, an mPTP opener, 20 min before HSYA, attenuated the protective effect of HSYA.Our study confirmed that protective effect of HSYA may be conferred through its free radical scavenger action followed by inhibiting the opening of mPTP during reperfusion and HSYA might act as a promising therapeutic agent against cerebral I/R injury.

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Eccentric contraction induces inflammatory responses in rat skeletal muscle: role of tumor necrosis factor-α

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00480.2009 ◽

2010 ◽

Vol 298 (3) ◽

pp. R599-R607 ◽

Cited By ~ 58

Author(s):

Peng Liao ◽

Jinping Zhou ◽

Li Li Ji ◽

Yong Zhang

Keyword(s):

Skeletal Muscle ◽

Oxidative Damage ◽

Time Course ◽

Inflammatory Responses ◽

Vastus Lateralis ◽

Reactive Oxygen Species Generation ◽

Eccentric Contraction ◽

Exercise Group ◽

Nuclear Accumulation ◽

Tnf Α

Eccentric contraction (EC) is known to elicit inflammation and damage in skeletal muscle. Proinflammatory cytokine TNF-α plays an important role in this pathogenesis, but the time course of its response to EC and the regulatory mechanisms involved are not clear. The purpose of the study is twofold: 1) to investigate the gene expression of TNF-α in rat muscle during and after an acute bout of downhill running and the associated oxidoreductive (redox) changes; and 2) to examine whether EC activates muscle ubiquitin-proteolytic pathway resulting in necrosis and oxidative damage. Female Sprague-Dawley rats (age 3 mo) were randomly divided into five groups ( n = 6) that ran on treadmill at 25 m/min at −10% grade for 1 h ( group 1) or 2 h ( group 2) and were killed immediately; ran for 2 h and killed at 6 h after exercise ( group 3), ran for 2 h and killed at 24 h after exercise ( group 4); and killed at rest as controls ( group 5). TNF-α mRNA and protein content showed progressive increases in the deep portion of vastus lateralis (DVL) and gastrocnemius muscles during and after EC. These changes were accompanied by a progressive decrease of mitochondrial aconitase activity and NF-κB activation. After 2 h of exercise, elevated levels of serum TNF-α, endotoxin, creatine kinase, and lipid peroxidation marker were evident and persisted through 24 h postexercise. At 24 h, there were marked increases in H2O2 concentration, myleoperoxidase activity, and endotoxin level, along with nuclear accumulation of p65, in both muscles. mRNA level of ubiquitin-conjugating enzymes (E2)-14k was progressively upregulated during exercise and recovery, whereas the expression of the Toll-like receptor 4 (TLR4) in DVL was downregulated in both muscles. We conclude that prolonged EC induces TNF-α expression possibly due to NF-κB activation stimulated by increased reactive oxygen species generation and endotoxin release. These inflammatory and prooxidative responses may underlie the processes of muscle proteolysis and oxidative damage.

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