Upregulated-gene expression of pro-inflammatory cytokines, oxidative stress and apoptotic markers through inflammatory, oxidative and apoptosis mediated signaling pathways in bovine pneumonia

2021 ◽  
pp. 104935
Author(s):  
Aftab Shaukat ◽  
Sana Hanif ◽  
Irfan Shaukat ◽  
Rizwan Shukat ◽  
Shahid Ali Rajput ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Apoptotic Markers ◽  
Pro Inflammatory Cytokines

Putative biomarkers for early detection of mastitis in cattle

2020 ◽  
Vol 60 (14) ◽  
pp. 1721
Author(s):  
Zul I. Huma ◽  
Neelesh Sharma ◽  
Sarabpreet Kour ◽  
Suhasani Tandon ◽  
Praveen Kumar Guttula ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Mammary Gland ◽  
Inflammatory Cytokines ◽  
Experimental Validation ◽  
Bioinformatics Analysis ◽  
In Silico Analysis ◽  
Oxidative Biomarkers ◽  
Silico Analysis ◽  
Pro Inflammatory Cytokines

Context Mastitis is an inflammation of mammary gland parenchyma, and is an unending cause of economic loss to the dairy industry. The interest in research on biomarker discovery for the diagnosis of bovine mastitis stems largely from the need to identify reliable biomarkers. Aim To determine the putative biomarkers of mastitis by using bioinformatics analysis, and experimental validation of pro-inflammatory cytokines and oxidative stress biomarkers of the mammary gland in healthy and diseased animals. Methods Various in silico analysis tools were applied to screen for gene expression in mastitis. Milk, as well as blood samples, was collected aseptically from the animals, which were then classified into three groups; namely, clinical, subclinical and control. Samples were subjected to assay of pro-inflammatory cytokines and oxidative biomarkers using enzyme-linked immunosorbent assay kits and the prescribed methodology respectively. Key results In silico analysis revealed that mastitis reduces the expression of fat metabolism and immune system-related genes, whereas it increased the expression of inflammatory genes. On laboratory analysis of cytokines and acute phase protein, it was revealed that interleukin-1∝, interleukin-8 and haptoglobin were significantly (P < 0.01) increased in both blood serum and milk whey in subclinical and clinical mastitis cows. On analysis of oxidative biomarkers, our results showed that oxidative stress was significantly (P < 0.05) increased with progression of mastitis in dairy cows. There was a significant (P < 0.05) increase in the blood serum level of malondialdehyde and nitric oxide, and a decrease in the level of anti-oxidant enzymes – glutathione peroxidase, superoxide dismutase and catalase – compared with healthy animals. Conclusion In conclusion, bioinformatics analysis of high-throughput gene expression revealed the involvement of multiple pathways, including the inflammatory pathway, fatty acid pathway and triglyceride synthesis pathway, in mastitis. Experimental validation confirmed that interleukin-8 and haptoglobin are putative early diagnostic markers for mastitis in dairy cattle. This study also concluded that milk can be used for the detection of cytokines as a non-invasive technique.

scholarly journals Methanol Extract of Chasmanthera dependens Stem Mitigates against Mechanisms Involved in Piroxicam-induced Liver Damage in Rat

2020 ◽  
pp. 16-28
Author(s):  
Tijani Stephanie Abiola ◽  
Olori Ogaraya David ◽  
Farombi Ebenezer Olatunde
Keyword(s):  
Oxidative Stress ◽  
Liver Function ◽  
Oral Administration ◽  
Inflammatory Cytokines ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Dependent Manner ◽  
Apoptotic Markers ◽  
Glutamyl Transferase ◽  
Pro Inflammatory Cytokines

Chasmanthera dependens has been claimed by tradition healers as a therapeutic agent in many diseases including hepatotoxicity. This study sought to evaluate the possible mechanisms involved in the hepatoprotective potential of tannin-rich extract of Chasmanthera dependens stem (TRECDS). Thirty two male Wistar rats (100- 130 g) were divided into four groups of eight rats per group labelled as group 1,2,3  and 4. The rats were treated orally for ten days consecutively.  Group 1 served as control group and received normal saline, group 2 rats received 40 mg/kg piroxicam alone, groups 3-4 were treated with 40 mg/kg piroxicam and 200 and 400 mg/kg TREDS respectively concomitantly. All the experimental rats were fed with standard rat chows. Twenty four hours after, blood was collected to obtain serum; liver was excised to prepare homogenate and histology staining under pentobarbital sodium anaesthesia. Liver function test (aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT)) and oxidative stress (superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and lipid peroxidation (LPO)) biomarkers were assessed. Pro-inflammatory cytokines (tumor necrosis factor-α (TNF- α), interleukin-1β (IL-1β)) and apoptotic markers; caspase-3 (CASP-3) and caspase-9 (CAPS-9), cytochrome-c (CYT-c)) were also assessed. The results showed that piroxicam administration caused hepatic damage as was evident in the histological assessment with increased serum activities of liver function markers, levels of pro-inflammatory cytokines and apoptotic markers. TRECDS also showed significant attenuation of the oxidative stress by decreasing the LPO level and increasing the activities of SOD, CAT and GSH level. Oral administration of TRECDS also restores the morphological structure of the liver in a dose-dependent manner. Conclusion: Oral administration of TRECDS exhibited protective potential against piroxicam-induced hepatotoxicity.

scholarly journals Modulation of Bovine Endometrial Cell Receptors and Signaling Pathways as a Nanotherapeutic Exploration against Dairy Cow Postpartum Endometritis

Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1516
Author(s):  
Ayodele Olaolu Oladejo ◽  
Yajuan Li ◽  
Xiaohu Wu ◽  
Bereket Habte Imam ◽  
Jie Yang ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Signal Transduction Pathway ◽  
Endometrial Cell ◽  
Cell Receptors ◽  
Endometrial Cells ◽  
Microbial Invasion ◽  
Pass Through ◽  
Pro Inflammatory Cytokines

In order to control and prevent bovine endometritis, there is a need to understand the molecular pathogenesis of the infectious disease. Bovine endometrium is usually invaded by a massive mobilization of microorganisms, especially bacteria, during postpartum dairy cows. Several reports have implicated the Gram-negative bacteria in the pathogenesis of bovine endometritis, with information dearth on the potentials of Gram-positive bacteria and their endotoxins. The invasive bacteria and their ligands pass through cellular receptors such as TLRs, NLRs, and biomolecular proteins of cells activate the specific receptors, which spontaneously stimulates cellular signaling pathways like MAPK, NF-kB and sequentially triggers upregulation of pro-inflammatory cytokines. The cascade of inflammatory induction involves a dual signaling pathway; the transcription factor NF-κB is released from its inhibitory molecule and can bind to various inflammatory genes promoter. The MAPK pathways are concomitantly activated, leading to specific phosphorylation of the NF-κB. The provision of detailed information on the molecular pathomechanism of bovine endometritis with the interaction between host endometrial cells and invasive bacteria in this review would widen the gap of exploring the potential of receptors and signal transduction pathways in nanotechnology-based drug delivery system. The nanotherapeutic discovery of endometrial cell receptors, signal transduction pathway, and cell biomolecules inhibitors could be developed for strategic inhibition of infectious signals at the various cell receptors and signal transduction levels, interfering on transcription factors activation and pro-inflammatory cytokines and genes expression, which may significantly protect endometrium against postpartum microbial invasion.

The protective effects of carvacrol and thymol against paracetamol–induced toxicity on human hepatocellular carcinoma cell lines (HepG2)

2016 ◽  
Vol 35 (12) ◽  
pp. 1252-1263 ◽  
Author(s):  
SS Palabiyik ◽  
E Karakus ◽  
Z Halici ◽  
E Cadirci ◽  
Y Bayir ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Hepg2 Cells ◽  
Folk Medicine ◽  
Hepatoprotective Activity ◽  
High Dose ◽  
Protective Effects ◽  
And Oxidative Stress ◽  
Pro Inflammatory Cytokines

Acetaminophen (APAP) overdose could induce liver damage and lead to acute liver failure. The treatment of APAP overdoses could be improved by new therapeutic strategies. Thymus spp., which has many beneficial effects and has been used in folk medicine, is one such potential strategy. In the present study, the hepatoprotective activity of the main constituents of Thymus spp., carvacrol and thymol, were evaluated in light of APAP-induced hepatotoxicity. We hoped to understand the hepatoprotective mechanism of these agents on the antioxidant system and pro-inflammatory cytokines in vitro. Dose-dependent effects of thymol and carvacrol (25, 50, and 100 µM) were tested on cultured HepG2 cells. N-Acetylcysteine (NAC) was tested as positive control. We showed that APAP inhibited HepG2 cell growth by inducing inflammation and oxidative stress. Incubating APAP-exposed HepG2 cells with carvacrol and thymol for 24 h ameliorated this inflammation and oxidative stress. We also evaluated alanine transaminase and lactate dehydrogenase levels of HepG2 cells. We found that thymol and carvacrol protected against APAP-induced toxicity in HepG2 cells by increasing antioxidant activity and reducing pro-inflammatory cytokines, such as tumor necrosis factor α and interleukin 1β. Taking together high-dose thymol and carvacrol treatment has an effect close to NAC treatment in APAP toxicity, but thymol has better treatment effect than carvacrol.

scholarly journals Cystine reduces tight junction permeability and intestinal inflammation induced by oxidative stress in Caco-2 cells

Amino Acids ◽  
2021 ◽  
Author(s):  
Tatsuya Hasegawa ◽  
Ami Mizugaki ◽  
Yoshiko Inoue ◽  
Hiroyuki Kato ◽  
Hitoshi Murakami
Keyword(s):  
Oxidative Stress ◽  
Tight Junction ◽  
Mrna Expression ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Whole Cells ◽  
Intestinal Barrier Dysfunction ◽  
Pro Inflammatory Cytokines

AbstractIntestinal oxidative stress produces pro-inflammatory cytokines, which increase tight junction (TJ) permeability, leading to intestinal and systemic inflammation. Cystine (Cys2) is a substrate of glutathione (GSH) and inhibits inflammation, however, it is unclear whether Cys2 locally improves intestinal barrier dysfunction. Thus, we investigated the local effects of Cys2 on oxidative stress-induced TJ permeability and intestinal inflammatory responses. Caco-2 cells were cultured in a Cys2-supplemented medium for 24 h and then treated with H2O2 for 2 h. We assessed TJ permeability by measuring transepithelial electrical resistance and the paracellular flux of fluorescein isothiocyanate–dextran 4 kDa. We measured the concentration of Cys2 and GSH after Cys2 pretreatment. The mRNA expression of pro-inflammatory cytokines was assessed. In addition, the levels of TJ proteins were assessed by measuring the expression of TJ proteins in the whole cells and the ratio of TJ proteins in the detergent-insoluble fractions to soluble fractions (IS/S ratio). Cys2 treatment reduced H2O2-induced TJ permeability. Cys2 did not change the expression of TJ proteins in the whole cells, however, suppressed the IS/S ratio of claudin-4. Intercellular levels of Cys2 and GSH significantly increased in cells treated with Cys2. Cys2 treatment suppressed the mRNA expression of pro-inflammatory cytokines, and the mRNA levels were significantly correlated with TJ permeability. In conclusion, Cys2 treatment locally reduced oxidative stress-induced intestinal barrier dysfunction possively due to the mitigation of claudin-4 dislocalization. Furthermore, the effect of Cys2 on the improvement of intestinal barrier function is related to the local suppression of oxidative stress-induced pro-inflammatory responses.

scholarly journals Biotribological Tests of Osteochondral Grafts after Treatment with Pro-Inflammatory Cytokines

Cartilage ◽  
2021 ◽  
pp. 194760352199490
Author(s):  
Christoph Bauer ◽  
Hakan Göçerler ◽  
Eugenia Niculescu-Morzsa ◽  
Vivek Jeyakumar ◽  
Christoph Stotter ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Cytokines ◽  
Metabolic Activity ◽  
Wear Debris ◽  
Cartilage Tissue ◽  
Test Fluid ◽  
Osteochondral Grafts ◽  
Extracellular Matrix Components ◽  
Proteoglycan Content ◽  
Pro Inflammatory Cytokines

ObjectiveDuring osteoarthritis progression, cartilage degrades in a manner that influences its biomechanical and biotribological properties, while chondrocytes reduce the synthesis of extracellular matrix components and become apoptotic. This study investigates the effects of inflammation on cartilage under biomechanical stress using biotribological tests.MethodsBovine osteochondral grafts from five animals were punched out from the medial condyle and treated with or without pro-inflammatory cytokines (interleukin-1β [IL-1β], tumor necrosis factor-α [TNF-α], IL-6) for 2 weeks. After incubation, biotribological tests were performed for 2 hours (alternating 10 minutes test and pause respectively at 39°C, 180 N, 1 Hz, and 2 mm stroke). Before and after testing, the cartilage surface was imaged with a 3-dimensional microscope. During testing, the coefficient of friction (COF) was measured, while gene expression analysis and investigation of metabolic activity of chondrocytes were carried out after testing. Histological sections of the tissue and wear debris from the test fluid were also analyzed.ResultsAfter biotribological tests, surface cracks were found in both treated and untreated osteochondral grafts. In treated grafts, the COF increased, and the proteoglycan content in the cartilage tissue decreased, leading to structural changes. Chondrocytes from treated grafts showed increased expression of genes encoding for degradative enzymes, while cartilage-specific gene expression and metabolic activity exhibited no significant differences between treated and untreated groups. No measurable difference in the wear debris in the test fluid was found.ConclusionsTreatment of osteochondral grafts with cytokines results in a significantly increased COF, while also leading to significant changes in cartilage proteoglycan content and cartilage matrix compression during biotribological tests.

Pro-inflammatory Cytokines Up-regulate MUC1 Gene Expression in Oral Epithelial Cells

2003 ◽  
Vol 82 (11) ◽  
pp. 883-887 ◽  
Author(s):  
X. Li ◽  
L. Wang ◽  
D.P. Nunes ◽  
R.F. Troxler ◽  
G.D. Offner
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Inflammatory Cytokines ◽  
Oral Epithelial Cells ◽  
Muc1 Gene ◽  
Oral Epithelial ◽  
Pro Inflammatory Cytokines
Sign in / Sign up

Export Citation Format

Share Document