scholarly journals Borate reduces experimental supra-celiac aortic clamping-induced oxidative stress in lung and kidney, but fails to prevent organ damage

2021 ◽  
Vol 29 (3) ◽  
pp. 320-329
Author(s):  
Tünay Kurtoğlu ◽  
Selim Durmaz ◽  
Ömer Faruk Rahman ◽  
Nesibe Kahraman Çetin ◽  
Mustafa Yılmaz ◽  
...  
Keyword(s):  
Dimethyl Sulfoxide ◽  
Ischemia Reperfusion ◽  
Interleukin 1 ◽  
Control Group ◽  
Nuclear Factor ◽  
Necrosis Factor Alpha ◽  
Aortic Clamping ◽  
Nuclear Factor Kappa ◽  
Histological Damage ◽  
Nuclear Factor Kappa Beta

Background: This study aims to investigate the effects of 2-aminoethoxydiphenyl borate (2-APB) on aortic clamping-induced lung and kidney tissue oxidation, tissue inflammation, and histological damage in a rat model. Methods: A total of 28 adult female Wistar albino rats were randomly allocated to four equal groups: Control group, ischemia-reperfusion group, dimethyl sulfoxide group, and 2-APB group. Animals in the control group underwent median laparotomy. In the remaining groups, supra-celiac aorta was clamped for 45 min and, then, reperfusion was constituted for 60 min. The 2-APB (2 mg/kg) was administered before clamping. The remaining groups received saline (ischemia-reperfusion group) or dimethyl sulfoxide (dimethyl sulfoxide group). Kidney and lung tissue samples were harvested at the end of reperfusion. Results: Aortic occlusion caused increased tissue total oxidant status and reduced total antioxidant status and glutathione levels in the ischemia-reperfusion and dimethyl sulfoxide groups. Tissue interleukin-1 beta and tumor necrosis factor-alpha levels, nuclear factor kappa beta activation, and histological damage severity scores were also higher in these groups. The 2-APB treatment eliminated the increase in total oxidant status and the decrease in total antioxidant status and glutathione levels. It also caused a decrease in the interleukin-1 beta levels, although it did not significantly alter the tumor necrosis factor-alpha levels, nuclear factor kappa beta immunoreactivity, and histological damage scores. Conclusion: Borate exerted a beneficial antioxidant effect as evidenced by reduced oxidative stress; however, it did not inhibit nuclear factor kappa beta activation and prevent histological damage in supra-celiac aortic clamping-induced kidney and lung injury in rats.

Nuclear Factor κB and Anesthetic Preconditioning during Myocardial Ischemia-Reperfusion

2004 ◽  
Vol 100 (3) ◽  
pp. 540-546 ◽  
Author(s):  
Caiyun Zhong ◽  
Yamei Zhou ◽  
Hong Liu
Keyword(s):  
Ischemia Reperfusion ◽  
Interleukin 1 ◽  
Intercellular Adhesion Molecule ◽  
Nuclear Factor ◽  
Intercellular Adhesion Molecule 1 ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Nf Kappab ◽  
Myocardial Ischemia Reperfusion ◽  
Oxide Synthase

Background Volatile anesthetic preconditioning (APC) protects against myocardial ischemia-reperfusion (IR) injury, but the precise mechanisms underlying this phenomenon remain undefined. To investigate the molecular mechanism of APC in myocardial protection, the activation of nuclear factor (NF) kappaB and its regulated inflammatory mediators expression were examined in the current study. Methods Hearts from male rats were isolated, Langendorff perfused, and randomly assigned to one of three groups: (1) the control group: hearts were continuously perfused for 130 min; (2) the IR group: 30 min of equilibration, 15 min of baseline, 25 min of ischemia, 60 min of reperfusion; and (3) the APC + IR group: 30 min of equilibration, 10 min of sevoflurane exposure and a 5-min washout, 25 min of global ischemia, 60 min of reperfusion. Tissue samples were acquired at the end of reperfusion. NF-kappaB activity was determined by electrophoretic mobility shift assay. The NF-kappaB inhibitor, IkappaB-alpha, was determined by Western blot analysis. Myocardial inflammatory mediators, including tumor necrosis factor alpha, interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase, were also assessed by Western blot analysis. Results Nuclear factor kappaB-DNA binding activity was significantly increased at the end of reperfusion in rat myocardium, and cytosolic IkappaB-alpha was decreased. Supershift assay revealed the involvement of NF-kappaB p65 and p50 subunits. APC with sevoflurane attenuated NF-kappaB activation and reduced the expression of tumor necrosis factor alpha, interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase. APC also reduced infarct size and creatine kinase release and improved myocardial left ventricular developed pressure during IR. Conclusions The results of this study indicate that attenuation of NF-kappaB activation and subsequent down-regulation of NF-kappaB-dependent inflammatory gene expression plays an important role in the protective mechanism of APC against acute myocardial IR injury.

scholarly journals A20 of nucleus pulposus cells plays a self-protection role via the nuclear factor-kappa B pathway in the inflammatory microenvironment

2020 ◽  
Vol 9 (5) ◽  
pp. 225-235
Author(s):  
Xin Peng ◽  
Cong Zhang ◽  
Jun-Ping Bao ◽  
Lei Zhu ◽  
Rui Shi ◽  
...  
Keyword(s):  
Nucleus Pulposus ◽  
Messenger Rna ◽  
Nuclear Factor Kappa B ◽  
Intervertebral Discs ◽  
Control Group ◽  
Nuclear Factor ◽  
Nucleus Pulposus Cells ◽  
Necrosis Factor Alpha ◽  
Nuclear Factor Kappa ◽  
Tnf Α

Aims Inflammatory response plays a pivotal role in the pathophysiological process of intervertebral disc degeneration (IDD). A20 (also known as tumour necrosis factor alpha-induced protein 3 (TNFAIP3)) is a ubiquitin-editing enzyme that restricts nuclear factor-kappa B (NF-κB) signalling. A20 prevents the occurrence of multiple inflammatory diseases. However, the role of A20 in the initiation of IDD has not been elucidated. The aim of the study was to investigate the effect of A20 in senescence of TNF alpha (TNF-α)-induced nucleus pulposus cells (NPCs). Methods Immunohistochemical staining was performed to observe the expression of A20 in normal and degenerated human intervertebral discs. The NPCs were dissected from the tail vertebrae of healthy male Sprague-Dawley rats and were cultured in the incubator. In the experiment, TNF-α was used to mimic the inflammatory environment of IDD. The cell viability and senescence were examined to investigate the effect of A20 on TNF-α-treated NPCs. The expression of messenger RNA (mRNA)-encoding proteins related to matrix macromolecules (collagen II, aggrecan) and senescence markers (p53, p16). Additionally, NF-κB/p65 activity of NPCs was detected within different test compounds. Results The expression of A20 was upregulated in degenerate human intervertebral discs. The A20 levels of NPCs in TNF-α inflammatory microenvironments were dramatically higher than those of the control group. TNF-α significantly decreased cell proliferation potency but increased senescence-associated beta-galactosidase (SA-β-Gal) activity, the expression of senescence-associated proteins, the synthesis of extracellular matrix, and G1 cycle arrest. The senescence indicators and NF-κB/p65 expression of A20 downregulated group treated with TNF-α were significantly upregulated compared to TNF-α-treated normal NPCs. Conclusion A20 has a self-protective effect on the senescence of NPCs induced by TNF-α. The downregulation of A20 in NPCs exacerbated the senescence of NPCs induced by TNF-α. Cite this article: Bone Joint Res. 2020;9(5):225–235.

scholarly journals Efek Ekstrak Etanol Daging Putih Semangka dan Simvastatin Terhadap Aktivasi Nuclear Factor Kappa Beta (NF- kβ) Aorta Tikus Rattus Norvegicus yang Diberi Diet Aterogenik

2018 ◽  
Vol 11 (2) ◽  
Author(s):  
Dafrosia Darmi Manggasa
Keyword(s):  
Rattus Norvegicus ◽  
Atherogenic Diet ◽  
Control Group ◽  
Antioxidant Compounds ◽  
Standard Diet ◽  
Nuclear Factor ◽  
Control Group Design ◽  
Nuclear Factor Kappa ◽  
Watermelon Rind ◽  
Nuclear Factor Kappa Beta

Atherogenic diet can lead to dyslipidemia condition that trigger increase Reactive Oxygen Species (ROS) and oxidative stress. The increasing of ROS can activate transcription factor Nuclear Factor Kappa Beta (NF-kβ). Activated NF-kβ induce proinflammatory cytokines that will increase the atherosclerosis progressivity. Watermelon rind had proven to have antioxidant compounds that can inhibit ROS. This study was aimed to prove the effect of watermelon rind extract and simvastatin to decrease the NF-kβ aktivation of Rattus norvegicus with atherogenic diet. This research was using Post Test Only Control Group Design. The samples were divided into five groups: (i) standard diet (K(-)), (ii) atherogenic diet (K(+)), (iii) atherogenic diet + watermelon rind extract 250 mg/kgBW/day, (iv) atherogenic diet + watermelon rind 500 mg/kgBW/day, and (v) the atherogenic diet + simvastatin 0.9 mg/kgBW/day. Atherogenic diet was given for 8 weeks. NF-kβ were measured by immunohistochemistry. Data were analyzed with ANOVA and post hoc test. The results showed a significant decrease mean NF-kβ activation after treatment of watermelon rind extract of 250 mg/kg/day (p =0,000), dose of 500 mg/kg/day (p = 0.000), and simvastatin dose of 0.9 mg/kg/day could reduced NF-kβ significantly (p = 0,000) compared with atherogenic diet group. It concluded that the watermelon rind extract dose 500 mg/kgBW/day was equivalent to simvastatin 0,9 mg/kgBW/day in lowering the NF-kβ activation rats with atherogenic diet.

scholarly journals RvD1 Attenuated Susceptibility to Ischemic AKI in Diabetes by Downregulating Nuclear Factor-κ B Signal and Inhibiting Apoptosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Zheng Li ◽  
Zhiwen Liu ◽  
Hengcheng Lu ◽  
Wenni Dai ◽  
Junxiang Chen ◽  
...  
Keyword(s):  
Renal Function ◽  
Clinical Study ◽  
Inflammatory Response ◽  
Ischemia Reperfusion ◽  
Animal Experiments ◽  
Ischemic Injury ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Nuclear Factor ◽  
Histological Damage

BackgroundAcute kidney injury (AKI), when occurring in diabetic kidney disease (DKD), is known to be more severe and difficult to recover from. Inflammation and apoptosis may contribute to the heightened sensitivity of, and non-recovery from, AKI in patients with DKD. Resolvin D1 (RvD1) is a potent lipid mediator which can inhibit the inflammatory response and apoptosis in many diseases. However, it has been reported that the RvD1 levels were decreased in diabetes, which may explain why DKD is more susceptible to AKI.MethodsFor animal experiments, diabetic nephropathy (DN) mice were induced by streptozotocin (STZ) injection intraperitoneally. Renal ischemia–reperfusion was used to induce AKI. Blood urea nitrogen (BUN) and serum creatinine were determined using commercial kits to indicate renal function. Renal apoptosis was examined by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Real-time polymerase chain reaction (PCR) was used to detect the marker of inflammatory response. Western blot was used to detect the expression of nuclear factor-κB (NF-κB)-related proteins. For clinical study, 12 cases diagnosed with DKD were enrolled in this study, and an equal number of non-diabetic renal disease patients (NDKD) were recruited as a control group. The serum RvD1 in DKD or NDKD patients were detected through an ELISA kit.ResultsIn clinical study, we found that the serum RvD1 levels were decreased in DKD patients compared to those in NDKD patients. Decreased serum RvD1 levels were responsible for the susceptibility to ischemic AKI in DKD patients. In animal experiments, both the serum RvD1 and renal ALX levels were downregulated. RvD1 treatment could ameliorate renal function and histological damage after ischemic injury in DN mice. RvD1 treatment also could inhibit the inflammatory response. Di-tert-butyl dicarbonate (BOC-2) treatment could deteriorate renal function and histological damage after ischemic injury in non-diabetic mice. RvD1 could inhibit the NF-κB activation and suppress inflammatory response mainly by inhibiting NF-κB signaling.ConclusionRvD1 attenuated susceptibility to ischemic AKI in diabetes by downregulating NF-κB signaling and inhibiting apoptosis. Downregulated serum RvD1 levels could be the crucial factor for susceptibility to ischemic AKI in diabetes.

scholarly journals The Effect of Mesenchymal Stem Cell Wharton’s Jelly on Nuclear Factor Kappa Beta and Interleukin-10 Levels in Osteoarthritis Rat Model

2020 ◽  
Vol 8 (B) ◽  
pp. 350-357
Author(s):  
Vivi Sofia ◽  
Moch Saiful Bachri ◽  
Endrinaldi Endrinaldi
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Wharton’S Jelly ◽  
Joint Disease ◽  
Control Group ◽  
Nuclear Factor ◽  
Wharton's Jelly ◽  
Knee Oa ◽  
Nuclear Factor Kappa ◽  
Nuclear Factor Kappa Beta

BACKGROUND: Osteoarthritis (OA) is a degenerative joint disease in one or more joints characterized by changes in pathological structures such as cartilage, hypertrophy, and remodeling of the subchondral bone and secondary inflammation of the synovium membrane, causing changes in joint components such as cells, matrices, and molecular production. At the molecular level, an imbalance between catabolic and anabolic activities in joint cartilage results in OA. Nuclear factor kappa beta (NFκβ) is a cytokine that plays an important role in the signaling pathway of the pathogenesis of OA in causing an inflammatory reaction, whereas interleukin (IL)-10 is an anti-inflammatory cytokine that is involved in the pathogenesis of OA. AIM: This study aims to prove the influence before and after administration mesenchymal stem cells from Wharton’s jelly on the serum NFκβ and IL-10 levels in OA rat models. MATERIALS AND METHODS: This research is an experimental study with the design of post-test-only control group design. The sample consisted of 16 OA rats as a control group and 16 OA rats treated with MSC-WJ as a treatment group. OA induction is done by injection of monosodium iodoacetate (MIA) into the intra-articular right knee. Giving MSC-WJ is done in the 3rd week after MIA induction. The serum NFκβ and IL-10 levels were measured after 3 weeks treated with MSC-WJ using the ELISA method. The statistical test used is an independent t-test. p < 0.05 was said to be statistically significant. RESULTS: From the research results obtained, serum levels of knee OA of rat knee OA treated with mesenchymal stem cell Wharton jelly are lower than serum NFκβ levels of knee OA of the rat that is not treated, but the difference in levels of NFκβ is not significant (p > 0.05). The serum IL-10 level of rat OA of knee treated with mesenchymal stem cell Wharton jelly was higher than the serum IL-10 level of rat OA of the knee that was not treated, difference in levels of IL-10, is significant (p < 0.05). CONCLUSION: This study concluded that MSC-WJ significantly decreased the serum NFκβ levels of OA rats and not significantly increased the serum IL-10 levels of OA rats.

scholarly journals Inhibition of Leukocyte Entry into the Brain by the Selectin Blocker Fucoidin Decreases Interleukin-1 (IL-1) Levels but Increases IL-8 Levels in Cerebrospinal Fluid during Experimental Pneumococcal Meningitis in Rabbits

2000 ◽  
Vol 68 (6) ◽  
pp. 3153-3157 ◽  
Author(s):  
Christian Østergaard ◽  
Runa Vavia Yieng-Kow ◽  
Thomas Benfield ◽  
Niels Frimodt-Møller ◽  
Frank Espersen ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Pneumococcal Meningitis ◽  
Interleukin 1 ◽  
Treated Group ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference ◽  
The Brain ◽  
Experimental Pneumococcal Meningitis

ABSTRACT The polysaccharide fucoidin is a selectin blocker that inhibits leukocyte recruitment into the cerebrospinal fluid (CSF) during experimental pneumococcal meningitis. In the present study, the effect of fucoidin treatment on the release of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1), and IL-8 into the CSF was investigated. Rabbits (n = 7) were treated intravenously with 10 mg of fucoidin/kg of body weight every second hour starting 4 h after intracisternal inoculation of ∼106 CFU of Streptococcus pneumoniae type 3 (untreated control group, n = 7). CSF samples were obtained every second hour during a 16-h study period. Treatment with fucoidin caused a consistent and significant decrease in CSF IL-1 levels (in picograms per milliliter) between 12 and 16 h (0 versus 170, 0 versus 526, and 60 versus 1,467, respectively;P < 0.02). A less consistent decrease in CSF TNF-α levels was observed in the fucoidin-treated group, but with no significant difference between the two groups (P > 0.05). In contrast, there was no attenuation in CSF IL-8 levels. Indeed, there was a significant increase in CSF IL-8 levels (in picograms per milliliter) in the fucoidin-treated group at 10 and 12 h (921 versus 574 and 1,397 versus 569, respectively;P < 0.09). In conclusion, our results suggest that blood-derived leukocytes mainly are responsible for the release of IL-1 and to some degree TNF-α into the CSF during pneumococcal meningitis, whereas IL-8 may be produced by local cells within the brain.

Oxydative stress markers and cytokine levels in rosuvastatin-medicated hypercholesterolemia patients

2018 ◽  
Vol 44 (4) ◽  
pp. 530-538
Author(s):  
Aysun Çetin ◽  
İhsan Çetin ◽  
Semih Yılmaz ◽  
Ahmet Şen ◽  
Göktuğ Savaş ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Interleukin 1 ◽  
Paraoxonase 1 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Phenotypic Effect ◽  
Necrosis Factor Alpha ◽  
Stress Markers ◽  
Tnf Α ◽  
Before And After

Abstract Background Limited research is available concerning the relationship between oxidative stress and inflammation parameters, and simultaneously the effects of rosuvastatin on these markers in patients with hypercholesterolemia. We aimed to investigate the connection between cytokines and oxidative stress markers in patients with hypercholesterolemia before and after rosuvastatin treatment. Methods The study consisted of 30 hypercholesterolemic patients diagnosed with routine laboratory tests and 30 healthy participants. The lipid parameters, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), paraoxonase-1 (PON1) and malondialdehyde (MDA) levels in controls and patients with hypercholesterolemia before and after 12-week treatment with rosuvastatin (10 mg/kg/day), were analyzed by means of enzyme-linked immunosorbent assay. Results It was found that a 12-week cure with rosuvastatin resulted in substantial reductions in IL-1β, IL-6 and TNF-α and MDA levels as in rising activities of PON1 in patients with hypercholesterolemia. Before treatment, the PON1 levels were significantly negatively correlated with TNF-α and IL-6 in control group, while it was positively correlated with TNF-α in patients. Conclusion Our outcomes provide evidence of protected effect of rosuvastatin for inflammation and oxidative damage. It will be of great interest to determine whether the correlation between PON1 and cytokines has any phenotypic effect on PON1.

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