scholarly journals 3-Indolepropionic Acid Prevented Chlorpyrifos-Induced Hepatorenal Toxicities in Rats By Improving Anti-Inflammatory, Antioxidant And Apoptotic Responses and Abating DNA Damage

2021 ◽  
Author(s):  
Solomon E. Owumi ◽  
Eseroghene S. Najophe ◽  
Moses T. Otunla
Keyword(s):  
Dna Damage ◽  
Caspase 3 ◽  
Corn Oil ◽  
Interleukin 1 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Liver And Kidney ◽  
Hepatorenal Function ◽  
The Individual

Abstract We examined the individual and combined effect of 3-Indolepropionic acid (IPA) and Chlorpyrifos (CPF) on rat hepatorenal function. The experimental cohorts (n=6) were treated per os for 14 consecutive days as follows: Control (Corn oil 2 mL/kg body weight), CPF alone (5 mg/kg), IPA alone (50 mg/kg) and the co-treated cohorts (CPF: 5 mg/kg + IPA: 25 or 50 mg/kg). Biomarkers of hepatorenal damage, antioxidant and myeloperoxidase (MPO) activities, the levels of nitric oxide (NO), lipid peroxidation (LPO) and reactive oxygen and nitrogen (RONS) species were spectrophotometrically evaluated. Besides, the concentration of tumour necrosis factor-alpha (TNF- α), interleukin-1 β (IL-1β) and caspase-3 activity and 8-hydroxy-2’-deoxyguanosine adducts (8-OHdG) was also assessed by Enzyme-Linked Immunosorbent Assay. Treatment with CPF alone increased biomarkers of hepatorenal toxicity was significantly (p<0.05) alleviated in rats co-exposed to CPF and IPA. Moreover, the decrease in antioxidant status as antioxidant elevation in RONS and LPO were lessened (p<0.05) in rats co-treated with CPF and IPA. CPF mediated increases in TNF-α, IL-1β, NO, MPO and caspase-3 activity were reduced (p<0.05) in the liver and kidney of rats co-exposed to CPF and IPA. In addition, 8-OHdG adducts formation were reduced in rats treated with 3-IPA dose-dependently. Light microscopic examination showed that histopathological lesions severity induced by CPF were alleviated in rats co-exposed to IPA and CPF. In conclusion, the results demonstrated that rats co-exposed to IPA and CPF exhibited reduced CPF-induced oxidative stress, inflammation, DNA damage and caspase-3 activation of the liver and kidney.

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.

scholarly journals Guaiane-Type Sesquiterpenoids From Dendranthema morifolium (Ramat.) S. Kitam Flowers Protect H9c2 Cardiomyocyte From LPS-Induced Injury

2019 ◽  
Vol 14 (7) ◽  
pp. 1934578X1986417
Author(s):  
Beibei Zhang ◽  
Mengnan Zeng ◽  
Meng Li ◽  
Wenjing Chen ◽  
Benke Li ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Creatine Phosphate ◽  
Cardiomyocyte Apoptosis ◽  
Exocyclic Double Bond ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Caspase 9 ◽  
Necrosis Factor Alpha ◽  
Thiazolyl Blue Tetrazolium Bromide ◽  
Tnf Α

This study investigated the protective effects of guaiane-type sesquiterpenoids isolated from Dendranthema morifolium (Ramat.) S. Kitam flowers on lipopolysaccharide (LPS)-induced injury in H9c2 cardiomyocyte. Cell viability was determined by thiazolyl blue tetrazolium bromide (MTT). The content of released tumor necrosis factor alpha (TNF- α) and interleukin 6 (IL-6) was evaluated by enzyme-linked immunosorbent assay. The levels of lactate dehydrogenase (LDH) and creatine phosphate kinase (CK) were measured by using commercial available kits. The protein expression levels of pelF2 α, GRP78, Bax, caspase-3, caspase-9, Bcl-2, LC3-II, and p62 were measured by in-cell Western. Flow cytometry was used to detect H9c2 cardiomyocyte apoptosis. Compounds 5, 7, 1, 8, and 2 exhibited the effects of cardioprotection and activity sequence enhancement. The levels of IL-6, TNF- α, LDH, CK, pelF2 α, GRP78, Bax, caspase-3, caspase-9, p62, and H9c2 cardiomyocyte apoptosis were increased in LPS-treated H9c2 cardiomyocyte, while those of Bcl-2 and LC3-II were decreased. These effects could be effectively reversed by compounds 5, 7, 1, 8, and 2. Results demonstrated that the guaiane-type sesquiterpenoids could prevent LPS-induced injury in cardiomyocyte by decreasing endoplasmic reticulum (ER) stress, apoptosis, and autophagy as well as downregulating the inflammatory mediators. In addition, the active groups of guaiane-type sesquiterpenoids might be the angelate at C-8 and the exocyclic double bond at C-11.

Proinflammatory cytokine levels in patients with conversion disorder

2013 ◽  
Vol 25 (3) ◽  
pp. 137-143 ◽  
Author(s):  
Utkan Tiyekli ◽  
Okan Çalıyurt ◽  
Nimet Dilek Tiyekli
Keyword(s):  
Acute Phase ◽  
Proinflammatory Cytokine ◽  
Interleukin 1 ◽  
Conversion Disorder ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference ◽  
Cytokine Levels ◽  
As Stress

ObjectiveIt was aimed to evaluate the relationship between proinflammatory cytokine levels and conversion disorder both commonly known as stress regulated.MethodBaseline proinflammatory cytokine levels–[Tumour necrosis factor alpha (TNF‐α), Interleukin‐1 beta (IL‐1β), Interleukin‐6 (IL‐6)]–were evaluated with enzyme‐linked immunosorbent assay in 35 conversion disorder patients and 30 healthy controls. Possible changes in proinflammatory cytokine levels were evaluated again, after their acute phase in conversion disorder patients.ResultsStatistically significant decreased serum TNF‐α levels were obtained in acute phase of conversion disorder. Those levels increased after acute conversion phase. There were no statistically significant difference observed between groups in serum IL‐1β and (IL‐6) levels.ConclusionsStress associated with conversion disorder may suppress immune function in acute conversion phase and may have diagnostic and therapeutic value.

Astaxanthin prevents lung injury due to hyperoxia and inflammation

2020 ◽  
Vol 23 ◽  
Author(s):  
Hasan Akduman ◽  
Cüneyt Tayman ◽  
Ufuk Çakir ◽  
Esra Çakir ◽  
Dilek Dilli ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Interleukin 1 ◽  
Survival Rates ◽  
Lipid Hydroperoxide ◽  
Treated Group ◽  
Lung Damage ◽  
Pregnant Rats ◽  
Necrosis Factor Alpha ◽  
Total Thiol ◽  
Tnf Α

Background/aim: We aimed to ascertain the effects of astaxanthin on the lungs of rat pups with bronchopulmonary dysplasia (BPD) induced by hyperoxia and lipopolysaccharide (LPS). Materials and methods: Forty-two newborn Wistar rats born to spontaneous pregnant rats were divided into three groups: Hyperoxia (95% O2) + lipopolysaccharide (LPS) group, hyperoxia + LPS + astaxhantin group and control: no treatment group (21% O2). Pups in the hyperoxia + LPS + astaxanthin group were given 100 mg/kg/day oral astaxanthin from the first day to the fifth day. Histopathologic and biochemical evaluations including glutathione (GSH), total antioxidant status (TAS), total oxidant status (TOS), lipid hydroperoxide (LPO), 8-hydroxydeoxyguanosine (8-OHdG), advanced oxidation protein products (AOPP), myeloperoxidase (MPO), total thiol, tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL1β) and caspase-3 activities were performed. Results: A better survival rates and weight gain were demonstrated in the hyperoxia + LPS + astaxanthin group (p <0.001). In the histopathologic evaluation, the severity of lung damage was significantly reduced in the hyperoxia+LPS+astaxanthin group, as well as decreased apoptosis (ELİSA for caspase-3) (p <0.001). The biochemical analyses of lung tissues TAS, GSH, Total thiol levels were significantly higher in the astaxanthin treated group compared to hyperoxia + LPS group (p <0.05) while TOS, AOPP, LPO, 8-OHdG, MPO levels were significantly lower (p <0.001). In addition, unlike the hyperoxia + LPS group, TNF-α and IL-1β levels in lung tissue were significantly lower in the astaxanthin-treated group (p <0.001). Conclusion: Astaxanthin was shown to reduce lung damage caused by inflammation and hyperoxia with its antiinflammatory, anti-oxidant, anti-apoptotic properties and to protect the lung from severe destruction.

scholarly journals Effects of Selenium-Enriched Protein fromGanoderma lucidumon the Levels of IL-1βand TNF-α, Oxidative Stress, and NF-κB Activation in Ovalbumin-Induced Asthmatic Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Guan Min-chang ◽  
Tang Wei-hong ◽  
Xu Zhen ◽  
Sun Jie
Keyword(s):  
Oxidative Stress ◽  
Interleukin 1 ◽  
Experimental Conditions ◽  
Necrosis Factor Alpha ◽  
Organic Selenium ◽  
Inorganic Selenium ◽  
Tnf Α ◽  
Liver And Kidney ◽  
Factor Alpha ◽  
Endogenous Antioxidant

The purpose of this study was to compare the effect and toxicity of organic selenium (Pro-Se) with inorganic selenium (IOSe) in preventing asthma in ovalbumin-induced asthmatic mice. After the mice were treated orally with Pro-Se and IOSe, respectively, the plasma Se levels, Se accumulation in liver and kidney, tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), oxidative stress, and NF-κB activation in lung were examined. The results showed that the serumal Se levels in the mice fed the Pro-Se were significant (P<0.01) elevations. It results in restoration of the level of endogenous antioxidant enzyme, lower levels of TNF-αand IL-1β, and activated NF-κB in the asthmatic mice. Our experiments have demonstrated profound differences between the activities of organic selenium and inorganic selenium in experimental conditions. These data provide an important proof of the concept that organic selenium might be a new potential therapy for the management of childhood asthma in humans.

Investigation of DNA damage, oxidative stress, and inflammation in synthetic cannabinoid users

2020 ◽  
Vol 39 (11) ◽  
pp. 1454-1462
Author(s):  
EM Guler ◽  
MY Bektay ◽  
AG Akyildiz ◽  
BH Sisman ◽  
FV Izzettin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Interleukin 1 ◽  
Synthetic Cannabinoids ◽  
Public Health Problem ◽  
Total Antioxidant Status ◽  
Stress Index ◽  
Important Public Health Problem ◽  
Necrosis Factor Alpha ◽  
Tnf Α

Background: The widespread use of synthetic cannabinoids (SCs) among youth has become an important public health problem. Several life-threatening side effects of SC have been reported, including cardiovascular, gastrointestinal, neurological, renal, metabolic, ophthalmologic, and pulmonary effects, besides skin toxicity and hepatotoxicity. Methods: Given that high levels of SC can lead to oxidative stress, DNA damage, and inflammation, it has been aimed in this study to investigate the effects of SC in aspects of primary DNA damage, plasma total oxidant status (TOS)/total antioxidant status (TAS), thiol–disulfide homeostasis, myeloperoxidase (MPO) level, and cytokine levels (interleukin 1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α)) of 40 SC users (SCUs) in Turkey. Results: Mean plasma TOS levels were significantly higher in the SCUs group than in the healthy group (HG). Similarly, mononuclear leukocyte DNA damage, plasma TOS, MPO activity, disulfide, oxidative stress index levels, IL-1β, IL-6, and TNF-α levels were significantly higher in the SCU group than in the HG, whereas plasma TAS, total, and native thiol levels were significantly lower in the SCU group than in the HG. Conclusion: It is concluded that SC can cause increase in oxidative stress and in inflammatory processes in addition to its potential for DNA damage. Additional studies with larger sample sizes and longer durations should be held to understand more specific outcomes of SC use.

Role of inflammation in the development of colorectal cancer

2020 ◽  
Vol 20 ◽  
Author(s):  
Sridhar Muthusami ◽  
R. Ileng Kumaran ◽  
Kokelavani Nampalli Babu ◽  
Sneha Krishnamoorthy ◽  
Akash Guruswamy ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Chronic Inflammation ◽  
Interleukin 1 ◽  
Cell Types ◽  
Model Systems ◽  
Cytokine Gene Expression ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Proinflammatory Molecules

: Chronic inflammation can lead to the development of many diseases including cancer. Inflammatory bowel disease (IBD) that includes both ulcerative colitis (UC) and Crohn's disease (CD) are risk factors for the development of colorectal cancer (CRC). Many cytokines produced primarily by the gut immune cells either during or in response to localized inflammation in the colon and rectum are known to stimulate the complex interactions between the different cell types in the gut environment resulting in acute inflammation. Subsequently, chronic inflammation together with genetic and epigenetic changes has been shown to lead to the development and progression of CRC. Various cell types present in the colon such as enterocytes, Paneth cells, goblet cells and macrophages express receptors for inflammatory cytokines and respond to tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6 and other cytokines. Among the several cytokines produced, TNF-α and IL-1β are the key proinflammatory molecules that play critical roles in the development of CRC. The current review is intended to consolidate the published findings to focus on the role of proinflammatory cytokines, namely TNF-α and IL-1β, on inflammation (and the altered immune response) in the gut, to better understand the development of CRC in IBD, using various experimental model systems, preclinical and clinical studies. Moreover, this review also highlights the current therapeutic strategies available (monotherapy and combination therapy), to alleviate the symptoms or treat inflammationassociated CRC by using monoclonal antibodies or aptamers to block proinflammatory molecules, inhibitors of tyrosine kinases in inflammatory signaling cascade, competitive inhibitors of proinflammatory molecules, and the nucleic acid drugs like small activating RNAs (saRNAs) or microRNA (miRNA) mimics to activate tumor suppressor or repress oncogene/proinflammatory cytokine gene expression.

scholarly journals Glycyrrhizin Attenuates Carcinogenesis by Inhibiting the Inflammatory Response in a Murine Model of Colorectal Cancer

2021 ◽  
Vol 22 (5) ◽  
pp. 2609
Author(s):  
Guifeng Wang ◽  
Keiichi Hiramoto ◽  
Ning Ma ◽  
Nobuji Yoshikawa ◽  
Shiho Ohnishi ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Stem Cell ◽  
Inflammatory Response ◽  
Murine Model ◽  
Licorice Root ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Stem Cell Markers ◽  
Tnf Α

Glycyrrhizin (GL), an important active ingredient of licorice root, which weakens the proinflammatory effects of high-mobility group box 1 (HMGB1) by blocking HMGB1 signaling. In this study, we investigated whether GL could suppress inflammation and carcinogenesis in an azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced murine model of colorectal cancer. ICR mice were divided into four groups (n = 5, each)—control group, GL group, colon cancer (CC) group, and GL-treated CC (CC + GL) group, and sacrificed after 20 weeks. Plasma levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-α were measured using an enzyme-linked immunosorbent assay. The colonic tissue samples were immunohistochemically stained with DNA damage markers (8-nitroguanine and 8-oxo-7,8-dihydro-2′-deoxy-guanosine), inflammatory markers (COX-2 and HMGB1), and stem cell markers (YAP1 and SOX9). The average number of colonic tumors and the levels of IL-6 and TNF-α in the CC + GL group were significantly lower than those in the CC group. The levels of all inflammatory and cancer markers were significantly reduced in the CC + GL group. These results suggest that GL inhibits the inflammatory response by binding HMGB1, thereby inhibiting DNA damage and cancer stem cell proliferation and dedifferentiation. In conclusion, GL significantly attenuates the pathogenesis of AOM/DSS-induced colorectal cancer by inhibiting HMGB1-TLR4-NF-κB signaling.

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.

scholarly journals Artemisinin Ameliorates Osteoarthritis by Inhibiting the Wnt/β-Catenin Signaling Pathway

2018 ◽  
Vol 51 (6) ◽  
pp. 2575-2590 ◽  
Author(s):  
Gang Zhong ◽  
Ruiming Liang ◽  
Jun Yao ◽  
Jia Li ◽  
Tongmeng Jiang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Cruciate Ligament ◽  
Interleukin 1 ◽  
Cartilage Degradation ◽  
Chondrocyte Apoptosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cell Viability Assay ◽  
Necrosis Factor Alpha ◽  
Anti Inflammatory

Background/Aims: Current drug therapies for osteoarthritis (OA) are not practical because of the cytotoxicity and severe side-effects associated with most of them. Artemisinin (ART), an antimalarial agent, is well known for its safety and selectivity to kill injured cells. Based on its anti-inflammatory activity and role in the inhibition of OA-associated Wnt/β-catenin signaling pathway, which is crucial in the pathogenesis of OA, we hypothesized that ART might have an effect on OA. Methods: The chondro-protective and antiarthritic effects of ART on interleukin-1-beta (IL-1β)-induced and OA patient-derived chondrocytes were investigated in vitro using cell viability assay, glycosaminoglycan secretion, immunofluorescence, quantitative reverse transcription-polymerase chain reaction, and western blotting. We also used OA model rats constructed by anterior cruciate ligament transection and medial meniscus resection (ACLT+MMx) in the joints to investigate the effects of ART on OA by gross observation, morphological staining, immunohistochemistry, and enzyme-linked immunosorbent assay. Results: ART exhibited potent anti-inflammatory effects by inhibiting the expression of proinflammatory chemokines and cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor alpha, and matrix metallopeptidase-13. It also showed favorable chondro-protective effect as evidenced by enhanced cell proliferation and viability, increased glycosaminoglycan deposition, prevention of chondrocyte apoptosis, and degeneration of cartilage. Further, ART inhibited OA progression and cartilage degradation via the Wnt/β-catenin signaling pathway, suggesting that it might serve as a Wnt/β-catenin antagonist to reduce inflammation and prevent cartilage degradation. Conclusion: In conclusion, ART alleviates IL-1β-mediated inflammatory response and OA progression by regulating the Wnt/β-catenin signaling pathway. Thereby, it might be developed as a potential therapeutic agent for OA.

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