scholarly journals Gingerol Fraction from Zingiber officinale Protects against Gentamicin-Induced Nephrotoxicity

2014 ◽  
Vol 58 (4) ◽  
pp. 1872-1878 ◽  
Author(s):  
Francisco A. P. Rodrigues ◽  
Mara M. G. Prata ◽  
Iris C. M. Oliveira ◽  
Natacha T. Q. Alves ◽  
Rosa E. M. Freitas ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitrosative Stress ◽  
Oral Treatment ◽  
Control Group ◽  
Mrna Levels ◽  
Sod Activity ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Ifn Γ ◽  
Nephroprotective Effect

ABSTRACTNephrotoxicity is the main complication of gentamicin (GM) treatment. GM induces renal damage by overproduction of reactive oxygen species and inflammation in proximal tubular cells. Phenolic compounds from ginger, called gingerols, have been demonstrated to have antioxidant and anti-inflammatory effects. We investigated if oral treatment with an enriched solution of gingerols (GF) would promote a nephroprotective effect in an animal nephropathy model. The following six groups of male Wistar rats were studied: (i) control group (CT group); (ii) gingerol solution control group (GF group); (iii) gentamicin treatment group (GM group), receiving 100 mg/kg of body weight intraperitoneally (i.p.); and (iv to vi) gentamicin groups also receiving GF, at doses of 6.25, 12.5, and 25 mg/kg, respectively (GM+GF groups). Animals from the GM group had a significant decrease in creatinine clearance and higher levels of urinary protein excretion. This was associated with markers of oxidative stress and nitric oxide production. Also, there were increases of the mRNA levels for proinflammatory cytokines (tumor necrosis factor alpha [TNF-α], interleukin-1β [IL-1β], IL-2, and gamma interferon [IFN-γ]). Histopathological findings of tubular degeneration and inflammatory cell infiltration reinforced GM-induced nephrotoxicity. All these alterations were attenuated by previous oral treatment with GF. Animals from the GM+GF groups showed amelioration in renal function parameters and reduced lipid peroxidation and nitrosative stress, in addition to an increment in the levels of glutathione (GSH) and superoxide dismutase (SOD) activity. Gingerols also promoted significant reductions in mRNA transcription for TNF-α, IL-2, and IFN-γ. These effects were dose dependent. These results demonstrate that GF promotes a nephroprotective effect on GM-mediated nephropathy by oxidative stress, inflammatory processes, and renal dysfunction.

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 The effect of long-term dehydration and subsequent rehydration on markers of inflammation, oxidative stress and apoptosis in the camel kidney

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Mahmoud A. Ali ◽  
Hassan Abu Damir ◽  
Osman M. Ali ◽  
Naheed Amir ◽  
Saeed Tariq ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Water Conservation ◽  
Mesangial Cells ◽  
Expression Level ◽  
Kidney Cortex ◽  
Mrna Levels ◽  
Sod Activity ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
Different Response

Abstract Background Dehydration has deleterious effects in many species, but camels tolerate long periods of water deprivation without serious health compromise. The kidney plays crucial role in water conservation, however, some reports point to elevated kidney function tests in dehydrated camels. In this work, we investigated the effects of dehydration and rehydration on kidney cortex and medulla with respect to pro-inflammatory markers, oxidative stress and apoptosis along with corresponding gene expression. Results The cytokines IL-1β and IL-18 levels were significantly elevated in the kidney cortex of dehydrated camel, possibly expressed by tubular epithelium, podocytes and/or mesangial cells. Elevation of IL-18 persisted after rehydration. Dehydration induced oxidative stress in kidney cortex evident by significant increases in MDA and GSH, but significant decreases in SOD and CAT. In the medulla, CAT decreased significantly, but MDA, GSH and SOD levels were not affected. Rehydration abolished the oxidative stress. In parallel with the increased levels of MDA, we observed increased levels of PTGS1 mRNA, in MDA synthesis pathway. GCLC mRNA expression level, involved in GSH synthesis, was upregulated in kidney cortex by rehydration. However, both SOD1 and SOD3 mRNA levels dropped, in parallel with SOD activity, in the cortex by dehydration. There were significant increases in caspases 3 and 9, p53 and PARP1, indicating apoptosis was triggered by intrinsic pathway. Expression of BCL2l1 mRNA levels, encoding for BCL-xL, was down regulated by dehydration in cortex. CASP3 expression level increased significantly in medulla by dehydration and continued after rehydration whereas TP53 expression increased in cortex by rehydration. Changes in caspase 8 and TNF-α were negligible to instigate extrinsic apoptotic trail. Generally, apoptotic markers were extremely variable after rehydration indicating that animals did not fully recover within three days. Conclusions Dehydration causes oxidative stress in kidney cortex and apoptosis in cortex and medulla. Kidney cortex and medulla were not homogeneous in all parameters investigated indicating different response to dehydration/rehydration. Some changes in tested parameters directly correlate with alteration in steady-state mRNA levels.

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

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.

scholarly journals Protective effects of bisoprolol against cadmium-induced myocardial toxicity through inhibition of oxidative stress and NF-κΒ signalling in rats

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Jinhua Liu ◽  
Ying Xie ◽  
Zhujun Han ◽  
Hailong Wang ◽  
Wenhu Xu
Keyword(s):  
Oxidative Stress ◽  
Cardiac Injury ◽  
Therapeutic Drug ◽  
Control Group ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Tissue Samples ◽  
Gum Acacia ◽  
Tnf Α ◽  
Creatine Kinase Mb

Abstract Introduction The aim of the study was to investigate the mitigative effects of bisoprolol (BIS) in cadmium-induced myocardial toxicity on oxidative stress and its inhibitive effect on nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signalling in rats. Material and Methods Male albino Wistar rats were assigned to control, Cd, BIS 2 (2 mg/kg b.w.) and BIS 8 (8 mg/kg b.w.) groups with nine rats in each. Over four weeks, the control group was administered 1% gum acacia, all other groups received 3mg/kg b.w. CdCl2 dissolved in distilled water, and the BIS groups were additionally given bisoprolol in gum acacia. Blood samples were collected for biochemical estimations. Blood pressure and serum biomarker (lactate dehydrogenase, aspirate transaminase, alanine transferase and creatine kinase-MB, enzyme (superoxide dismutase, lipid hydroxy peroxidase, catalase and malondialdehyde), and tumour necrosis factor alpha (TNF-α) concentrations were measured. Western blot analysis was conducted for NF-κB and glutathione S-transferase (GST). After sacrificing the rats, cardiac tissue samples were examined histopathologically. Results Our findings pointed to a significant decrease (P < 0.05) in the studied serum biomarkers and levels of the relevant enzymes in the BIS 8 group compared to the Cd group. A significant decrease (P < 0.05) in NF-kB p65 expression and TNF-α levels was noted in the BIS 8 group relative to the BIS 2 and Cd groups, indicating a reduction at a higher dose. In microscopy, histopathological changes in the cardiac muscles of the BIS 8 group were evident compared to those of the Cd group. Conclusion BIS seemed to have protective effects against cardiac injury induced by cadmium and could be considered a novel therapeutic drug and prognostic biomarker in the pathology of the many cardiovascular diseases caused by heavy metal intake.

scholarly journals Fasudil attenuates Neuro-Inflammation and Oxidative Stress via Rhoa/Rock Pathways in Delayed Neuropsychologic Sequelae Mice Model

2021 ◽  
Author(s):  
Xiang Yan ◽  
Meng Fu ◽  
Ye Gao ◽  
Qin Han ◽  
Shuang Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuroprotective Effect ◽  
Carbon Monoxide Poisoning ◽  
Immunofluorescence Staining ◽  
Control Group ◽  
Spatial Learning And Memory ◽  
Mrna Levels ◽  
Co Poisoning ◽  
Mice Model ◽  
Tnf Α

Abstract Background Delayed neuropsychologic sequelae is common in patients after carbon monoxide poisoning without effective methods worldwide. Fasudil exerts neuroprotective effect and alleviates oxidative stress in some neurodegenerative disorders. However, the mechanism between DNS and FS remains unclear. The study aims to explore the efficacy and mechanism of Fasudil in DNS mice model. Objective The delayed neuropsychologic sequelae model was induced with a hyperbaric oxygen chamber. All rats were randomly assigned to three groups (n=10): air control group (AC), CO poisoning group (CO), and CO poisoning +Fasudil group (CO+FS). Rats in the CO+FS group were given Fasudil (10 mg/kg/day, ip). The morris water maze was documented to estimate spatial learning and memory of mice. The demyelination state in brain was observed through LFB staining. The protein of MBP was examined with immunofluorescence staining. The levels of IL-6, TNF-α, TGF-β, SOD, and MDA were examined by ELISA. The mRNA levels of Rho, ROCK2, MLC1 and MYPT1 were analyzed by rt-PCR. Result The cognitive impairment in the CO+FS group were significantly reduced than those of the CO group (P<0.05). LFB staining and immunofluorescence staining of MBP results showed that FS significantly treatment attenuated demyelination (P<0.05). Compared with the CO group, the levels of TNF-α, IL-6, MDA, ROCK2, MLC1, and MYPT1 significantly decreased (P<0.05), and the levels of SOD were significantly increased in the CO+FS group (P<0.05). Conclusion In a word, Fasudil attenuated delayed neuropsychologic sequelae by inhibiting inflammation, oxidative stress and downregulating Rho/ROCK pathway in DNS mice model. We conclude that Fasudil may be a novel treatment for delayed neuropsychologic sequelae.

scholarly journals Co-Exposure of Cardiomyocytes to IFN-γ and TNF-α Induces Mitochondrial Dysfunction and Nitro-Oxidative Stress: Implications for the Pathogenesis of Chronic Chagas Disease Cardiomyopathy

2021 ◽  
Vol 12 ◽  
Author(s):  
João Paulo Silva Nunes ◽  
Pauline Andrieux ◽  
Pauline Brochet ◽  
Rafael Ribeiro Almeida ◽  
Eduardo Kitano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Mitochondrial Dysfunction ◽  
Chagas Disease ◽  
Nitrosative Stress ◽  
Acid Oxidation ◽  
Oxidative And Nitrosative Stress ◽  
Human Cardiomyocytes ◽  
Tnf Α ◽  
Ifn Γ

Infection by the protozoan Trypanosoma cruzi causes Chagas disease cardiomyopathy (CCC) and can lead to arrhythmia, heart failure and death. Chagas disease affects 8 million people worldwide, and chronic production of the cytokines IFN-γ and TNF-α by T cells together with mitochondrial dysfunction are important players for the poor prognosis of the disease. Mitochondria occupy 40% of the cardiomyocytes volume and produce 95% of cellular ATP that sustain the life-long cycles of heart contraction. As IFN-γ and TNF-α have been described to affect mitochondrial function, we hypothesized that IFN-γ and TNF-α are involved in the myocardial mitochondrial dysfunction observed in CCC patients. In this study, we quantified markers of mitochondrial dysfunction and nitro-oxidative stress in CCC heart tissue and in IFN-γ/TNF-α-stimulated AC-16 human cardiomyocytes. We found that CCC myocardium displayed increased levels of nitro-oxidative stress and reduced mitochondrial DNA as compared with myocardial tissue from patients with dilated cardiomyopathy (DCM). IFN-γ/TNF-α treatment of AC-16 cardiomyocytes induced increased nitro-oxidative stress and decreased the mitochondrial membrane potential (ΔΨm). We found that the STAT1/NF-κB/NOS2 axis is involved in the IFN-γ/TNF-α-induced decrease of ΔΨm in AC-16 cardiomyocytes. Furthermore, treatment with mitochondria-sparing agonists of AMPK, NRF2 and SIRT1 rescues ΔΨm in IFN-γ/TNF-α-stimulated cells. Proteomic and gene expression analyses revealed that IFN-γ/TNF-α-treated cells corroborate mitochondrial dysfunction, transmembrane potential of mitochondria, altered fatty acid metabolism and cardiac necrosis/cell death. Functional assays conducted on Seahorse respirometer showed that cytokine-stimulated cells display decreased glycolytic and mitochondrial ATP production, dependency of fatty acid oxidation as well as increased proton leak and non-mitochondrial oxygen consumption. Together, our results suggest that IFN-γ and TNF-α cause direct damage to cardiomyocytes’ mitochondria by promoting oxidative and nitrosative stress and impairing energy production pathways. We hypothesize that treatment with agonists of AMPK, NRF2 and SIRT1 might be an approach to ameliorate the progression of Chagas disease cardiomyopathy.

scholarly journals Effects of dietary licorice extract on serum Biochemical index, tissues antioxidant capacity and immunity function of weaned piglets

2020 ◽  
Author(s):  
You Ting ◽  
Tang Jia Yong ◽  
Jia Gang ◽  
Liu Guang Mang ◽  
Tian Gang ◽  
...  
Keyword(s):  
Antioxidant Capacity ◽  
Density Lipoprotein ◽  
Control Group ◽  
Mrna Levels ◽  
Weaned Piglets ◽  
Sod Activity ◽  
Inflammatory Genes ◽  
Tnf Α ◽  
Licorice Extract ◽  
Serum Biochemical

Abstract Background: This study investigated the effects of dietary licorice extract (LE) on antioxidant capacity and immunity in weaned piglets. A total of 96 DLY (Duroc × Landrace × Yorkshire) weaned piglets were randomly assigned to four treatments. The control group were fed a corn–soybean meal-based diet (basal diet, BD), and three LE level groups were fed on BD supplied with 50、150 and 250 mg/kg LE. The trial lasted 5 weeks. At day 35, six piglets per treatment were killed and blood, liver, spleen, and thymus were collected.Results: The result showed that: 1)Dietary LE increased (P < 0.05) activity of the alkaline phosphatase (ALP) and reduced (P < 0.05) the activity of glutamic oxalacetic transaminase (AST), 50 mg / kg LE reduced (P < 0.05) total cholesterol (TC) and high density lipoprotein cholesterol (HDL-C) in serum. 2) The addition of 150 and 250 mg / kg LE increased (P < 0.05) glutathion peroxidase (GSH-Px) activity in liver and spleen, increased (P < 0.05) the total antioxidant capacity (T-AOC) in serum and spleen . 50 mg / kg LE increased (P < 0.05) the total superoxide dismutase (T-SOD) activity in serum. Three doses of LE reduced (P < 0.05) serum malondialdehyde content (MDA). 3) 150 mg / kg LE increased (P < 0.05) serum IgG level. 4) Dietary LE down-regulated (P < 0.05) the mRNA levels of 7 immune-related genes (IL-6, IL-8, IL-10, IL-1β, TNF-α, MCP-1, ICAM-1) in the thymus; 50 mg / kg LE and 150 mg / kg LE down-regulated (P < 0.05) the mRNA levels of TNF-α, while 250 mg / kg LE up-regulated the mRNA levels of 2 inflammatory genes (IL-1β, and ICAM-1) in the spleen; three levels of LE down-regulated (P < 0.05 the mRNA levels of 3 inflammatory genes (IL-6, TNF-α, ICAM-1) in the liver.Conclusions: In summary, LE supplementation regulates the activity of serum biochemical enzyme, improves the antioxidant capacity and immune function of in serum, liver, spleen and thymus, those improvement may contributes to the promotion of growth performance of weaned piglets. In general, 150 mg / kg LE exhibits better effect.

Opium may affect coronary artery disease by inducing inflammation but not through the expression of CD9, CD36, and CD68

2021 ◽  
pp. jim-2021-001935
Author(s):  
Mohammad Amin Momeni-Moghaddam ◽  
Gholamreza Asadikaram ◽  
Mohammad Masoumi ◽  
Erfan Sadeghi ◽  
Hamed Akbari ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Messenger Rna ◽  
Molecular Mechanisms ◽  
Control Group ◽  
Mrna Levels ◽  
Tnf Α ◽  
Opium Addiction ◽  
Ifn Γ ◽  
Artery Disease

The molecular mechanisms of opium with regard to coronary artery disease (CAD) have not yet been determined. The aim of the present study was to evaluate the effect of opium on the expression of scavenger receptors including CD36, CD68, and CD9 tetraspanin in monocytes and the plasma levels of tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), malondialdehyde (MDA), and nitric oxide metabolites (NOx) in patients with CAD with and without opium addiction. This case–control study was conducted in three groups: (1) opium-addicted patients with CAD (CAD+OA, n=30); (2) patients with CAD with no opium addiction (CAD, n=30); and (3) individuals without CAD and opium addiction as the control group (Ctrl, n=17). Protein and messenger RNA (mRNA) levels of CD9, CD36, and CD68 were evaluated by flow cytometry and reverse transcription-quantitative PCR methods, respectively. Consumption of atorvastatin, aspirin, and glyceryl trinitrate was found to be higher in the CAD groups compared with the control group. The plasma level of TNF-α was significantly higher in the CAD+OA group than in the CAD and Ctrl groups (p=0.001 and p=0.005, respectively). MDA levels significantly increased in the CAD and CAD+OA groups in comparison with the Ctrl group (p=0.010 and p=0.002, respectively). No significant differences were found in CD9, CD36, CD68, IFN-γ, and NOx between the three groups. The findings demonstrated that opium did not have a significant effect on the expression of CD36, CD68, and CD9 at the gene and protein levels, but it might be involved in the development of CAD by inducing inflammation through other mechanisms.

Erythropoietic Stimuli and Response in Hereditary Spherocytosis

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5377-5377
Author(s):  
Susana Rocha ◽  
Petronila Rocha-Pereira ◽  
Elisabeth Bayer Castro ◽  
Esmeralda Cleto ◽  
Fátima Ferreira ◽  
...  
Keyword(s):  
Hemolytic Anemia ◽  
Hereditary Spherocytosis ◽  
Reticulocyte Count ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Mean Cell Volume ◽  
Tnf Α ◽  
Immune Hemolytic Anemia ◽  
Ifn Γ ◽  
Erythropoietic Response

Abstract Hereditary Spherocytosis (HS) is the most common non-immune hemolytic anemia in Europe. HS ranges from assymptomatic to transfusion-dependent hemolytic anemia and is clinically classified as mild, moderate or severe. Clinical, biochemical and molecular heterogeneous patterns are HS trademarks. In a previous work, we reported that in HS patients the erythropoietic response appears to be impaired in the more severe cases of the disease, since erythropoietin (EPO) levels did not correlate with reticulocyte count or with reticulocyte production index (RPI) [Rocha S. et al. (2005) Br J Haematol. 131(4):534]. It is known that spherocytes are removed by splenic macrophages. The activation of these cells is associated with cytokine release, namely, tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ), both known as EPO inhibitors. The aim of our work was to evaluate the erythropoietic stimuli and response according to HS severity and to clarify the role of these cytokines in HS. We studied 31 HS patients and 25 healthy individuals as the control group. The HS group included only unsplenectomised patients classified as presenting mild (n=19), moderate (n=9) or severe HS (n=3) according to the Guidelines for the diagnosis and management of hereditary spherocytosis [Bolton-Maggs et al. (2004) Br J Haematol. 126(4):455]. The basic hematological study was performed in all samples, as well as the reticulocyte count and RPI calculation; the plasma levels of EPO and soluble transferrin receptor (sTfR) (as markers of erythropoietic stimuli), of bilirubin (as a marker of hemolysis) and of TNF-α and IFN-γ (known as EPO inhibitors) were also determined. Data was analysed according to the severity of HS and versus the control group. Erythrocyte count, hemoglobin concentration, hematocrit and mean cell volume were found to be significantly lower in patients than in controls and their values decreased with HS severity; for MCHC, RDW, reticulocytes, RPI, bilirubin, EPO and sTfR patients presented significantly higher values than controls, and their values increased with HS severity. However, the increment in EPO and sTfR levels was more marked than for reticulocytes and RPI. As for TNF-α and IFN-γ no differences were found between patients and controls or between HS severities; no correlations with the other studied variables were observed. In mild HS patients, sTfR was found to be statistically and positively correlated with reticulocytes (r=0.783; p&lt;0.001), RPI (r=0.748; p&lt;0.001) and bilirubin (r=0.870; p&lt;0.001); in patients with more severe forms (moderate and severe HS) these correlations were lower and only a statistically and positively correlation between sTfR and reticulocytes (r=0.657; p&lt;0.05) was found. Our results confirm the inadequate erythropoietic response in the more severe cases of HS, given that, the erythropoietic stimuli (shown by higher EPO, sTfR and indirectly, by bilirubin levels) was not able to trigger an adequate erythropoietic response as shown by the reticulocyte number and RPI, as occured in mild HS patients. Our hypothesis, that this disturbance could be due to an increase in TNF-α and IFN-γ, was not confirmed, as we did not found any significant increase in these cytokines that could explain the non adequate erythropoietic response in moderate/severe HS patients. In conclusion, the erythropoietic stimuli seem to increase with HS severity; however, the response to that stimulus appears to be impaired in the more severe cases of HS. Further studies are needed to clarify this erythropoietic disturbance in HS patients, which may contribute to the severity of the clinical presentation of the disease.

Tangeretin Inhibits Oxidative Stress and Inflammation via Upregulating Nrf-2 Signaling Pathway in Collagen-Induced Arthritic Rats

Pharmacology ◽  
2019 ◽  
Vol 104 (3-4) ◽  
pp. 187-195 ◽  
Author(s):  
Xing Li ◽  
Peigen Xie ◽  
Yu Hou ◽  
Shudong Chen ◽  
Peiheng He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Chinese Herb ◽  
Biological Properties ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Ifn Γ ◽  
Anti Inflammatory

Background/Aims: Tangeretin (TAN), a major phytochemical in tangerine peels and an important Chinese herb, has multiple biological properties, especially antioxidative and anti-inflammatory effects. However, the mechanisms remain unclear. Based on these findings, the aim of the present study was to assess the antioxidant and anti-inflammatory properties of TAN in bovine type II collagen-induced arthritis rats. Methods: TAN (50 mg/kg) was given orally once daily for 14 days. The effects of treatment were evaluated by biochemical assay (articular elastase, myeloperoxidase, end products of lipid peroxidation [MDA], antioxidant enzyme, such as superoxide dismutase, catalase, glutathione), nitric oxide, and inflammatory cytokines (interleukin-1β [IL-1β], ­IL-10, tumor necrosis factor-alpha [TNF-α], interferon-γ [IFN-γ], and prostaglandin E2 [PGE2]). The protective effects of TAN against rheumatoid arthritis (RA) were evident from the decrease in arthritis scoring. Furthermore, the Nrf-2 signaling pathway was assessed to illustrate the molecular mechanism. Results: TAN had therapeutic effects on RA by decreasing the oxidative stress damage and regulating inflammatory cytokine expression, including suppression of the accumulation of MDA products, decreasing the IL-1β, TNF-α, IFN-γ, and PGE2 levels, enhancing the IL-10 and the activity of antioxidant enzymes, which was through upregulating Nrf-2 signaling pathway. Conclusion: TAN might have potential as a therapeutic agent for the treatment of RA.

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