Prophylaxis With Diosmin Mitigates Kidney Damage Induced by Gentamicin in Rats

2021 ◽  
Author(s):  
Seyed Sajad Hossieni Geshnigani ◽  
Masoud Mahdavinia ◽  
Mojtaba Kalantar ◽  
Mehdi Goudarzi ◽  
Layasadat Khorsandi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glutathione Peroxidase ◽  
Bacterial Infections ◽  
Interleukin 1 ◽  
Kidney Injury ◽  
Aminoglycoside Antibiotic ◽  
Tnf Α ◽  
Male Wistar Rats ◽  
Serum Blood Urea Nitrogen ◽  
Factor Α

Abstract Background Gentamicin is a crucial aminoglycoside antibiotic but it is used only to treat severe bacterial infections, because of its high nephrotoxicity among patients. We evaluated the preventive effects of diosmin (as a natural ingredient) on gentamicin-related renal damage in rats. MethodsIn this research, 28 male Wistar rats were assigned to 4 groups: control, gentamicin (100 mg/kg, (i.p.), daily for 1 week), and gentamicin plus diosmin (50mg/kg, p.o., daily for two weeks), diosmin (50mg/kg/day, p.o. for two weeks). After, the final gavage, blood specimens were gathered for determining serum blood urea nitrogen (BUN) and creatinine. kidneys used for biochemical, inflammation and histological test.Results Creatinine, BUN, nitric oxide, malondialdehyde, TNF-α and IL-1β concentrations significantly increased and glutathione, catalase, glutathione peroxidase, and superoxide dismutase activities decreased after gentamicin treatment. Creatinine, BUN, nitric oxide, malondialdehyde, tumour necrosis factor α (TNF-α), interleukin 1 beta (IL-1β) concentrations significantly reduced and glutathione level, catalase and glutathione peroxidase activities significantly increased via co-administration with diosmin. ConclusionDiosmin had ameliorative impacts against gentamicin-related kidney injury that can be owing to its antioxidant, and anti-inflammatory activities.

Molecular Mechanisms of Curcumin in Neuroinflammatory Disorders: A Mini Review of Current Evidences

2019 ◽  
Vol 19 (3) ◽  
pp. 247-258 ◽  
Author(s):  
Mahsa Hatami ◽  
Mina Abdolahi ◽  
Neda Soveyd ◽  
Mahmoud Djalali ◽  
Mansoureh Togha ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
English Language ◽  
Molecular Mechanisms ◽  
Randomized Clinical Trials ◽  
Mitochondrial Dynamics ◽  
Nuclear Factor Κb ◽  
General Term ◽  
Neuroinflammatory Disease ◽  
Tnf Α ◽  
Factor Α

Objective: Neuroinflammatory disease is a general term used to denote the progressive loss of neuronal function or structure. Many neuroinflammatory diseases, including Alzheimer’s, Parkinson’s, and multiple sclerosis (MS), occur due to neuroinflammation. Neuroinflammation increases nuclear factor-κB (NF-κB) levels, cyclooxygenase-2 enzymes and inducible nitric oxide synthase, resulting in the release of inflammatory cytokines, such as interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). It could also lead to cellular deterioration and symptoms of neuroinflammatory diseases. Recent studies have suggested that curcumin (the active ingredient in turmeric) could alleviate the process of neuroinflammatory disease. Thus, the present mini-review was conducted to summarize studies regarding cellular and molecular targets of curcumin relevant to neuroinflammatory disorders. Methods: A literature search strategy was conducted for all English-language literature. Studies that assessed the various properties of curcuminoids in respect of neuroinflammatory disorders were included in this review. Results: The studies have suggested that curcuminoids have significant anti- neuroinflammatory, antioxidant and neuroprotective properties that could attenuate the development and symptom of neuroinflammatory disorders. Curcumin can alleviate neurodegeneration and neuroinflammation through multiple mechanisms, by reducing inflammatory mediators (such as TNF-α, IL-1β, nitric oxide and NF-κB gene expression), and affect mitochondrial dynamics and even epigenetic changes. Conclusion: It is a promising subject of study in the prevention and management of the neuroinflammatory disease. However, controlled, randomized clinical trials are needed to fully evaluate its clinical potential.

scholarly journals Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

Tumor necrosis factor-α and interleukin-1 β levels in recurrent and persistent otitis media with effusion

2002 ◽  
Vol 126 (4) ◽  
pp. 417-422 ◽  
Author(s):  
Sertac Yetiser ◽  
Bulent Satar ◽  
Atilla Gumusgun ◽  
Faruk Unal ◽  
Yalcin Ozkaptan
Keyword(s):  
Tumor Necrosis Factor ◽  
Otitis Media ◽  
Tumor Necrosis ◽  
Otitis Media With Effusion ◽  
Interleukin 1 ◽  
Tertiary Referral Center ◽  
Adenoid Tissue ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

OBJECTIVE: Based on interleukin (IL)-1β and tumor necrosis factor (TNF)-α levels in effusions, our goals were to specify either recurrent or persistent otitis media with effusion (OME) is a mid stage in the development of chronic disease and to identify the factors that have an influence on cytokine levels. STUDY DESIGN: Samples from groups with recurrent (n = 15) and persistent (n = 39) OME were essayed for IL-1 β and TNF-α. Children were also grouped with respect to age, sex, quality of effusion, and the presence of pharyngeal adenoid tissue. SETTING: Tertiary referral center. RESULTS: In recurrent and persistent OME groups, IL-1β was higher than TNF-α ( P < 0.01). IL-β was higher in recurrent OME than in persistent OME ( P < 0.05). CONCLUSION: Recurrent OME seems to be closer to the chronic stage of the disease relative to persistent OME in terms of higher IL-1 β levels. Each exacerbation of acute disease in recurrent otitis media is likely to be mediated by IL-1 β. SIGNIFICANCE: We were able to clarify that recurrent OME is a stage that occurs before chronic OME. Therefore, the prevention of acute attacks in recurrent disease would also impede long-term damage to the middle ear.

Arginase 1 is expressed in myelocytes/metamyelocytes and localized in gelatinase granules of human neutrophils

Blood ◽  
2006 ◽  
Vol 109 (7) ◽  
pp. 3084-3087 ◽  
Author(s):  
Lars C. Jacobsen ◽  
Kim Theilgaard-Mönch ◽  
Erik I. Christensen ◽  
Niels Borregaard
Keyword(s):  
Nitric Oxide ◽  
Immune Responses ◽  
Tissue Regeneration ◽  
Human Neutrophils ◽  
Arginase 1 ◽  
Tnf Α ◽  
Activated Neutrophils ◽  
Factor Α ◽  
Oxide Synthase ◽  
Extracellular Environment

Abstract Arginase 1 (ARG1) metabolizes arginine, thus reducing the availability of arginine as a substrate for nitric oxide synthase (NOS). The decreased production of nitric oxide (NO) by NOS and the production of ornithine by ARG1 affect immune responses and tissue regeneration at sites of infection, respectively. We here demonstrate that ARG1 is synthesized in myelocytes/metamyelocytes and is stored in gelatinase granules. In accordance with this, activated neutrophils coreleased ARG1 and gelatinase to the extracellular environment on stimulation with phorbol-12-myristate 13-acetate (PMA), formyl-methionyl-leucyl-phenylalanine (fMLP), or tumor necrosis factor α (TNF-α). Overall, these findings define ARG1 as a genuine gelatinase granule protein and support a model in which activated neutrophils release ARG1 at sites of infection to modulate immune responses and promote tissue regeneration.

Oxymatrine inhibits lipopolysaccharide-induced inflammation by down-regulating Toll-like receptor 4/nuclear factor-kappa B in macrophages

2015 ◽  
Vol 93 (4) ◽  
pp. 253-260 ◽  
Author(s):  
Yu Zhang ◽  
Ruhong Yan ◽  
Yae Hu
Keyword(s):  
Nitric Oxide ◽  
Interleukin 1 ◽  
Chinese Herb ◽  
Mrna Levels ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Anti Inflammatory

Oxymatrine (OMT) is the quinolizidine alkaloid extracted from the Chinese herb Sophora flavescens Ait. that has many pharmacological effects and is used for the treatment of some inflammatory diseases. In this study, RAW264.7 cells and THP-1 differentiated macrophages were pretreated with various concentrations of OMT at 2 h prior to treatment with lipopolysaccharide (LPS) (1.0 μg/mL) for different durations. We detected the anti-inflammatory effect of OMT in LPS-stimulated macrophages and investigated the molecular mechanism. We showed that OMT pretreatment significantly inhibited the LPS-induced secretion of nitric oxide (NO), interleukin-1 beta (IL-1β), and tumor necrosis factor-alpha (TNF-α) in supernatant, attenuated the mRNA levels of inducible nitric oxide synthase (iNOS), IL-1β, TNF-α, and Toll-like receptor 4 (TLR4), increased TLR4 and phosphorylation of inhibitor of kappa B-alpha (p-IBα) in cytosol, and decreased the nuclear level of nuclear factor-κB (NF-κB) p65 in macrophages. In conclusion, OMT exerts anti-inflammatory properties in LPS-stimulated macrophages by down-regulating the TLR4/NF-κB pathway.

Predisposition to Hyperthyroidism May Be Influenced by Functional TNF-α, IL-1, IL-6, and IL-10 Polymorphisms: A Meta-Analysis

2020 ◽  
Vol 181 (12) ◽  
pp. 956-965
Author(s):  
Hong Ma ◽  
Ting Tan ◽  
Jie Wu ◽  
Juan Chen ◽  
Xiaohong Zhang
Keyword(s):  
Meta Analysis ◽  
Interleukin 1 ◽  
Interleukin 10 ◽  
Interleukin 4 ◽  
Asian Origin ◽  
Tnf Α ◽  
Caucasian Origin ◽  
Meta Analyses ◽  
Factor Α ◽  
Necrosis Factor

<b><i>Background:</i></b> Predisposition to hyperthyroidism may be influenced by functional gene polymorphisms in tumor necrosis factor-α (<i>TNF-α</i>), interleukin-1 (<i>IL-1</i>), interleukin-4 (<i>IL-4</i>), interleukin-6 (<i>IL-6</i>), and interleukin-10 (<i>IL-10</i>). However, the results of the studies published so far remain discrepant, so we conducted a meta-analysis to more robustly investigate relationships between <i>TNF-α</i>/<i>IL-1/IL-4/IL-6/IL-10</i> polymorphisms and predisposition to hyperthyroidism. <b><i>Methods:</i></b> A comprehensive literature retrieval from PubMed, Embase, Web of Science, WanFang, VIP, and CNKI was endorsed by the authors, and 38 studies were found to be eligible for pooled meta-analyses. <b><i>Results:</i></b> We found that genotypic frequencies of <i>TNF-α</i> −308 G/A, <i>IL-1A</i> −889 C/T, <i>IL-6</i> −174 G/C, <i>IL-6</i> −572 G/C, <i>IL-10</i> −819 C/T, and <i>IL-10</i> −1082 A/G polymorphisms among cases were significantly different from those among controls. Moreover, we also found that genotypic frequencies of <i>TNF-α</i> −308 G/A and <i>IL-6</i> −174 G/C polymorphisms among cases of Caucasian origin were significantly different from those among Caucasian controls, and genotypic frequencies of <i>IL-1A</i> −889 C/T, <i>IL-1B</i> −511 C/T, <i>IL-6</i> −174 G/C, <i>IL-6</i> −572 G/C, and <i>IL-10</i> −1,082 A/G polymorphisms among cases of Asian origin were also significantly different from those among Asian controls. <b><i>Conclusions:</i></b> This meta-analysis suggests that <i>TNF-α</i> −308 G/A, <i>IL-1A</i> −889 C/T, <i>IL-1B</i> −511 C/T, <i>IL-6</i> −174 G/C, <i>IL-6</i> −572 G/C, <i>IL-10</i> −819 C/T, and <i>IL-10</i> −1,082 A/G polymorphisms may influence predisposition to hyperthyroidism in certain ethnic groups.

The Augmented Productions of Neopterin and Cytokines from Macrophages/monocytes in vitro

Pteridines ◽  
1996 ◽  
Vol 7 (3) ◽  
pp. 72-76
Author(s):  
Tadashi Lizuka ◽  
Mitsuyo Sasaki ◽  
Hitomi Kamisako ◽  
Ko Oishi ◽  
Shigeru Uemura ◽  
...  
Keyword(s):  
Kawasaki Disease ◽  
Interleukin 1 ◽  
Poly I:C ◽  
Recombinant Interferon ◽  
Preliminary Examination ◽  
Tnf Α ◽  
Ifn Γ ◽  
Factor Α ◽  
Necrosis Factor

Summary In Kawasaki disease patients, increases in excretion of urinary neopterin coincided with fever and monocytosis in peripheral blood. We examined the products of neopterin, tumor necrosis factor-α (TNFα) and Interleukin-1 β (1L-1β) from healthy adult macrophages/monocytes (Mφ>/M), after stimulation with several activators to obtain some understanding of Kawasaki disease. Upon stimulation with either lipopolysaccharide (LPS) or polyinosinate-polycytidylate (Poly I:C), the Mφ/M released neopterin and pyogenic products (TNF-α or 1L-1β). The release of neopterin was eliminated by the addition of the anti-interferon-y antibody. The production of both TNF-α, 1L-1β and neopterin from Mφ/M upon stimulation of LPS was augmented in a co-culture with low dose recombinant interferon-y (rIFN-γ). Upon stimulation with rIFN-γ alone, however, the Mφ/M released neopterin but not the pyogenic products. A preliminary examination failed to detect. any difference in the response of the Mφ/M in adults annd children after stimulation with LPS. We concluded that some endotoxins could trigger the onset of Kawasaki disease and that endogenous IFN-γ can play an important role in the abnormality of Kawasaki disease patients

scholarly journals Inhibition of TNF-α production contributes to the attenuation of LPS-induced hypophagia by pentoxifylline

2000 ◽  
Vol 279 (6) ◽  
pp. R2113-R2120 ◽  
Author(s):  
M. H. Porter ◽  
B. J. Hrupka ◽  
G. Altreuther ◽  
M. Arnold ◽  
W. Langhans
Keyword(s):  
Bacterial Infections ◽  
Tumor Necrosis ◽  
Low Dose ◽  
Potent Inhibitor ◽  
Muramyl Dipeptide ◽  
High Dose ◽  
Tnf Α ◽  
Anorectic Effect ◽  
Factor Α ◽  
Necrosis Factor

Cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) are assumed to mediate anorexia during bacterial infections. To improve our understanding of the role that these two cytokines serve in mediating infection during anorexia, we investigated the ability of pentoxifylline (PTX), a potent inhibitor of TNF-α production, to block the anorectic effects of the bacterial products lipopolysaccharide (LPS) and muramyl dipeptide (MDP) in rats. Intraperitoneally injected PTX (100 mg/kg body wt) completely eliminated the anorectic effect of intraperitoneally injected LPS (100 μg/kg body wt) and attenuated the anorectic effect of a higher dose of intraperitoneally injected LPS (250 μg/kg body wt). Concurrently, PTX pretreatment suppressed low-dose LPS-induced TNF-α production by more than 95% and IL-1β production 39%, as measured by ELISA. Similarly, high-dose LPS-induced TNF-α production was reduced by ∼90%. PTX administration also attenuated the tolerance that is normally observed with a second injection of LPS. In addition, PTX pretreatment attenuated the hypophagic effect of intraperitoneally injected MDP (2 mg/kg body wt) but had no effect on the anorectic response to intraperitoneally injected recombinant human TNF-α (150 ug/kg body wt). The results suggest that suppression of TNF-α production is sufficient to attenuate LPS- and MDP-induced anorexia. This is consistent with the hypothesis that TNF-α plays a major role in the anorexia associated with bacterial infection.

scholarly journals Phytosterols Suppress Phagocytosis and Inhibit Inflammatory Mediators via ERK Pathway on LPS-Triggered Inflammatory Responses in RAW264.7 Macrophages and the Correlation with Their Structure

Foods ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 582 ◽  
Author(s):  
Yuan ◽  
Zhang ◽  
Shen ◽  
Jia ◽  
Xie
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Responses ◽  
Ester Group ◽  
No Production ◽  
Raw264.7 Macrophages ◽  
Extracellular Signal ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase

Phytosterols, found in many commonly consumed foods, exhibit a broad range of physiological activities including anti-inflammatory effects. In this study, the anti-inflammatory effects of ergosterol, β-sitosterol, stigmasterol, campesterol, and ergosterol acetate were investigated in lipopolysaccharide (LPS)-induced RAW264.7 macrophages. Results showed that all phytosterol compounds alleviated the inflammatory reaction in LPS-induced macrophage models; cell phagocytosis, nitric oxide (NO) production, release of tumor necrosis factor-α (TNF-α), and expression and activity of pro-inflammatory mediator cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and phosphorylated extracellular signal-regulated protein kinase (p-ERK) were all inhibited. The anti-inflammatory activity of β-sitosterol was higher than stigmasterol and campesterol, which suggests that phytosterols without a double bond on C-22 and with ethyl on C-24 were more effective. However, inconsistent results were observed upon comparison of ergosterol and ergosterol acetate (hydroxy or ester group on C-3), which suggest that additional research is still needed to ascertain the contribution of structure to their anti-inflammatory effects.

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