scholarly journals Anti-inflammatory effect of gold nanoparticles supported on metal oxides

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takashi Fujita ◽  
Maeva Zysman ◽  
Dan Elgrabli ◽  
Toru Murayama ◽  
Masatake Haruta ◽  
...  
Keyword(s):  
Chemical Nature ◽  
Inflammatory Mediator ◽  
Catalytic Performance ◽  
Phagocytic Capacity ◽  
Au Nps ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Inflammatory Profile ◽  
Particle Internalization ◽  
Inflammatory Effect

AbstractGold (Au) can be deposited as nanoparticles (NPs) smaller than 10 nm in diameter on a variety of metal oxide (MOx) NPs. Au/MOx have high catalytic performance and selective oxidation capacity which could have implications in terms of biological activity, and more specifically in modulation of the inflammatory reaction. Therefore, the aim of this study was to examine the effect of Au/TiO2, Au/ZrO2 and Au/CeO2 on viability, phagocytic capacity and inflammatory profile (TNF-α and IL-1β secretion) of murine macrophages. The most important result of this study is an anti-inflammatory effect of Au/MOx depending on the MOx nature with particle internalization and no alteration of cell viability and phagocytosis. The effect was dependent on the MOx NPs chemical nature (Au/TiO2 > Au/ZrO2 > Au/CeO2 if we consider the number of cytokines whose concentration was reduced by the NPs), and on the inflammatory mediator considered. The effect of Au/TiO2 NPs was not related to Au NPs size (at least in the case of Au/TiO2 NPs in the range of 3–8 nm). To the best of our knowledge, this is the first demonstration of an anti-inflammatory effect of Au/MOx.

scholarly journals Anti-Inflammatory Effect of Gold Nanoparticles Supported on Metal Oxides 

2021 ◽  
Author(s):  
Takeshi Fujita ◽  
Maéva ZYSMAN ◽  
Dan Elgrabli ◽  
Toru Murayama ◽  
Masatake Haruta ◽  
...  
Keyword(s):  
Chemical Nature ◽  
Inflammatory Mediator ◽  
Catalytic Performance ◽  
Phagocytic Capacity ◽  
Au Nps ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Inflammatory Profile ◽  
Particle Internalization ◽  
Inflammatory Effect

Abstract Gold (Au) can be deposited as nanoparticles (NPs) smaller than 10 nm in diameter on a variety of metal oxide (MOx) NPs. Au/MOx NPs have high catalytic performance and selective oxidation capacity which could have implications in terms of biological activity, and more specifically in modulation of the inflammatory reaction. Therefore, the aim of this study was to examine the effect of Au/TiO2, Au/ZrO2 and Au/Ce/O2 on viability, phagocytic capacity and inflammatory profile (TNF-α and IL-1β secretion) of murine macrophages. The most important result of this study is an anti-inflammatory effect of Au/MOx NPs depending on the MOx nature with particle internalization and no alteration of cell viability and phagocytosis. The effect was dependent on the MOx NPs chemical nature (Au/TiO2> Au/ZrO2> Au/CeO2 if we consider the number of cytokines whose concentration was reduced by the NPs), and on the inflammatory mediator considered. The effect of Au/TiO2 NPs was not related to Au NPs size (at least in the case of Au/TiO2 NPs in the range of 3-8 nm). To the best of our knowledge, this is the first demonstration of an anti-inflammatory effect of Au/MOx NPs.

scholarly journals Dipterocarpus tuberculatus Roxb. Ethanol Extract Has Anti-Inflammatory and Hepatoprotective Effects In Vitro and In Vivo by Targeting the IRAK1/AP-1 Pathway

Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2529
Author(s):  
Haeyeop Kim ◽  
Woo Seok Yang ◽  
Khin Myo Htwe ◽  
Mi-Nam Lee ◽  
Young-Dong Kim ◽  
...  
Keyword(s):  
Ethanol Extract ◽  
Serum Levels ◽  
Hepatoprotective Activity ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Related Proteins ◽  
Pro Inflammatory Cytokines ◽  
Inflammatory Effect

Dipterocarpus tuberculatus Roxb. has been used traditionally as a remedy for many diseases, especially inflammation. Therefore, we analyzed and explored the mechanism of the anti-inflammatory effect of a Dipterocarpus tuberculatus Roxb. ethanol extract (Dt-EE). Dt-EE clearly and dose-dependently inhibited the expression of pro-inflammatory cytokines such as IL-6, TNF-α, and IL-1β in lipopolysaccharide (LPS)-treated RAW264.7 cells. Also, Dt-EE suppressed the activation of the MyD88/TRIF-mediated AP-1 pathway and the AP-1 pathway related proteins JNK2, MKK4/7, and TAK1, which occurred as a result of inhibiting the kinase activity of IRAK1 and IRAK4, the most upstream factors of the AP-1 pathway. Finally, Dt-EE displayed hepatoprotective activity in a mouse model of hepatitis induced with LPS/D-galactosamine (D-GalN) through decreasing the serum levels of alanine aminotransferase and suppressing the activation of JNK and IRAK1. Therefore, our results strongly suggest that Dt-EE could be a candidate anti-inflammatory herbal medicine with IRAK1/AP-1 inhibitory and hepatoprotective properties.

scholarly journals In vitro evidence for the involvement of H2S pathway in the effect of clodronate during inflammatory response

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rosangela Montanaro ◽  
Alessio D’Addona ◽  
Andrea Izzo ◽  
Carlo Ruosi ◽  
Vincenzo Brancaleone
Keyword(s):  
Inflammatory Markers ◽  
In Vitro Study ◽  
Inos Expression ◽  
Beneficial Effects ◽  
Tnf Α ◽  
Inflammatory State ◽  
Anti Inflammatory ◽  
Underlying Mechanisms ◽  
Inflammatory Effect

AbstractClodronate is a bisphosphonate agent commonly used as anti-osteoporotic drug. Throughout its use, additional anti-inflammatory and analgesic properties have been reported, although the benefits described in the literature could not solely relate to their inhibition of bone resorption. Thus, the purpose of our in vitro study is to investigate whether there are underlying mechanisms explaining the anti-inflammatory effect of clodronate and possibly involving hydrogen sulphide (H2S). Immortalised fibroblast-like synoviocyte cells (K4IM) were cultured and treated with clodronate in presence of TNF-α. Clodronate significantly modulated iNOS expression elicited by TNF-α. Inflammatory markers induced by TNF-α, including IL-1, IL-6, MCP-1 and RANTES, were also suppressed following administration of clodronate. Furthermore, the reduction in enzymatic biosynthesis of CSE-derived H2S, together with the reduction in CSE expression associated with TNF-α treatment, was reverted by clodronate, thus rescuing endogenous H2S pathway activity. Clodronate displays antinflammatory properties through the modulation of H2S pathway and cytokines levels, thus assuring the control of the inflammatory state. Although further investigation is needed to stress out how clodronate exerts its control on H2S pathway, here we showed for the first the involvement of H2S in the additive beneficial effects observed following clodronate therapy.

Intratracheal perfluorocarbons diminish LPS-induced increase in systemic TNF-α

2008 ◽  
Vol 294 (6) ◽  
pp. L1043-L1048 ◽  
Author(s):  
Wolfram Burkhardt ◽  
Petra Koehne ◽  
Heide Wissel ◽  
Susanne Graf ◽  
Hans Proquitté ◽  
...  
Keyword(s):  
Histological Evaluation ◽  
Partial Liquid Ventilation ◽  
Liquid Ventilation ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Spontaneously Breathing ◽  
Lower Expression ◽  
Mechanical Barrier ◽  
Low Serum ◽  
Inflammatory Effect

Perfluorocarbons (PFC) reduce the production of various inflammatory cytokines, including TNF-α. The anti-inflammatory effect is not entirely understood. If anti-inflammatory properties are caused by a mechanical barrier, PFC in the alveoli should have no effect on the inflammatory response to intravenous LPS administration. To test that hypothesis, rats ( n = 31) were administered LPS intravenously and were either spontaneously breathing (Spont), conventionally ventilated (CMV), or receiving partial liquid ventilation (PLV). Serum concentration of TNF-α was measured. The pulmonary expressions of TNF-α and TNF-α receptor 1 protein and of TNF-α and ICAM-1 mRNA were determined. LPS caused a significant ( P < 0.001) increase in serum TNF-α. Serum TNF-α concentration was similar in LPS/Spont (525 ± 180 pg/ml) and LPS/CMV (504 ± 154 pg/ml) but was significantly ( P < 0.001) lower in animals of the LPS/PLV group (274 ± 101 pg/ml). Immunohistochemical data on TNF-α protein expression showed a LPS-induced increase in TNF-α and TNF-α receptor 1 expression that was diminished by partial liquid ventilation. PCR measurements revealed a lower expression of TNF-α and ICAM-1 mRNA in LPS/PLV than in LPS/CMV or LPS/Spont animals. Semiquantitative histological evaluation revealed only minor alveolar inflammation with no significant differences between the groups. Low serum TNF-α concentration in PFC-treated animals is most likely explained by a decreased production of TNF-α in the lung.

scholarly journals Accumulation of Non-steroidal Anti-inflammatory Drugs by Gingival Fibroblasts

2006 ◽  
Vol 85 (5) ◽  
pp. 452-456 ◽  
Author(s):  
M.M. Zavarella ◽  
O. Gbemi ◽  
J.D. Walters
Keyword(s):  
Steady State ◽  
Connective Tissue ◽  
Inflammatory Mediator ◽  
Dependent Manner ◽  
Gingival Fibroblasts ◽  
Temperature Dependent ◽  
Tnf Α ◽  
Steady State Levels ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Non-steroidal anti-inflammatory drugs (NSAIDs) are used to manage pain and inflammatory disorders. We hypothesized that gingival fibroblasts actively accumulate NSAIDs and enhance their levels in gingival connective tissue. Using fluorescence to monitor NSAID transport, we demonstrated that cultured gingival fibroblasts transport naproxen in a saturable, temperature-dependent manner with a Km of 127 μg/mL and a Vmax of 1.42 ng/min/μg protein. At steady state, the intracellular/extracellular concentration ratio was 1.9 for naproxen and 7.2 for ibuprofen. Naproxen transport was most efficient at neutral pH and was significantly enhanced upon cell treatment with TNF-α. In humans, systemically administered naproxen attained steady-state levels of 61.9 μg/mL in blood and 9.4 μg/g in healthy gingival connective tissue, while ibuprofen attained levels of 2.3 μg/mL and 1.5 μg/g, respectively. Thus, gingival fibroblasts possess transporters for NSAIDs that are up-regulated by an inflammatory mediator, but there is no evidence that they contribute to elevated NSAID levels in healthy gingiva.

scholarly journals Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages

1992 ◽  
Vol 1 (6) ◽  
pp. 375-377 ◽  
Author(s):  
Fang Jun ◽  
Zheng Qin Yue ◽  
Wang Hong Bin ◽  
Ju Dian Wen ◽  
Yi Yang Hua
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Inflammatory Mediator ◽  
Platelet Activating Factor ◽  
Peritoneal Macrophages ◽  
Dependent Manner ◽  
Anti Inflammatory ◽  
Dose Dependent ◽  
Necrosis Factor ◽  
Inflammatory Effect

Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta. Previous experiments showed that it had strong anti-inflammatory effects. Tumour necrosis factor (TNF) is an important inflammatory mediator. In order to study the mechanism of the anti-inflammatory effect of EsA, it was determined whether TNF production from macrophages was altered by EsA under lipopolysaccharide (LPS) stimulated conditions. EsA was found to decrease both extracellular and cell associated TNF production in a dose dependent manner at concentrations higher than 1 μmol/l EsA. Previous studies have showed that EsA reduced the releasing of platelet activating factor (PAF) from rat macrophages. The reducing effects of EsA on the release of TNF and PAF may explain its anti-inflammatory effect.

Vanillin protects lipopolysaccharide-induced acute lung injury by inhibiting ERK1/2, p38 and NF-κB pathway

2019 ◽  
Vol 11 (16) ◽  
pp. 2081-2094 ◽  
Author(s):  
Tingting Guo ◽  
Zhenzhong Su ◽  
Qi Wang ◽  
Wei Hou ◽  
Junyao Li ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Western Blot ◽  
Lung Inflammation ◽  
Macrophage Activation ◽  
Myeloperoxidase Activity ◽  
Histopathological Changes ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Aim: Thus far, the anti-inflammatory effect of vanillin in acute lung injury (ALI) has not been studied. This study aimed to investigate the effect of vanillin in lipopolysaccharide (LPS)-induced ALI. Results & methodology: Our study detected the anti-inflammatory effects of vanillin by ELISA and western blot, respectively. Pretreatment of mice with vanillin significantly attenuated LPS-stimulated lung histopathological changes, myeloperoxidase activity and expression levels of proinflammatory cytokines by inhibiting the phosphorylation activities of ERK1/2, p38, AKT and NF-κB p65. In addition, vanillin inhibited LPS-induced TNF-α and IL-6 expression in RAW264.7 cells via ERK1/2, p38 and NF-κB signaling. Conclusion: Vanillin can inhibit macrophage activation and lung inflammation, which suggests new insights for clinical treatment of ALI.

Apoptosis perturbations and expression of regulatory inflammatory factors in cisplatin-depleted rat livers under l-arginine protection

2019 ◽  
Vol 97 (5) ◽  
pp. 359-369 ◽  
Author(s):  
Rehab M. El-Sayed ◽  
Hebatalla I. Ahmed ◽  
Abd El-Lateef S. Abd El-Lateef ◽  
Azza A. Ali
Keyword(s):  
Liver Function ◽  
Hepatic Injury ◽  
Inflammatory Factors ◽  
Protective Effects ◽  
Tnf Α ◽  
Apoptotic Marker ◽  
Apoptosis Markers ◽  
Anti Inflammatory ◽  
Rat Livers ◽  
Inflammatory Effect

Hepatic injury is one of the most common complications associated with cisplatin (CIS) use. Recently, liver protection lines are being discovered to stop the hepatic cell death due to inflammatory and apoptotic perturbations. l-arginine has protective effects in several models of liver injury. This study was designed to investigate the possible protective effect of l-arginine against CIS-induced acute hepatic injury in rats. Rats were divided into 4 groups: control, l-arginine, CIS, l-arginine + CIS. Liver function, oxidative stress, inflammatory cytokines, and apoptosis markers were assessed. l-arginine pretreatment protected the liver against CIS-induced toxicity as indicated by significantly alleviating the changes in liver function along with restoration of the antioxidant status. This finding was confirmed with the markedly improved pathological changes. l-arginine showed anti-inflammatory effect through the reduction of liver expression of iNOS, TNF-α, and NF-κβ, which were ameliorated to significant levels. Furthermore, l-arginine administration downregulated the liver expression of the apoptotic marker, caspase-3. The results recommend l-arginine as a hepatoprotective agent against CIS toxicity. Mostly, this hepatoprotective effect of l-arginine involved anti-inflammatory and anti-apoptotic activities.

scholarly journals Obesity Affects β2 Adrenergic Regulation of the Inflammatory Profile and Phenotype of Circulating Monocytes from Exercised Animals

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2630 ◽  
Author(s):  
Isabel Gálvez ◽  
Leticia Martín-Cordero ◽  
María Dolores Hinchado ◽  
Alberto Álvarez-Barrientos ◽  
Eduardo Ortega
Keyword(s):  
Inflammatory Response ◽  
Adrenergic Receptor ◽  
Acute Exercise ◽  
Inflammatory Responses ◽  
Adrenergic Regulation ◽  
Immune Stress ◽  
Β2 Adrenergic Receptor ◽  
Anti Inflammatory ◽  
Inflammatory Profile ◽  
Inflammatory Effect

Anomalous immune/inflammatory responses in obesity take place along with alterations in the neuroendocrine responses and dysregulation in the immune/stress feedback mechanisms. Exercise is a potential anti-inflammatory strategy in this context, but the influence of exercise on the β2 adrenergic regulation of the monocyte-mediated inflammatory response in obesity remains completely unknown. The first objective of this study was to analyze the effect of exercise on the inflammatory profile and phenotype of monocytes from obese and lean animals, and the second aim was to determine whether obesity could affect monocytes’ inflammatory response to β2 adrenergic activation in exercised animals. C57BL/6J mice were allocated to different lean or obese groups: sedentary, with acute exercise, or with regular exercise. The inflammatory profile and phenotype of their circulating monocytes were evaluated by flow cytometry in the presence or absence of the selective β2 adrenergic receptor agonist terbutaline. Exercise caused an anti-inflammatory effect in obese individuals and a pro-inflammatory effect in lean individuals. β2 adrenergic receptor stimulation exerted a global pro-inflammatory effect in monocytes from exercised obese animals and an anti-inflammatory effect in monocytes from exercised lean animals. Thus, β2 adrenergic regulation of inflammation in monocytes from exercised animals seems to depend on the inflammatory basal set-point.

scholarly journals Anti-Inflammatory Effect of Musa acuminata Stem

2020 ◽  
Vol 14 (02) ◽  
pp. 294-298
Author(s):  
Maharani Laillyza Apriasari ◽  
Selviana Rizky Pramitha ◽  
Dewi Puspitasari ◽  
Diah Savitri Ernawati
Keyword(s):  
Treatment Group ◽  
Musa Acuminata ◽  
Control Group ◽  
Control Group Design ◽  
Treatment Groups ◽  
Tnf Α ◽  
Significant Difference ◽  
Anti Inflammatory ◽  
Mucosal Wound ◽  
Inflammatory Effect

Abstract Objective This study was designed to assess the anti-inflammatory effect of Musa acuminata through the expression of tumor necrosis factor-α (TNF-α) and nuclear factor kappa β (NF-κB) after 3 days of application of Musa acuminata stem extract (MASE) gel on oral mucosal wound. Materials and Methods An experimental study with post-test only control group design was conducted. Twenty male Rattus norvegicus (Wistar) were injured on their left buccal mucosa and treated three times a day with MASE gel of varying concentrations: 0% (as control), MASE 25%, MASE 37.5%, and MASE 50%. On day 3, a biopsy was performed on each mucosal wound for later immunohistochemical analysis for the expressions of TNF-α and NF-κB. Results The highest expression of TNF-α was observed in the control group (13.20 ± 1.79), while the lowest was in the treatment group using 50% MASE (6.40 ± 1.14). Meanwhile the comparison between treatment groups did not highlight any significant difference (p > 0.05). The highest expression of NF-κB was observed in the control group (13.20 ± 1.30), whereas the lowest was in the treatment group using MASE 50% (6.40 ± 1.14). NF-κB was significantly lower in the treatment group using MASE 50% when compared with other treatment groups (p < 0.05). Conclusion Application of MASE on mucosal wound reduces the expression of TNF-α and NF-κB at all concentrations. The anti-inflammatory effect of MASE 50% was the strongest one.

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