scholarly journals Anti-Arthritis Effect through the Anti-Inflammatory Effect of Sargassum muticum Extract in Collagen-Induced Arthritic (CIA) Mice

Molecules ◽  
2019 ◽  
Vol 24 (2) ◽  
pp. 276 ◽  
Author(s):  
Hyelin Jeon ◽  
Weon-Jong Yoon ◽  
Young-Min Ham ◽  
Seon-A Yoon ◽  
Se Kang

(1) Background: Rheumatoid arthritis is a chronic autoimmune disease that causes progressive articular damage and functional loss. It is characterized by synovial inflammation that leads to progressive cartilage destruction. For this reason, research on functional foods that reduce the inflammatory response are under progress. (2) Methods: We focused on the anti-inflammatory effects of Sargassum muticum, and confirmed the effect of the extract on the collagen-induced arthritis (CIA) DBA/1J mice model. (3) Results: The extract was given at concentrations of 50, 100, and 200 mg/kg, and the arthritis score and edema volume of the experimental group were significantly different from the CIA group. The level of interleukin (IL)-6, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ were determined in serum and lymphocytes. The expression of these cytokines in the serum remarkably decreased from S. muticum extract (SME)100 mg/kg, and decreased from SME 200 mg/kg in lymphocytes. Also, immunohistochemical analysis of IL-6 and TNF-α in the joints revealed that the inflammatory response was noticeably lower when treated with S. muticum extract. (4) Conclusions: This study provides results of the experiment of S. muticum extract treatment in a mouse model. The treatment was found to contribute to the alleviation of edema and symptoms by reducing the expression of inflammatory cytokines. It was concluded that it may be a useful substance to help in the mitigation of arthritis symptoms.

2021 ◽  
Vol 9 (4) ◽  
pp. 207-224
Author(s):  
Paloma E Pinto ◽  
◽  
Aloisio M Requião-Moura

Renal ischemia is a major problem in the world that lead to renal failure for which no effective treatment is available. Renal ischemia involves a robust inflammatory response, involving up-regulated chemokine expression and leukocyte accumulation, contributes to the mechanism of renal injury and renal failure. IL-37 is a new human cytokine and has an anti-inflammatory function. Currently, it is unknown whether IL-37 suppresses renal inflammatory response to ischemia. We tested the hypothesis that expression of human IL-37 in mouse protects the renal against ischemic injury through suppression of the renal inflammatory response. IL-37 Tg and WT mice were subjected to right renal nephrectomy to induce unilateral model of ischemia the microvascular clamp was positioned around the left renal pedicles. Serum sampling for measurements of TNF-α, IL-1β, Caspase3, MDA, HMGB1, urea and creatinine. Hematoxylin-eosin staining for histological analysis. The resulted data showed that IL-37 has anti-inflammatory effects in renal IRI as evidenced by significant reduction of the inflammatory markers levels TNF-α, IL-1β and HMGB1. IL-37 has potent antioxidant and anti-apoptotic effects with significant reduction in MDA and caspace-3 respectively


2021 ◽  
Vol 9 (1) ◽  
pp. 110-122

Interleukin-32 (IL-32) is discovered as proinflammatory cytokine by inducing IL-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α. However, there are unclear data regarding IL-32β associated with worsening of myocardial injury after cardiac ischemia and reperfusion (I/R). In this study, we investigate the prognostic value of IL-32β in inflammatory response after myocardial injury. Anesthetized mice subjected to the myocardial ischemia for 30 min and 2 hours reperfusion. Expression and Regulation of IL-32β were measured by RNA Isolation and Real-Time Polymerase Chain Reaction, inflammatory response in blood and myocardial tissue, were assayed accordingly by ELISA and Western blotting, while Echo for cardiac elements measurement. The I/R group had a significantly higher expression level of IL-32β (0.643±0.012, vs. sham group 0.121±0.013; P<0.05) and associated with worsen myocardial injury, and low cardiac function. In-conclusion, IL-32β might be a new marker associated with adverse event after myocardial injury and may contribute with cardiac remodeling.


2021 ◽  
Vol 9 (4) ◽  
pp. 207-224

Renal ischemia is a major problem in the world that lead to renal failure for which no effective treatment is available. Renal ischemia involves a robust inflammatory response, involving up-regulated chemokine expression and leukocyte accumulation, contributes to the mechanism of renal injury and renal failure. IL-37 is a new human cytokine and has an anti-inflammatory function. Currently, it is unknown whether IL-37 suppresses renal inflammatory response to ischemia. We tested the hypothesis that expression of human IL-37 in mouse protects the renal against ischemic injury through suppression of the renal inflammatory response. IL-37 Tg and WT mice were subjected to right renal nephrectomy to induce unilateral model of ischemia the microvascular clamp was positioned around the left renal pedicles. Serum sampling for measurements of TNF-α, IL-1β, Caspase3, MDA, HMGB1, urea and creatinine. Hematoxylin-eosin staining for histological analysis. The resulted data showed that IL-37 has anti-inflammatory effects in renal IRI as evidenced by significant reduction of the inflammatory markers levels TNF-α, IL-1β and HMGB1. IL-37 has potent antioxidant and anti-apoptotic effects with significant reduction in MDA and caspace-3 respectively. Keywords: Renal ischemia, IL-37, TNF-α, IL-1β, Caspase-3


2021 ◽  
Vol 9 (4) ◽  
pp. 207-224
Author(s):  
Paloma E. Pinto

Renal ischemia is a major problem in the world that lead to renal failure for which no effective treatment is available. Renal ischemia involves a robust inflammatory response, involving up-regulated chemokine expression and leukocyte accumulation, contributes to the mechanism of renal injury and renal failure. IL-37 is a new human cytokine and has an anti-inflammatory function. Currently, it is unknown whether IL-37 suppresses renal inflammatory response to ischemia. We tested the hypothesis that expression of human IL-37 in mouse protects the renal against ischemic injury through suppression of the renal inflammatory response. IL-37 Tg and WT mice were subjected to right renal nephrectomy to induce unilateral model of ischemia the microvascular clamp was positioned around the left renal pedicles. Serum sampling for measurements of TNF-α, IL-1β, Caspase3, MDA, HMGB1, urea and creatinine. Hematoxylin-eosin staining for histological analysis. The resulted data showed that IL-37 has anti-inflammatory effects in renal IRI as evidenced by significant reduction of the inflammatory markers levels TNF-α, IL-1β and HMGB1. IL-37 has potent antioxidant and anti-apoptotic effects with significant reduction in MDA and caspace-3 respectively.


Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu

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.


2021 ◽  
Vol 22 (14) ◽  
pp. 7482
Author(s):  
Hwan Lee ◽  
Zhiming Liu ◽  
Chi-Su Yoon ◽  
Linsha Dong ◽  
Wonmin Ko ◽  
...  

Aging is associated with immune disregulation and oxidative stress which lead to inflammation and neurodegenerative diseases. We have tried to identify the anti-neuroinflammatory and anti-inflammatory components of Coreopsis lanceolata L. The dried flowers of C. lanceolata were extracted with 70% EtOH, and the obtained extract was divided into CH2Cl2, EtOAc, n-BuOH, and H2O fractions. The CH2Cl2 fraction was separated using silica gel and C-18 column chromatography to yield phenylheptatriyne (1), 2′-hydroxy-3,4,4′-trimethoxychalcone (2), and 4′,7-dimethoxyflavanone (3). Additionally, the EtOAc fraction was subjected to silica gel, C-18, and Sephadex LH-20 column chromatography to yield 8-methoxybutin (4) and leptosidin (5). All the compounds isolated from C. lanceolata inhibited the production of nitric oxide (NO) in LPS-induced BV2 and RAW264.7 cells. In addition, phenylheptatriyne and 4′,7-dimethoxyflavanone reduced the secretion of inflammatory cytokines, tumor necrosis factor alpha (TNF-α), and interleukin (IL)-6. Among them, phenylheptatriyne was significantly downregulated in the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2). Subsequently, phenylheptatriyne also effectively inhibited nuclear factor-kappa B (NF-κB) activation in LPS-stimulated BV2 and RAW264.7 cells. Based on these results, the anti-neuroinflammatory effect of phenylheptatriyne isolated from C. lanceolata was confirmed, which may exert a therapeutic effect in treatment of neuroinflammation-related diseases.


Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 716
Author(s):  
Oksana Sintsova ◽  
Irina Gladkikh ◽  
Anna Klimovich ◽  
Yulia Palikova ◽  
Viktor Palikov ◽  
...  

Currently the TRPV1 (transient receptor potential vanilloid type 1) channel is considered to be one of the main targets for pro-inflammatory mediators including TNF-α. Similarly, the inhibition of TRPV1 activity in the peripheral nervous system affects pro-inflammatory mediator production and enhances analgesia in total. In this study, the analgesic and anti-inflammatory effects of HCRG21, the first peptide blocker of TRPV1, were demonstrated in a mice model of carrageenan-induced paw edema. HCRG21 in doses of 0.1 and 1 mg/kg inhibited edema formation compared to the control, demonstrated complete edema disappearance in 24 h in a dose of 1 mg/kg, and effectively reduced the productionof TNF-α in both doses examined. ELISA analysis of blood taken 24 h after carrageenan administration showed a dramatic cytokine value decrease to 25 pg/mL by HCRG21 versus 100 pg/mL in the negative control group, which was less than the TNF-α level in the intact group (40 pg/mL). The HCRG21 demonstrated potent analgesic effects on the models of mechanical and thermal hyperalgesia in carrageenan-induced paw edema. The HCRG21 relief effect was comparable to that of indomethacin taken orally in a dose of 5 mg/kg, but was superior to this nonsteroidal anti-inflammatory drug (NSAID) in duration (which lasted 24 h) in the mechanical sensitivity experiment. The results confirm the existence of a close relationship between TRPV1 activity and TNF-α production once again, and prove the superior pharmacological potential of TRPV1 blockers and the HCRG21 peptide in particular.


Pharmaceutics ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 143 ◽  
Author(s):  
Jingnan Zhao

Gold nanocages (AuNCs) are biocompatible and porous nanogold particles that have been widely used in biomedical fields. In this study, hyaluronic acid (HA) and peptide- modified gold nanocages (HA-AuNCs/T/P) loaded with 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide (TPCA-1) were prepared to investigate their potential for combating inflammation. TPCA-1 was released from AuNCs, intracellularly when HA was hydrolyzed by hyaluronidase. HA-AuNCs/T/P show a much higher intracellular uptake than AuNCs/T/P, and exhibit a much higher efficacy on the suppression of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) than free TPCA-1, suggesting great improvement to the anti-inflammatory efficacy of TPCA-1 through the application of AuNCs. HA-AuNCs/T/P can also reduce the production of reactive oxygen species in inflammatory cells. This study suggests that HA-AuNCs/T/P may be potential agents for anti-inflammatory treatment, and are worthy of further investigation.


2017 ◽  
Vol 12 (1) ◽  
pp. 35 ◽  
Author(s):  
Dian Ratih Laksmitawati ◽  
Anisa Widyastuti ◽  
Nadia Karami ◽  
Ervi Afifah ◽  
Dwi Davidson Rihibiha ◽  
...  

<p class="Abstract">In this study, the anti-inflammatory potential of <em>Anredera </em>cordifolia and <em>Piper </em>crocatum extracts on lipopolysaccharide-induced murine macrophage cell line (RAW 264.7) was observed. Cell viability assay was performed with MTS assay. Parameters measured to determine the anti-inflammatory activity were interleukin-1β (IL-1β), tumor necrosis factor (TNF)-α, nitric oxide (NO) and IL-6. Both <em>A. </em>cordifolia and<em> P. </em>crocatum at concentration of 50 µg/mL in cell line resulted significant decrease in TNF-α level (250.3 and 242.5 pg/mL respectively). <em>A. </em>cordifolia showed significant decrease in IL-1β level at 50 µg/mL and IL-6 level at 10 µg/mL, whilst <em>P. </em>crocatum  showed significant decrease IL-1β level in three concentrations with lowest level at 50 µg/mL.<em> A. </em>cordifolia showed lowest decrease in NO level at 50 µg/mL but not comparable with normal cells, whilst <em>P. </em>crocatum showed significant decrease in NO level at 50 µg/mL. This research revealed that <em>A. </em>cordifolia and<em> P. </em>crocatum possess the anti-inflammatory potential indicated by the inhibitory activity of the inflammatory mediators including, TNF-α, IL-1β, IL-6, and NO.</p>


2003 ◽  
Vol 12 (6) ◽  
pp. 323-328 ◽  
Author(s):  
Shigeru Abe ◽  
Naho Maruyama ◽  
Kazumi Hayama ◽  
Hiroko Ishibashi ◽  
Shigeharu Inoue ◽  
...  

Background:In aromatherapy, essential oils are used as anti-inflammatory remedies, but experimental studies on their action mechanisms are very limited.Aims:To assess their anti-inflammatory activities, effects of essential oils on neutrophil activation were examinedin vitro.Methods:Neutrophil activation was measured by tumor necrosis factor-alpha (TNF-α)-induced adherence reaction of human peripheral neutrophils.Results:All essential oils tested at 0.1% concentration suppressed TNF-α-induced neutrophil adherence, and, in particular, lemongrass, geranium and spearmint oils clearly lowered the reaction even at 0.0125%. Similar inhibitory activities for the neutrophil adherence were obtained by their major constituent terpenoids: citral, geraniol, citronellol and carvone. In contrast, very popular essential oils, tea tree oil and lavender oil, did not display the inhibitory activity at the concentration.Conclusion:Thus, some essential oils used as anti-inflammatory remedies suppress neutrophil activation by TNF-α at a low concentration (0.0125-0.025%)in vitro.


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