scholarly journals Evaluation of the anti-inflammatory effect of telmisartan as an adjuvant therapy to nsaid in the management of knee osteoarthritis; a clinical prospective study

2018 ◽  
Vol 9 (SPL1) ◽  
Author(s):  
Mohammed M Mohammed
Keyword(s):  
Adjuvant Therapy ◽  
Partial Agonist ◽  
Serum Levels ◽  
Joint Disease ◽  
Peroxisome Proliferator ◽  
Knee Oa ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Hs Crp ◽  
Inflammatory Effect

Osteoarthritis (OA)is a degenerative joint disease caused by gradual loss of cartilage. Telmisartan is an Angiotensin II receptor antagonist,and act as a partial agonist on the nuclear peroxisome proliferator-activated receptor-gamma (PPAR-γ),that has been reported to exert anti-inflammatory effects. This study was designed to evaluate the potential anti-inflammatory effect oftelmisartan in patients with knee OA.42 patients with painful knee OA were allocated into 2 groups,group (1): patients treated with naproxen tablets (500 mg/12 hr),telmisartan tablets (40 mg/day) and omeprazole (20 mg/day) for 3 months,while group (2): patients treated with naproxen tablets (500 mg/12hr) and omeprazole (20 mg/day) for 3 months. The serum levels of IL-1β,high-sensitivity C-reactive protein (hs-CRP),TNF-α anderythrocyte sedimentation rate (ESR) were measured before and after 3 months of treatment.Telmisartan when used in combination with naproxen resulted in significant decrease in serum levels of IL-1β and hs-CRP,higher than that produced by naproxen when used alone. The mean TNF-α level and ESR was decreased non-significantly in both study groups. Administration of telmisartan as an adjuvant therapy to naproxen in knee OA patients produced a significant decrease in the serum levels of IL-1β and hs-CRP,though no clear effect on TNF-α and ESR was noticed after 3 months treatment. Accordingly,many promising preventive strategies emerged from the available results since telmisartan relatively reduce the inflammatory burden in OA patients.

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 δ-Tocotrienol, Isolated from Rice Bran, Exerts an Anti-Inflammatory Effect via MAPKs and PPARs Signaling Pathways in Lipopolysaccharide-Stimulated Macrophages

2018 ◽  
Vol 19 (10) ◽  
pp. 3022 ◽  
Author(s):  
Junjun Shen ◽  
Tao Yang ◽  
Youzhi Xu ◽  
Yi Luo ◽  
Xinyue Zhong ◽  
...  
Keyword(s):  
Rice Bran ◽  
Molecular Mechanisms ◽  
Mitogen Activated Protein Kinase ◽  
Peroxisome Proliferator ◽  
Activator Protein 1 ◽  
Peroxisome Proliferator Activated Receptor ◽  
Tnf Α ◽  
Mitogen Activated Protein ◽  
Anti Inflammatory ◽  
Inflammatory Effect

δ-Tocotrienol, an important component of vitamin E, has been reported to possess some physiological functions, such as anticancer and anti-inflammation, however their molecular mechanisms are not clear. In this study, δ-tocotrienol was isolated and purified from rice bran. The anti-inflammatory effect and mechanism of δ-tocotrienol against lipopolysaccharides (LPS) activated pro-inflammatory mediator expressions in RAW264.7 cells were investigated. Results showed that δ-tocotrienol significantly inhibited LPS-stimulated nitric oxide (NO) and proinflammatory cytokine (TNF-α, IFN-γ, IL-1β and IL-6) production and blocked the phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular regulated protein kinases 1/2 (ERK1/2). δ-Tocotrienol repressed the transcriptional activations and translocations of nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1), which were closely related with downregulated cytokine expressions. Meanwhile, δ-tocotrienol also affected the PPAR signal pathway and exerted an anti-inflammatory effect. Taken together, our data showed that δ-tocotrienol inhibited inflammation via mitogen-activated protein kinase (MAPK) and peroxisome proliferator-activated receptor (PPAR) signalings in LPS-stimulated macrophages.

scholarly journals Baicalin Administered Orally After Ischemia/Reperfusion Alleviated Brain Injury in Mice by Inhibiting Inflammation and Edema

2019 ◽  
Vol 14 (5) ◽  
pp. 1934578X1984303
Author(s):  
Byoungho Lee ◽  
Chiyeon Lim ◽  
Sehyun Lim ◽  
Suin Cho
Keyword(s):  
Lipid Peroxidation ◽  
Brain Injury ◽  
Ischemia Reperfusion ◽  
Serum Levels ◽  
Pharmacological Activities ◽  
Once Daily ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Water Contents ◽  
Inflammatory Effect

Baicalin is a natural product isolated from Scutellaria genus and has been reported to have many different pharmacological activities, which include anti-viral, anti-inflammatory, and anti-allergic effects. We investigated the effects of baicalin administered after I/R-induced brain injury in a mouse model. I/R-induced brain injury was induced by MCAO for 2 h. Baicalin was orally administered to mice once daily for 2 consecutive days after 2 h of reperfusion. Single daily oral administrations of baicalin at 10, 30, or 100 mg/kg/day for 2 consecutively days after I/R significantly reduced infarct volumes, edema indices, and water contents in mouse brains, serum levels of AQP-4. IL-1β, TNF-α, and ROS, and lipid peroxidation levels in brain ipsilateral hemispheres were suppressed by baicalin. This result is believed to be due to the anti-inflammatory effect of baicalin and its downregulation of AQP-4 protein expression in affected brain tissues after I/R-induced brain injury in mice.

scholarly journals Zerumbone Suppresses Enterotoxigenic Bacteroides fragilis Infection-Induced Colonic Inflammation through Inhibition of NF-κΒ

2019 ◽  
Vol 20 (18) ◽  
pp. 4560 ◽  
Author(s):  
Soonjae Hwang ◽  
Minjeong Jo ◽  
Ju Eun Hong ◽  
Chan Oh Park ◽  
Chang Gun Lee ◽  
...  
Keyword(s):  
Bacteroides Fragilis ◽  
Serum Levels ◽  
Colonic Inflammation ◽  
Colon Cells ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide ◽  
Inflammatory Effect ◽  
E Cadherin

Enterotoxigenic Bacteroides fragilis (ETBF) is human intestinal commensal bacterium and a potent initiator of colitis through secretion of the metalloprotease Bacteroides fragilis toxin (BFT). BFT induces cleavage of E-cadherin in colon cells, which subsequently leads to NF-κB activation. Zerumbone is a key component of the Zingiber zerumbet (L.) Smith plant and can exhibit anti-bacterial and anti-inflammatory effects. However, whether zerumbone has anti-inflammatory effects in ETBF-induced colitis remains unknown. The aim of this study was to determine the anti-inflammatory effect of orally administered zerumbone in a murine model of ETBF infection. Wild-type C57BL/6 mice were infected with ETBF and orally administered zerumbone (30 or 60 mg/kg) once a day for 7 days. Treatment of ETBF-infected mice with zerumbone prevented weight loss and splenomegaly and reduced colonic inflammation with decreased macrophage infiltration. Zerumbone treatment significantly decreased expression of IL-17A, TNF-α, KC, and inducible nitric oxide synthase (iNOS) in colonic tissues of ETBF-infected mice. In addition, serum levels of KC and nitrite was also diminished. Zerumbone-treated ETBF-infected mice also showed decreased NF-κB signaling in the colon. HT29/C1 colonic epithelial cells treated with zerumbone suppressed BFT-induced NF-κB signaling and IL-8 secretion. However, BFT-mediated E-cadherin cleavage was unaffected. Furthermore, zerumbone did not affect ETBF colonization in mice. In conclusion, zerumbone decreased ETBF-induced colitis through inhibition of NF-κB signaling.

Anti-Inflammatory Effects of Garlic Consumption and Regular Exercise in Sedentary Overweight Individuals

2020 ◽  
Vol 24 (2) ◽  
Author(s):  
Farhad Gholami ◽  
Jabar Bashiri ◽  
Naser Amanollahi
Keyword(s):  
Exercise Intervention ◽  
Experimental Period ◽  
Serum Levels ◽  
Regular Exercise ◽  
Lifestyle Modifications ◽  
Significance Level ◽  
Tnf Α ◽  
Significant Difference ◽  
Anti Inflammatory ◽  
Hs Crp

Background: A sedentary lifestyle can result in chronic inflammation, which is a risk factor for Cardiovascular Disease (CVD). Lifestyle modifications, including physical activity and herbal supplements, may have health benefits. Objectives: The present study aimed to investigate the effect of regular exercise and garlic consumption on some inflammatory biomarkers in sedentary overweight individuals. Methods: Forty-four sedentary overweight male participants (20 - 30 years) were randomized to the following groups: Exercise + garlic (ES), exercise + placebo (E), garlic (G), and placebo (P). The training protocol included 20 - 45 minutes of walking/running at 60 to 75% of the maximum heart rate, three sessions per week for eight weeks. Participants consumed two capsules containing 500 milligrams of garlic powder or placebo (starch) per day. Before and 48 h after the exercise intervention and supplement administration, blood samples were collected to assess the hs-CRP and TNF-α serum levels. One-way ANOVA and Tukey’s post hoc tests were used to analyze the data at a significance level of P < 0.05. Results: A significant difference was observed between the groups regarding the hs-CRP and TNF-α levels after the experimental period (P < 0.05). There was a significant difference between EG and placebo groups (P < 0.05). Conclusions: Based on the findings, garlic consumption, along with exercise training could exert anti-inflammatory properties in overweight subjects.

GH-releasing peptide-2 administration prevents liver inflammatory response in endotoxemia

2008 ◽  
Vol 294 (1) ◽  
pp. E131-E141 ◽  
Author(s):  
Miriam Granado ◽  
Ana Isabel Martín ◽  
María López-Menduiña ◽  
Asunción López-Calderón ◽  
M. Angeles Villanúa
Keyword(s):  
Receptor Agonist ◽  
Serum Levels ◽  
Ghrelin Receptor ◽  
Nonparenchymal Cells ◽  
Tnf Α ◽  
Igf I ◽  
Ghrelin Receptor Agonist ◽  
Anti Inflammatory ◽  
Inflammatory Effect

It has been reported that growth hormone (GH)-releasing peptide-2 (GHRP-2), a ghrelin receptor agonist, has an anti-inflammatory effect. We investigated whether this GH secretagogue attenuates liver injury in LPS-treated rats. Wistar rats were simultaneously injected (ip) with LPS (1 mg/kg) and/or GHRP-2 (100 μg/kg). Serum levels of aspartate and alanine transaminases were measured as an index of liver damage. Circulating nitrites/nitrates and hepatic IGF-I and TNF-α were evaluated as possible mediators of GHRP-2 actions. LPS increased serum levels of transaminases and nitrites/nitrates. Moreover, LPS increased hepatic TNF-α and decreased hepatic IGF-I mRNAs. GHRP-2 administration attenuated the effects of LPS on transaminases, nitrites/nitrates, TNF-α, and IGF-I in vivo. This GHRP-2 effect does not seem to be due to modifications in food intake, since fasting did not modify serum levels of transaminases, serum nitrites/nitrates, and hepatic TNF-α mRNA both in vehicle rats and in LPS-injected rats. To elucidate whether GHRP-2 is acting directly on the liver, cocultures of hepatocytes and nonparenchymal cells and monocultures of isolated hepatocytes were incubated with LPS and GHRP-2. The ghrelin receptor agonist prevented an endotoxin-induced increase in transaminases and nitrite/nitrate release as well as in TNF-α mRNA and increased IGF-I mRNA from cocultures of hepatocytes and nonparenchymal cells, but not from monocultures. In summary, these data indicate that GHRP-2 has a protective effect on the liver in LPS-injected rats that seems to be mediated by IGF-I, TNF-α, and nitric oxide. Our data also suggest that the anti-inflammatory effect of GHRP-2 in the liver is exerted on nonparenchymal cells.

Radioprotective effect of pioglitazone against genotoxicity induced by ionizing radiation in human healthy lymphocytes

2020 ◽  
Vol 18 ◽  
Author(s):  
Roya Kazemi ◽  
Seyed Jalal Hosseinimehr
Keyword(s):  
Ionizing Radiation ◽  
Human Lymphocytes ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
The Mean ◽  
Anti Inflammatory ◽  
Sensitizing Effect ◽  
Binucleated Lymphocytes ◽  
Inflammatory Effect

Objective: Pioglitazone (PG) is used to control high blood sugar in patients with type 2 diabetes mellitus. PG acts as a peroxisome proliferator-activated receptor γ agonist. In addition to the insulin-sensitizing effect, PG possesses anti-inflammatory effect. In this study, the protective effect of PG was evaluated against DNA damage induced by ionizing radiation in human healthy lymphocytes. Methods: The microtubes containing human whole blood were treated with PG at various concentrations (1-50 μM) for three hours. Then, the blood samples were irradiated with X-ray. Lymphocytes were cultured for determining the frequency of micronuclei as a genotoxicity biomarker in binucleated lymphocytes. Results: The mean percentage of micronuclei was significantly increased in human lymphocytes when were exposed to IR, while it was decreased in lymphocytes pre-treated with PG. The maximum reduction in the frequency of micronuclei in irradiated lymphocytes was observed at 5 μM of PG treatment (48% decrease). Conclusion: The anti-inflammatory property is suggested the mechanism action of PG for protection human lymphocytes against genotoxicity induced by ionizing radiation.

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.

scholarly journals In Vitro Evaluation of the Anti-Inflammatory Effect of KMUP-1 and in Vivo Analysis of Its Therapeutic Potential in Osteoarthritis

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 615
Author(s):  
Shang-En Huang ◽  
Erna Sulistyowati ◽  
Yu-Ying Chao ◽  
Bin-Nan Wu ◽  
Zen-Kong Dai ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Antioxidant Properties ◽  
Serum Levels ◽  
Gene Expressions ◽  
Tnf Α ◽  
Anti Inflammatory

Osteoarthritis is a degenerative arthropathy that is mainly characterized by dysregulation of inflammatory responses. KMUP-1, a derived chemical synthetic of xanthine, has been shown to have anti-inflammatory and antioxidant properties. Here, we aimed to investigate the in vitro anti-inflammatory and in vivo anti-osteoarthritis effects of KMUP-1. Protein and gene expressions of inflammation markers were determined by ELISA, Western blotting and microarray, respectively. RAW264.7 mouse macrophages were cultured and pretreated with KMUP-1 (1, 5, 10 μM). The productions of TNF-α, IL-6, MMP-2 and MMP- 9 were reduced by KMUP-1 pretreatment in LPS-induced inflammation of RAW264.7 cells. The expressions of iNOS, TNF-α, COX-2, MMP-2 and MMP-9 were also inhibited by KMUP-1 pretreatment. The gene expression levels of TNF and COX families were also downregulated. In addition, KMUP-1 suppressed the activations of ERK, JNK and p38 as well as phosphorylation of IκBα/NF-κB signaling pathways. Furthermore, SIRT1 inhibitor attenuated the inhibitory effect of KMUP-1 in LPS-induced NF-κB activation. In vivo study showed that KMUP-1 reduced mechanical hyperalgesia in monoiodoacetic acid (MIA)-induced rats OA. Additionally, KMUP-1 pretreatment reduced the serum levels of TNF-α and IL-6 in MIA-injected rats. Moreover, macroscopic and histological observation showed that KMUP-1 reduced articular cartilage erosion in rats. Our results demonstrated that KMUP-1 inhibited the inflammatory responses and restored SIRT1 in vitro, alleviated joint-related pain and cartilage destruction in vivo. Taken together, KMUP-1 has the potential to improve MIA-induced articular cartilage degradation by inhibiting the levels and expression of inflammatory mediators suggesting that KMUP-1 might be a potential therapeutic agent for OA.

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