Curcumin ameliorates ethanol and nonethanol experimental pancreatitis

2003 ◽  
Vol 284 (1) ◽  
pp. G85-G95 ◽  
Author(s):  
Ilya Gukovsky ◽  
Christopher N. Reyes ◽  
Eva C. Vaquero ◽  
Anna S. Gukovskaya ◽  
Stephen J. Pandol
Keyword(s):  
Transcription Factor ◽  
Inflammatory Response ◽  
Neutrophil Infiltration ◽  
Experimental Pancreatitis ◽  
Early Event ◽  
Pancreatic Acini ◽  
Activation Of Transcription ◽  
Tnf Α ◽  
Severity Of The Disease ◽  
Oxide Synthase

Treatments for pancreatitis are limited. Activation of transcription factor NF-κB, a key regulator of inflammatory molecule expression, is an early event in experimental pancreatitis and correlates with the inflammatory response. We report here that curcumin, a natural phytochemical known to inhibit NF-κB and activator protein (AP)-1, another important proinflammatory transcription factor, ameliorates pancreatitis in two rat models. In both cerulein pancreatitis and pancreatitis induced by a combination of ethanol diet and low-dose CCK, curcumin improved the severity of the disease as measured by a number of parameters (histology, serum amylase, pancreatic trypsin, and neutrophil infiltration). Curcumin markedly inhibited NF-κB and AP-1 activation, assessed by DNA binding and degradation of inhibitory IκB proteins, and the induction of mRNAs for cytokines IL-6 and TNF-α, the chemokine KC, and inducible nitric oxide synthase in pancreas. Curcumin also blocked CCK-induced NF-κB and AP-1 activation in isolated pancreatic acini. Our findings indicate that blocking key signals of the inflammatory response ameliorates pancreatitis in both ethanol and nonethanol models. They suggest that curcumin, which is currently in clinical trials for cancer prevention, may be useful for treatment of pancreatitis.

Calcium and ROS-mediated activation of transcription factors and TNF-α cytokine gene expression in macrophages exposed to ultrafine particles

2004 ◽  
Vol 286 (2) ◽  
pp. L344-L353 ◽  
Author(s):  
D. M. Brown ◽  
K. Donaldson ◽  
P. J. Borm ◽  
R. P. Schins ◽  
M. Dehnhardt ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Intracellular Calcium ◽  
Alveolar Macrophages ◽  
Calcium Concentration ◽  
Protein Release ◽  
Human Monocytes ◽  
Blood Monocytes ◽  
Activation Of Transcription ◽  
Tnf Α

Ultrafine (Uf) particles are a component of particulate air pollution suggested to be responsible for the health effects associated with elevations of this pollutant. We have previously suggested that Uf particles, through the induction of oxidative stress, may induce inflammation in the lung, thus exacerbating preexisting illness in susceptible individuals. Alveolar macrophages are considered to play a key role in particlemediated inflammation and lung disease. The effect of Uf particles on rat alveolar macrophages and human blood monocytes was investigated with reference to the roles of calcium and reactive oxygen species (ROS). TNF-α protein release, intracellular calcium concentration, TNF-α mRNA expression, and transcription factor activation were studied as end points after treatment of rat alveolar macrophages or peripheral blood monocytes. The calcium channel blocker verapamil, the intracellular calcium chelator BAPTA-AM, the calmodulin inhibitor W-7, and the antioxidants Trolox and Nacystelin (NAL) were included in combination with Uf particles. Verapamil reduced intracellular calcium concentration in rat alveolar macrophages on stimulation with Uf particles. This effect was also apparent with transcription factor AP-1 activation. All antagonists and antioxidants reduced Uf-stimulated nuclear localization of the p50 and p65 subunits of NF-κB in human monocytes. Verapamil, BAPTA-AM, and NAL reduced Uf-stimulated TNF-α protein release, whereas only verapamil reduced Uf-stimulated mRNA expression in rat alveolar macrophages. In human monocytes, verapamil, Trolox, BAPTA-AM, and W-7 reduced Uf-stimulated TNF-α protein release. These findings suggest that Uf particles may exert proinflammatory effects by modulating intracellular calcium concentrations, activation of transcription factors, and cytokine production through a ROS-mediated mechanism.

scholarly journals Knockdown of TRIM8 Attenuates IL-1β-induced Inflammatory Response in Osteoarthritis Chondrocytes Through the Inactivation of NF-κB Pathway

2020 ◽  
Vol 29 ◽  
pp. 096368972094360
Author(s):  
Ruoxi Liu ◽  
Hao Wu ◽  
Huanjin Song
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Response ◽  
Interleukin 1 ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Prostaglandin E ◽  
Tnf Α ◽  
Osteoarthritis Chondrocytes ◽  
Oa Chondrocytes ◽  
Oxide Synthase

Osteoarthritis (OA) is a degenerative joint disease associated with inflammatory response. Tripartite motif 8 (TRIM8) is a member of TRIM family that has been found to regulate inflammation. The present study was aimed to evaluate the role of TRIM8 in OA chondrocytes. Our results showed that TRIM8 expression was significantly increased in interleukin 1 beta (IL-1β)-stimulated OA chondrocytes. To knock down the TRIM8 expression in chondrocytes, the chondrocytes were transfected with si-TRIM8. Knockdown of TRIM8 attenuated IL-1β-induced production of inflammatory mediators including nitric oxide and prostaglandin E2. The increased expression levels of inducible nitric oxide synthase and cyclooxygenase-2 in IL-1β-induced chondrocytes were suppressed by TRIM8 knockdown. The IL-1β-induced production of proinflammatory cytokines including TNF-α and IL-6 was significantly decreased after transfection with si-TRIM8. Besides, knockdown of TRIM8 mitigated the IL-1β-induced decrease in aggrecan and collagen-II proteins expression and increase in matrix-degrading enzymes in chondrocytes. Furthermore, TRIM8 knockdown prevented IL-1β-induced nuclear factor kappa B (NF-κB) activation in chondrocytes. Taken together, these findings indicated that knockdown of TRIM8 attenuates IL-1β-induced inflammatory response in OA chondrocytes through the inactivation of NF-κB pathway. Thus, targeting TRIM8 might provide therapeutic treatment for OA.

Triggering of inflammatory response by myeloperoxidase-oxidized LDLAn oral presentation of the data was given before the Congress of the Beligian Society of Internal Medicine.

2006 ◽  
Vol 84 (5) ◽  
pp. 805-812 ◽  
Author(s):  
Karim Zouaoui Boudjeltia ◽  
Ilham Legssyer ◽  
Pierre Van Antwerpen ◽  
Roger Lema Kisoka ◽  
Sajida Babar ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Oxidized Ldl ◽  
Fold Increase ◽  
Ldl Oxidation ◽  
Early Event ◽  
Modified Ldl ◽  
Tnf Α ◽  
Cell Medium ◽  
Oxidation Theory ◽  
Cellular Types

The oxidation theory proposes that LDL oxidation is an early event in atherosclerosis and that oxidized LDL contributes to atherogenesis in triggering inflammation. In contrast to the copper-modified LDL, there are few studies using myeloperoxidase-modified LDL (Mox-LDL) as an inflammation inducer. Our aim is to test whether Mox-LDL could constitute a specific inducer of the inflammatory response. Albumin, which is the most abundant protein in plasma and which is present to an identical concentration of LDL in the intima, was used for comparison. The secretion of IL-8 by endothelial cells (Ea.hy926) and TNF-α by monocytes (THP-1) was measured in the cell medium after exposure of these cells to native LDL, native albumin, Mox-LDL, or Mox-albumin. We observed that Mox-LDL induced a 1.5- and 2-fold increase (ANOVA; P < 0.001) in IL-8 production at 100 µg/mL and 200 µg/mL, respectively. The incubation of THP-1 cells with Mox-LDL (100 µg/mL) increased the production of TNF-α 2-fold over the control. Native LDL, albumin, and Mox-albumin showed no effect in either cellular types. The myeloperoxidase-modified LDL increase in cytokine release by endothelial and monocyte cells and by firing both local and systemic inflammation could induce atherogenesis and its development.

scholarly journals Docosahexaenoic fatty acid reduces the pro‐inflammatory response induced by IL-1β in astrocytes through inhibition of NF-κB and AP-1 transcription factor activation

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Emilia Zgórzyńska ◽  
Dawid Stulczewski ◽  
Barbara Dziedzic ◽  
Kuan-Pin Su ◽  
Anna Walczewska
Keyword(s):  
Transcription Factor ◽  
Fatty Acid ◽  
Inflammatory Response ◽  
Omega 3 ◽  
Age Related ◽  
Tnf Α ◽  
Key Factor ◽  
Range Of Functions ◽  
Cox 2 ◽  
Docosahexaenoic Fatty Acid

Abstract Background Astrocytes are responsible for a broad range of functions that maintain homeostasis in the brain. However, their response to the pro-inflammatory cytokines released by activated microglia in various neurological pathologies may exacerbate neurodegenerative processes. Accumulating evidence suggests that omega-3 docosahexaenoic fatty acid (DHA) has an anti-inflammatory effect in various cell cultures studies and in a variety of neurological disorders. In this study we examined the mechanism involved in the inhibition of the pro-inflammatory response by DHA in astrocytes treated with IL-1β. Methods and results Activation of the transcription factors NF-κB and AP-1 was measured in IL-1β-treated primary astrocytes incubated with various concentrations of DHA. COX-2 and iNOS protein expression was determined by Western blot, and TNF-α and IL-6 secretion was measured using ELISA-based assays. DHA treatment inhibited translocation of p65NF-κB to the nucleus, significantly lowered p65NF-κB protein level and fluorescence of p65NF-κB in the nucleus, reduced dose-dependently IκB protein phosphorylation, and the binding of the AP-1 transcription factor members (c-Jun/c-Fos) to the specific TPA-response element (TRE) of DNA. In addition, the expression of pro-inflammatory COX-2 and iNOS proteins was downregulated and TNF-α and IL-6 secretion was also reduced. Conclusions These results indicate that DHA is a powerful factor that reduces the pro-inflammatory response in astrocytes. Consequently, successful introduction of DHA into the astrocyte membranes can attenuate neuroinflammation, which is a key factor of age-related neurodegenerative disorders.

scholarly journals Clotrimazole Dampens Vaginal Inflammation and Neutrophil Infiltration in Response to Candida albicans Infection

2013 ◽  
Vol 57 (10) ◽  
pp. 5178-5180 ◽  
Author(s):  
Duncan Wilson ◽  
Betty Hebecker ◽  
David L. Moyes ◽  
Pedro Miramón ◽  
Nadja Jablonowski ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Candida Albicans ◽  
Inflammatory Response ◽  
Proinflammatory Cytokines ◽  
Fungal Growth ◽  
Neutrophil Infiltration ◽  
Content Type ◽  
Candida Albicans Infection ◽  
Low Levels ◽  
Factor C

ABSTRACTThe pathology of vulvovaginal candidiasis (VVC) caused byCandida albicansis associated with a nonprotective inflammatory response and is frequently treated with clotrimazole. We investigated the mechanisms by which clotrimazole resolves VVC. Low levels of clotrimazole, which do not block fungal growth, inhibit expression of a “danger response” transcription factor, c-Fos, block production of proinflammatory cytokines, and inhibit neutrophil infiltration to the site of infection.

Anti-coccidial and anti-apoptotic activities of palm pollen grains on Eimeria papillata-induced infection in mice

Biologia ◽  
2014 ◽  
Vol 69 (2) ◽  
Author(s):  
Mahmoud Metwaly ◽  
Mohamed Dkhil ◽  
Saleh Al-Quraishy
Keyword(s):  
Inflammatory Response ◽  
Pollen Grains ◽  
Pollen Extract ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Eimeria Papillata ◽  
Factor Alpha ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

AbstractThe present work aimed to study the effect of palm pollen extract (PPE) as an anticoccidial and anti-apoptotic modulator during the course of murine intestinal Eimeria papillata infection. The fact that PPE has an anticoccidial efficacy against intestinal E. papillata infection in mice has been clarified by the reduction of faecal output of oocysts on day five post infection from 49.5 × 103 to 34 × 103 oocyst/g. Moreover, the number of intracellular eimerian stages of zygots and developing oocysts decreased by about 89% and that of schizonts and gamonts to 42% and 72%, respectively. E. papillata infection also induced an increase in the number of apoptotic cells from 17.5 to 122.8 apoptotic nuclei/10 villous crypt units (VCU). In addition, it caused a state of systemic inflammatory response as revealed by an elevation in levels of the pro-inflammatory biomarkers, inducible nitric oxide synthase (iNOs) and tumor necrosis factor alpha (TNF-α) from 5.3 and 78.3 to 33 pmol ml−1 and 96.3 pg ml−1 in blood, respectively, with concurrent duplication in the total leucocytic number. Upon treatment of infected mice with the aqueous PPE, the activity of iNOs was reduced by 55% and the level of TNF-α was decreased by 30%. Moreover, the total leucocytic count was significantly reduced from 9.05 × 103 to 7.8 × 103 cells/mm3. Based on our results, PPE showed both anti-coccidial, anti-inflammatory and anti-apoptotic activities. So it can be used in developing new herbal medicine against animal coccidiosis and may be suitable agent for treating eimeriosis associated inflammatory response.

Sorghum Fermented by Aspergillus oryzae NK Enhances Inhibition of Vascular Inflammation in TNF-α-stimulated Human Aortic Smooth Muscle Cells

2018 ◽  
Vol 88 (5-6) ◽  
pp. 309-318
Author(s):  
Hae Seong Song ◽  
Jung-Eun Kwon ◽  
Hyun Jin Baek ◽  
Chang Won Kim ◽  
Hyelin Jeon ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Inflammatory Response ◽  
Smooth Muscle Cells ◽  
Adhesion Molecule ◽  
Vascular Inflammation ◽  
Muscle Cells ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Tnf Α ◽  
Cox 2

Abstract. Sorghum bicolor L. Moench is widely grown all over the world for food and feed. The effects of sorghum extracts on general inflammation have been previously studied, but its anti-vascular inflammatory effects are unknown. Therefore, this study investigated the anti-vascular inflammation effects of sorghum extract (SBE) and fermented extract of sorghum (fSBE) on human aortic smooth muscle cells (HASMCs). After the cytotoxicity test of the sorghum extract, a series of experiments were conducted. The inhibition effects of SBE and fSBE on the inflammatory response and adhesion molecule expression were measured using treatment with tumor necrosis factor-α (TNF-α), a crucial promoter for the development of atherosclerotic lesions, on HASMCs. After TNF-α (10 ng/mL) treatment for 2 h, then SBE and fSBE (100 and 200 μg/mL) were applied for 12h. Western blotting analysis showed that the expression of vascular cell adhesion molecule-1 (VCAM-1) (2.4-fold) and cyclooxygenase-2 (COX-2) (6.7-fold) decreased, and heme oxygenase-1 (HO-1) (3.5-fold) increased compared to the TNF-α control when treated with 200 μg/mL fSBE (P<0.05). In addition, the fSBE significantly increased the expression of HO-1 and significantly decreased the expression of VCAM-1 and COX-2 compared to the TNF-α control in mRNA level (P<0.05). These reasons of results might be due to the increased concentrations of procyanidin B1 (about 6-fold) and C1 (about 30-fold) produced through fermentation with Aspergillus oryzae NK for 48 h, at 37 °C. Overall, the results demonstrated that fSBE enhanced the inhibition of the inflammatory response and adherent molecule expression in HASMCs.

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