scholarly journals Ferulic Acid Improves Depressive-Like Behavior in Prenatally-Stressed Offspring Rats via Anti-Inflammatory Activity and HPA Axis

2019 ◽  
Vol 20 (3) ◽  
pp. 493 ◽  
Author(s):  
Xingxing Zheng ◽  
Ying Cheng ◽  
Yiwei Chen ◽  
Yisong Yue ◽  
Yingchun Li ◽  
...  
Keyword(s):  
Protein Expression ◽  
Ferulic Acid ◽  
Hpa Axis ◽  
Glucocorticoid Receptors ◽  
Metabolic Diseases ◽  
Inflammatory Activity ◽  
Tnf Α ◽  
Immobility Time ◽  
Prenatally Stressed ◽  
Anti Inflammatory

Prenatal stress (PS) can increase the risk of nervous, endocrine and metabolic diseases, and immune dysfunction. Ferulic acid (FA) is a dietary phenolic acid that has pharmacological properties, including potent anti-inflammatory action. We used male, prenatally-stressed offspring rats to investigate the anti-depressive-like effects and possible anti-inflammatory mechanism of FA. We determined the animal behaviors, and the mRNA expression and concentration of inflammatory cytokines, and HPA axis. In addition, we assessed the modulation of hippocampal nuclear factor-κB (NF-κB) activation, neuronal nitric oxide synthase (nNOS) and glucocorticoid receptors (GR) expression via western blotting and immunohistochemistry. Administration of FA (12.5, 25, and 50 mg/kg/day, i.g.) for 28 days markedly increased sucrose intake, and decreased immobility time and total number of crossings, center crossings, rearing, and grooming in the male PS offspring. FA significantly reduced IL-6, IL-1β, and TNF-α concentration and increased IL-10 concentration in male, prenatally-stressed offspring, stimulated by the NF-κB pathway. In addition, FA inhibited interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α), and increased interleukin-10 (IL-10) mRNA and protein expression. Furthermore, FA markedly decreased the serum adrenocorticotropin (ACTH) and corticosterone concentration by the increase of GR protein expression. Taken together, this study revealed that FA has anti-depressive-like effects in male, prenatally-stressed offspring, partially due to its anti-inflammatory activity and hypothalamic-pituitary-adrenal (HPA) axis.

Thymoquinone ameliorates NLRP3-mediated inflammation in the pancreas of albino Wistar rats fed ethanol and high-fat diet

2015 ◽  
Vol 26 (6) ◽  
Author(s):  
Suguna Periyanayagam ◽  
Geetha Arumugam ◽  
Aruna Ravikumar ◽  
Vijaiyan Siva Ganesan
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Mrna Expression ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Inflammatory Activity ◽  
High Fat ◽  
Caspase 1 ◽  
Tnf Α ◽  
Anti Inflammatory

AbstractInflammasomes are protein complexes that mediate the process of inflammation and tissue injury by regulating the level of cytokine production. Pancreatitis is a major gastrointestinal disorder characterized by painful inflammation in the pancreas. The aim of this study was to evaluate whether thymoquinone (TQ) exerts anti-inflammatory activity by influencing the expression of the apoptosis-associated speck-like protein (ASC) complex of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasomes in rats subjected to experimental pancreatitis.Male albino Wistar rats were randomly separated into four groups. Rats in groups 1 and 2 were fed with a normal diet for 90 days, and rats in groups 3 and 4 were administered with ethanol (EtOH) 8–12 g/kg/day orally and fed with a high-fat diet (HFD) for 90 days. In addition, rats in groups 2 and 4 were administered with 100 mg/kg body weight of TQ from the 31st day. The serum lipase (L)/amylase (A) ratio; the oxidative stress markers; the GSH/GSSG ratio; the mRNA expression of ASC, caspase-1, IL-1β, IL-18, and TNF-α; and the protein expression of ASC and caspase-1 in the pancreas were assessed.We observed a significant increase in the serum L/A ratio and oxidative stress, a decrease in the GSH/GSSG ratio, and a GST activity in EtOH- and HFD-fed rats. The mRNA expression of IL-1β, IL-18, and TNF-α was significantly reduced in TQ-coadministered rats than that in EtOH- and HFD-fed rats. The upregulation of mRNA and the protein expression of ASC and caspase-1 were significantly reduced in TQ-coadministered rats.TQ exerts the anti-inflammatory activity probably by downregulating the ASC expression to minimize the maturation of proinflammatory cytokines.

Piper sarmentosum extract alleviates inflammatory responses and improves barrier function in porcine intestinal epithelial (IPEC-J2) cells induced by lipopolysaccharide (LPS)

2020 ◽  
Author(s):  
Dingfa Wang ◽  
Luli Zhou ◽  
zhou Hanlin ◽  
Guanyu Hou
Keyword(s):  
Protein Expression ◽  
Signaling Pathway ◽  
Inflammatory Responses ◽  
Inflammatory Activity ◽  
Complete Medium ◽  
Metabolic Pathway Analysis ◽  
Metabolic Pattern ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Lps Treatment

Abstract Background: In this study, we investigated the anti-inflammatory effect of Piper sarmentosum extract (PSE) in the IPEC-J2 cells induced by lipopolysaccharide (LPS). Meanwhile, we also tested the metabolomics profile of cells treated by LPS and PSE. Method: IPEC-J2 cells (6×105 cell/well) were seeded on 6-well plates, and cells were divided into three treatments (control, LPS treatment and LPS + PSE-NB treatment). Each treatment was conducted in five replicates. After incubation for 24 h, cells in LPS + PSE-NB treatment were treated by media containing PSE-NB at 10 ug/ml (cells in control and LPS treatments were treated by complete medium). Cells were culture for 24 h, and cells in LPS treatment and LPS + PSE-NB treatment then were treated by media contain 1 μg/ml of LPS (cells in control was treated by complete medium) for another 24 h. After treatment, cells were used for gene expression assays, protein expression assays and metabolomics analysis.Results: We demonstrated that LPS stimulation significantly up-regulated the mRNA expression of IL-1, IL-6 and TNF-α (P < 0.05) compared with the control in the IPEC-J2 cells. Piper sarmentosum extract with n-butanol (PSE-NB) pre-treatment with 10 ug/mL before LPS stimulation significantly decreased the expression of IL-1, IL-6 and TNF-α compared with LPS treatment (P < 0.05). We found that PSE-NB improved the expression of intestinal tight junction proteins (ZO1 and Occludin) and NHE3 that were reduced by LPS stimulation (P < 0.05). Moreover, PSE-NB alleviated LPS-induced protein expression of p65 and p-p65 (P < 0.05) and inhibited the NF-κB signaling pathway. Metabolic pathway analysis indicated that PSE-NB exert anti-inflammatory activity mainly through affecting tryptophan metabolism. Its metabolic product, melatonin, has anti-inflammatory properties by inhibition of NF-κB activation, which consistent with our results regarding to anti-inflammatory activity of PSE-NB on inflammatory signaling pathway. Conclusion: These results suggested that PSE-NB might attenuate LPS-induced inflammatory responses in the IPEC-J2 cells by regulating inflammatory NF-κB signaling pathway and intracellular metabolic pattern.

scholarly journals Pirfenidone attenuates synovial fibrosis and postpones the progression of osteoarthritis by anti-fibrotic and anti-inflammatory properties in vivo and in vitro

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Qilu Wei ◽  
Ning Kong ◽  
Xiaohui Liu ◽  
Run Tian ◽  
Ming Jiao ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Fast Green ◽  
Expression Levels ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Safranin O ◽  
Tgf Β1

Abstract Background Osteoarthritis (OA) is a disease of the entire joint involving synovial fibrosis and inflammation. Pathological changes to the synovium can accelerate the progression of OA. Pirfenidone (PFD) is a potent anti-fibrotic drug with additional anti-inflammatory properties. However, the influence of PFD on OA is unknown. Methods Proliferation of human fibroblast-like synoviocytes (FLSs) after treatment with TGF-β1 or PFD was evaluated using a Cell Counting Kit-8 assay and their migration using a Transwell assay. The expression of fibrosis-related genes (COL1A1, TIMP-1, and ACTA-2) and those related to inflammation (IL-6 and TNF-α) was quantified by real-time quantitative PCR. The protein expression levels of COL1A1, α-SMA (coded by ACTA-2), IL-6 and TNF-α were measured by enzyme-linked immunosorbent assay. A rabbit model of OA was established and then PFD was administered by gavage. The expression of genes related to fibrosis (COL1A1, TIMP-1, and ADAM-12) and inflammation (IL-6 and TNF-α) was measured using RNA extracted from the synovium. Synovial tissue was examined histologically after staining with H&E, Masson’s trichrome, and immunofluorescence. Synovitis scores, the volume fraction of collagen, and mean fluorescence intensity were calculated. Degeneration of articular cartilage was analyzed using a Safranin O-fast green stain and OARSI grading. Results The proliferation of FLSs was greatest when induced with 2.5 ng/ml TGF-β1 although it did not promote their migration. Therefore, 2.5 ng/ml TGF-β1 was used to stimulate the FLSs and evaluate the effects of PFD, which inhibited the migration of FLSs at concentrations as low as 1.0 mg/ml. PFD decreased the expression of COL1A1 while TGF-β1 increased both mRNA and protein expression levels of IL-6 but had no effect on α-SMA or TNF-α expression. PFD decreased mRNA expression levels of COL1A1, IL-6, and TNF-α in vivo. H&E staining and synovitis scores indicated that PFD reduced synovial inflammation, while Masson’s trichrome and immunofluorescence staining suggested that PFD decreased synovial fibrosis. Safranin O-Fast Green staining and the OARSI scores demonstrated that PFD delayed the progression of OA. Conclusions PFD attenuated synovial fibrosis and inflammation, and postponed the progression of osteoarthritis in a modified Hulth model of OA in rabbits, which was related to its anti-fibrotic and anti-inflammatory properties.

scholarly journals Fisetin inhibits lipopolysaccharide-induced inflammatory response by activating β-catenin, leading to a decrease in endotoxic shock

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ilandarage Menu Neelaka Molagoda ◽  
Jayasingha Arachchige Chathuranga C Jayasingha ◽  
Yung Hyun Choi ◽  
Rajapaksha Gedara Prasad Tharanga Jayasooriya ◽  
Chang-Hee Kang ◽  
...  
Keyword(s):  
Glycogen Synthase ◽  
Endotoxic Shock ◽  
Inflammatory Activity ◽  
Prostaglandin E ◽  
Necrosis Factor Alpha ◽  
Zebrafish Larvae ◽  
Proinflammatory Mediators ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Gsk 3Β

AbstractFisetin is a naturally occurring flavonoid that possesses several pharmacological benefits including anti-inflammatory activity. However, its precise anti-inflammatory mechanism is not clear. In the present study, we found that fisetin significantly inhibited the expression of proinflammatory mediators, such as nitric oxide (NO) and prostaglandin E2 (PGE2), and cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Additionally, fisetin attenuated LPS-induced mortality and abnormalities in zebrafish larvae and normalized the heart rate. Fisetin decreased the recruitment of macrophages and neutrophils to the LPS-microinjected inflammatory site in zebrafish larvae, concomitant with a significant downregulation of proinflammatory genes, such as inducible NO synthase (iNOS), cyclooxygenase-2a (COX-2a), IL-6, and TNF-α. Fisetin inhibited the nuclear localization of nuclear factor-kappa B (NF-κB), which reduced the expression of pro-inflammatory genes. Further, fisetin inactivated glycogen synthase kinase 3β (GSK-3β) via phosphorylation at Ser9, and inhibited the degradation of β-catenin, which consequently promoted the localization of β-catenin into the nucleus. The pharmacological inhibition of β-catenin with FH535 reversed the fisetin-induced anti-inflammatory activity and restored NF-κB activity, which indicated that fisetin-mediated activation of β-catenin results in the inhibition of LPS-induced NF-κB activity. In LPS-microinjected zebrafish larvae, FH535 promoted the migration of macrophages to the yolk sac and decreased resident neutrophil counts in the posterior blood island and induced high expression of iNOS and COX-2a, which was accompanied by the inhibition of fisetin-induced anti-inflammatory activity. Altogether, the current study confirmed that the dietary flavonoid, fisetin, inhibited LPS-induced inflammation and endotoxic shock through crosstalk between GSK-3β/β-catenin and the NF-κB signaling pathways.

Abstract 393: Anti-inflammatory Properties of Aqueous Extracts of Sesame Oil

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Krithika Selvarajan ◽  
Chandrakala Aluganti Narasimhulu ◽  
Reena Bapputty ◽  
Sampath Parthasarathy
Keyword(s):  
Protein Expression ◽  
Aqueous Extract ◽  
Dietary Intervention ◽  
Sesame Oil ◽  
Luciferase Assay ◽  
Treatment Modalities ◽  
Raw 264.7 Cells ◽  
Mrna Levels ◽  
Tnf Α ◽  
Anti Inflammatory

Background Dietary intervention to prevent atherosclerosis and inflammation has been a major focus in recent years. Sesame oil (SO), widely used in many Asian countries, has been reported to help reduce high blood pressure. It has also been shown to reduce plasma cholesterol, low density lipoprotein (LDL) cholesterol and triglyceride levels. We previously reported that SO was effective in inhibiting atherosclerosis in LDL-receptor negative mice. In this study we tested whether the aqueous, non-lipid components of SO might have anti-inflammatory effects. Methods Sesame oil was extracted using ethanol:water mixture, lyophilized and reconstituted in water. To study anti-inflammatory effect, RAW 264.7 cells (macrophage cell line) were treated with the aqueous extract in the presence or absence of lipopolysaccharide (LPS) for 24 hours. RNA was extracted using Trizol. mRNA expression of inflammatory cytokines such as IL-1α, IL-6 and TNF-α were analyzed by real time PCR. Protein expression was determined by western blot analysis. To identify the mechanism of action, we performed luciferase assay using HepG2-LXR reporter cell lines. Results LPS induced the expression of IL-1α, IL-6 and TNF-α mRNA levels in RAW cells. The extract alone did not significantly affect the expressions of inflammatory cytokine genes. However, when treated together with LPS, sesame oil aqueous extract inhibited the mRNA levels of these cytokines significantly. Treatment with LPS together with SO extract also decreased the protein expression of these cytokines. The SO extract induced LXR expression as identified by the luciferase assay system in HepG2-LXR reporter cells. Conclusion These findings suggest that the aqueous portion of SO might be effective in preventing inflammation. Furthermore, the activation of LXR might suggest additional effects on lipid metabolism. Identifying the specific components present in the aqueous extract will be instrumental in developing treatment modalities for atherosclerosis and other inflammatory conditions.

Abstract 035: Cholinergic Agonists Protect from the Development of Hypertension during Chronic Inflammatory Disease

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Keisa W Mathis
Keyword(s):  
Protein Expression ◽  
Lupus Erythematosus ◽  
Inflammatory Diseases ◽  
Autoimmune Disorder ◽  
Chronic Inflammatory Disease ◽  
Cholinergic Agonists ◽  
Inflammatory Pathway ◽  
Genetic Mouse Model ◽  
Tnf Α ◽  
Anti Inflammatory

Systemic lupus erythematosus (SLE) is an autoimmune disorder with prevalent hypertension. Previous studies using a genetic mouse model of SLE (NZBWF1) suggest chronic inflammation is an important contributor to SLE hypertension. A novel neuroimmune pathway involving the α7 subunit of the nicotinic acetylcholine receptor (α7nAChR) suppresses splenic cytokine release and reduces systemic inflammation upon stimulation. To test whether activation of this ‘cholinergic anti-inflammatory pathway’ at the level of the α7nAChR attenuates the development of hypertension during SLE, female SLE and control (NZW) mice were infused with nicotine hydrogen tartrate salt (2 mg/kg/day, SC) or saline for 7 days. Nicotine-treated SLE mice had lower splenic protein expression of TNF-α and IL-6 (normalized to β-actin) relative to saline-treated SLE mice (1.09±0.06 vs. 1.37±0.06 and 0.36±0.04 vs. 0.55±0.10; all p<0.05), suggesting efficacy of the therapy. Mean arterial pressure (MAP; mmHg) was increased in SLE mice compared to controls (140±4 vs. 114±2; p<0.001). Nicotine prevented the rise in MAP in SLE mice (129±4; p=0.022), but not controls (121±3). This protection from hypertension coincided with a 46±5% lower renal cortical TNF-α in nicotine-treated SLE mice compared to saline-treated SLE mice (0.39±0.04 vs. 0.73±0.18), which is important because it has been previously shown that renal TNF-α plays a mechanistic role in the development of hypertension during SLE. Because nicotine acts on both ganglionic and peripheral cholinergic receptors, in a subsequent study mice were administered the selective α7nAChR agonist, PNU-282987 (0.38 mg/kg/day, IP), or vehicle for 28 days. PNU-282987-treated SLE mice had lower splenic protein expression of TNF-α and IL-6 relative to saline-treated SLE mice (0.33±0.01 vs. 0.54±0.03 and 0.40±0.08 vs. 0.86±0.05; all p<0.05). MAP was increased in SLE mice compared to controls (138±2 vs. 122±5). PNU-282987 prevented the rise in MAP in SLE mice (128±4), but not controls (125±5). These data suggest the anti-inflammatory effects of cholinergic agonists may protect from SLE hypertension and that the cholinergic anti-inflammatory pathway may be an important target in hypertensive patients with chronic inflammatory diseases.

Anti-Inflammatory Activity of Ethanol Extract of Marine Sponge Petrosia Sp. by Supression the Level of Tumor Necrosis Factor-alpha

2021 ◽  
pp. 4435-4439
Author(s):  
Adryan Fristiohady ◽  
Muhammad Hajrul Malaka ◽  
Andi Rizqa Wahyuni Safitri ◽  
Dewo Diha ◽  
Saripuddin Saripuddin ◽  
...  
Keyword(s):  
Inflammatory Process ◽  
Oral Treatment ◽  
Ethanol Extract ◽  
The Body ◽  
Inflammatory Activity ◽  
Inflammatory Agent ◽  
Edema Volume ◽  
Group I ◽  
Tnf Α ◽  
Anti Inflammatory

Inflammation is the host's protective response to any stimulus that harms the body. Excessive inflammatory process causes tissue damage. Therefore, an anti-inflammatory agent is needed. The use of natural ingredients, especially sea sponges, is an option to reduce the side effects of anti-inflammatory agents. This utilization is related to the discovery of new agents. So, we tested the effect of the ethanol extract of Petrosia sp. as an anti-inflammatory agent. Animal induced with 1% carrageenan and left for 1 hour. After that the animals were divided into 6 groups (n = 4) and given oral treatment, namely: Group I (normal group); Group II (negative group); Group III (ethanol extract of Petrosia sp. Concentration of 0.05mg/ml); Group IV (ethanol extract of Petrosia sp. Concentration 0.1mg/ml); Group V (ethanol extract of Petrosia sp. Concentration 0.2mg/ml); and Group VI (positive group, Diclofenac Sodium). After 1 hour, the animals were measured for edema volume and plasma TNF-α levels. Based on the research conducted, the ethanol extract of Petrosia sp. decreased edema volume and plasma TNF-α levels in inflammatory mice. The concentration of 0.2mg/mL had a significant effect on the negative control used (p <0.05). On the other hand, Petrosia sp. indicates the presence of alkaloids, flavonoids, and steroids. They may play an important role in the anti-inflammatory process. Thus, it can be concluded that the ethanol extract of Petrosia sp. has anti-inflammatory activity.

scholarly journals Essential Oil of Myrtus communis Inhibits Inflammation in Rats by Reducing Serum IL-6 and TNF-α

2011 ◽  
Vol 6 (10) ◽  
pp. 1934578X1100601 ◽  
Author(s):  
Andrea Maxia ◽  
Maria Assunta Frau ◽  
Danilo Falconieri ◽  
Manvendra Singh Karchuli ◽  
Sanjay Kasture
Keyword(s):  
Essential Oil ◽  
Inflammatory Activity ◽  
Myrtus Communis ◽  
Ear Edema ◽  
Tnf Α ◽  
Cotton Pellet ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis

The topical anti-inflammatory activity of the essential oil of Myrtus communis L. was studied using croton oil induced ear edema and myeloperoxidase (MPO) activity in mice, and cotton pellet induced granuloma, and serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in rats. On topical application, the oil exhibited a significant decrease in the ear edema as well as MPO activity. The oil also inhibited cotton pellet-induced granuloma and serum TNF-α and IL-6. It can be concluded that the essential oil of Myrtus communis reduces leukocyte migration to the damaged tissue and exhibits anti-inflammatory activity.

scholarly journals Cerevisterol Alleviates Inflammation via Suppression of MAPK/NF-κB/AP-1 and Activation of the Nrf2/HO-1 Signaling Cascade

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 199 ◽  
Author(s):  
Md Badrul Alam ◽  
Nargis Sultana Chowdhury ◽  
Md Hossain Sohrab ◽  
Md Sohel Rana ◽  
Choudhury Mahmood Hasan ◽  
...  
Keyword(s):  
Endophytic Fungi ◽  
Fusarium Solani ◽  
Nuclear Translocation ◽  
Mapk Signaling ◽  
Inflammatory Activity ◽  
Signaling Cascade ◽  
Nuclear Factor ◽  
Tnf Α ◽  
Gene Assay ◽  
Anti Inflammatory

As part of our continuous effort to find potential anti-inflammatory agents from endophytic fungi, a Fusarium solani strain, isolated from the plant Aponogeton undulatus Roxb., was investigated. Cerevisterol (CRVS) was identified from endophytic fungi, a Fusarium solani strain, and moreover exhibited anti-inflammatory activity. However, the underlying mode of action remains poorly understood. The aim of this study is to reveal the potential mechanisms of CRVS against inflammation on a molecular level in LPS-activated RAW 264.7 peritoneal macrophage cells. CRVS was isolated from F. solani and characterized based on spectral data analysis. The MTT assay was performed to measure cell viability in CRVS-treated macrophages. Anti-inflammatory activity was assessed by measurement of nitric oxide (NO) and prostaglandin E2 (PGE2) levels, as well as the production of various cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and -6 (IL-6) in LPS-stimulated macrophages. RT-PCR and immunoblotting analyses were done to examine the expression of various inflammatory response genes. A reporter gene assay was conducted to measure the level of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and activator protein-1 (AP-1) transactivation. CRVS suppresses the LPS-induced production of NO and PGE2, which is a plausible mechanism for this effect is by reducing the expression of iNOS and COX-2. CRVS also decreases the expression of pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-1β. CRVS halted the nuclear translocation of NF-κB by blocking the phosphorylation of inhibitory protein κBα (IκBα) and suppressing NF-κB transactivation. The mitogen-activated protein kinases (MAPK) signaling pathways are also suppressed. CRVS treatment also inhibited the transactivation of AP-1 and the phosphorylation of c-Fos. Furthermore, CRVS could induce the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) by down-regulating Kelch-like ECH-associated protein 1 (Keap-1) and up-regulating hemeoxygenases-1 (HO-1) expression. The results suggest that CRVS acts as a natural agent for treating inflammatory diseases by targeting an MAPK, NF-κB, AP-1, and Nrf2-mediated HO-1 signaling cascade.

scholarly journals Beneficial Effects of Neurotensin in Murine Model of Hapten-Induced Asthma

2019 ◽  
Vol 20 (20) ◽  
pp. 5025 ◽  
Author(s):  
Ewelina Russjan ◽  
Katarzyna Kaczyńska
Keyword(s):  
Mast Cell ◽  
Murine Model ◽  
Airway Hyperreactivity ◽  
Inflammatory Activity ◽  
Atopic Asthma ◽  
Mast Cell Activation ◽  
Oxidative Stress Marker ◽  
Beneficial Effects ◽  
Tnf Α ◽  
Anti Inflammatory

Neurotensin (NT) demonstrates ambiguous activity on inflammatory processes. The present study was undertaken to test the potential anti-inflammatory activity of NT in a murine model of non-atopic asthma and to establish the contribution of NTR1 receptors. Asthma was induced in BALB/c mice by skin sensitization with dinitrofluorobenzene followed by intratracheal hapten provocation. The mice were treated intraperitoneally with NT, SR 142948 (NTR1 receptor antagonist) + NT or NaCl. Twenty-four hours after the challenge, airway responsiveness to nebulized methacholine was measured. Bronchoalveolar lavage fluid (BALF) and lungs were collected for biochemical and immunohistological analysis. NT alleviated airway hyperreactivity and reduced the number of inflammatory cells in BALF. These beneficial effects were inhibited by pretreatment with the NTR1 antagonist. Additionally, NT reduced levels of IL-13 and TNF-α in BALF and IL-17A, IL12p40, RANTES, mouse mast cell protease and malondialdehyde in lung homogenates. SR 142948 reverted only a post-NT TNF-α decrease. NT exhibited anti-inflammatory activity in the hapten-induced asthma. Reduced leukocyte accumulation and airway hyperresponsiveness indicate that this beneficial NT action is mediated through NTR1 receptors. A lack of effect by the NTR1 blockade on mast cell activation, oxidative stress marker and pro-inflammatory cytokine production suggests that other pathways can be involved, which requires further research.

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