scholarly journals Phyto-therapeutic potential of stem bark of the wonder tree, Prosopis cineraria (L.) Druce in LPS-induced mouse model: An Anti-Inflammatory Study

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Veena Sharma ◽  
Preeti Sharma
Keyword(s):  
Mouse Model ◽  
Therapeutic Potential ◽  
Stem Bark ◽  
Prosopis Cineraria ◽  
Anti Inflammatory

MAPK/AP-1-Targeted Anti-Inflammatory Activities of Xanthium strumarium

2016 ◽  
Vol 44 (06) ◽  
pp. 1111-1125 ◽  
Author(s):  
Muhammad Jahangir Hossen ◽  
Mi-Yeon Kim ◽  
Jae Youl Cho
Keyword(s):  
Mouse Model ◽  
Therapeutic Potential ◽  
Inflammatory Diseases ◽  
Elevated Serum ◽  
Human Monocyte ◽  
Serum Levels ◽  
Mitogen Activated Protein Kinase ◽  
Xanthium Strumarium ◽  
U937 Cells ◽  
Anti Inflammatory

Xanthium strumarium L. (Asteraceae), a traditional Chinese medicine, is prescribed to treat arthritis, bronchitis, and rhinitis. Although the plant has been used for many years, the mechanism by which it ameliorates various inflammatory diseases is not yet fully understood. To explore the anti-inflammatory mechanism of methanol extracts of X. strumarium (Xs-ME) and its therapeutic potential, we used lipopolysaccharide (LPS)-stimulated murine macrophage-like RAW264.7 cells and human monocyte-like U937 cells as well as a LPS/D-galactosamine (GalN)-induced acute hepatitis mouse model. To find the target inflammatory pathway, we used holistic immunoblotting analysis, reporter gene assays, and mRNA analysis. Xs-ME significantly suppressed the up-regulation of both the activator protein (AP)-1-mediated luciferase activity and the production of LPS-induced proinflammatory cytokines, including interleukin (IL)-1[Formula: see text], IL-6, and tumor necrosis factor (TNF)-[Formula: see text]. Moreover, Xs-ME strongly inhibited the phosphorylation of mitogen-activated protein kinase (MAPK) in LPS-stimulated RAW264.7 and U937 cells. Additionally, these results highlighted the hepatoprotective and curative effects of Xs-ME in a mouse model of LPS/D-GalN-induced acute liver injury, as assessed by elevated serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and histological damage. Therefore, our results strongly suggest that the ethnopharmacological roles of Xs-ME in hepatitis and other inflammatory diseases might result from its inhibitory activities on the inflammatory signaling of MAPK and AP-1.

scholarly journals New Class of Anti-Inflammatory Therapeutics Based on Gold (III) Complexes in Intestinal Inflammation–Proof of Concept Based on In Vitro and In Vivo Studies

2021 ◽  
Vol 22 (6) ◽  
pp. 3121
Author(s):  
Julia B. Krajewska ◽  
Jakub Włodarczyk ◽  
Damian Jacenik ◽  
Radzisław Kordek ◽  
Przemysław Taciak ◽  
...  
Keyword(s):  
Mouse Model ◽  
Intestinal Inflammation ◽  
Therapeutic Potential ◽  
Gastrointestinal Diseases ◽  
Neutral Red ◽  
Water Soluble ◽  
In Vivo Studies ◽  
Anti Inflammatory

Inflammatory bowel diseases (IBD) are at the top of the worldwide rankings for gastrointestinal diseases as regards occurrence, yet efficient and side-effect-free treatments are currently unavailable. In the current study, we proposed a new concept for anti-inflammatory treatment based on gold (III) complexes. A new gold (III) complex TGS 121 was designed and screened in the in vitro studies using a mouse macrophage cell line, RAW264.7, and in vivo, in the dextran sulphate sodium (DSS)-induced mouse model of colitis. Physicochemical studies showed that TGS 121 was highly water-soluble; it was stable in water, blood, and lymph, and impervious to sunlight. In lipopolysaccharide (LPS)-stimulated RAW264.7 cells, the complex showed a potent anti-inflammatory profile, as evidenced in neutral red uptake and Griess tests. In the DSS-induced mouse model of colitis, the complex administered in two doses (1.68 μg/kg, intragastrically, and 16.8 μg/kg, intragastrically, once daily) produced a significant (* p < 0.05) anti-inflammatory effect, as shown by macroscopic score. The mechanism of action of TGS 121 was related to the enzymatic and non-enzymatic antioxidant system; moreover, TGS 121 induced changes in the tight junction complexes expression in the intestinal wall. This is the first study proving that gold (III) complexes may have therapeutic potential in the treatment of IBD.

scholarly journals A Cell Penetrating Peptide from Type I Interferon Protects the Retina in a Mouse Model of Autoimmune Uveitis

2019 ◽  
Author(s):  
Chulbul M Ahmed ◽  
Cristhian J Ildefonso ◽  
Howard M Johnson ◽  
Alfred S Lewin
Keyword(s):  
Mouse Model ◽  
Therapeutic Potential ◽  
Type I ◽  
Cell Penetration ◽  
Autoimmune Uveitis ◽  
C Terminus ◽  
Tnf Α ◽  
A Cell ◽  
Anti Inflammatory ◽  
And Function

AbstractExperimental autoimmune uveitis (EAU) in rodents recapitulates many features of the disease in humans and has served as a useful tool for the development of therapeutics. A peptide from C-terminus of interferon α1, conjugated to palmitoyl-lysine for cell penetration, denoted as IFNα–C, was tested for its anti-inflammatory properties in ARPE-19 cells, followed by testing in a mouse model of EAU. Treatment with IFNα–C and evaluation by RT-qPCR showed the induction of anti-inflammatory cytokines and chemokine. Inflammatory markers induced by treatment with TNFα were suppressed when IFNα–C was simultaneously present. TNF-α mediated induction of NF-kB and signaling by IL-17A were attenuated by IFNα–C. Differentiated ARPE-19 cells were treated with TNFα in the presence or absence IFNα–C and analyzed by immmunhistochemistry. IFNα–C protected against the disruption integrity of tight junction proteins. Similarly, loss of transepithelial resistance caused by TNFα was prevented by IFNα–C. B10.RIII mice were immunized with a peptide from interphotoreceptor binding protein (IRBP) and treated by gavage with IFNα–C. Development of uveitis was monitored by histology, fundoscopy, SD-OCT, and ERG. Treatment with IFNα–C prevented uveitis in mice immunized with the IRBP peptide. Splenocytes isolated from mice with ongoing EAU exhibited antigenspecific T cell proliferation that was inhibited in the presence of IFNα–C. IFNα–C peptide exhibits anti-inflammatory properties and protects mice against damage to retinal structure and function suggesting that it has therapeutic potential for the treatment of autoimmune uveitis.

scholarly journals SO022PBI-4425, A NOVEL ANTI-INFLAMMATORY/FIBROTIC COMPOUND, IMPROVES KIDNEY FUNCTION AND GLOMERULAR INTEGRITY IN THE DIABETIC DB/DB MOUSE MODEL

2016 ◽  
Vol 31 (suppl_1) ◽  
pp. i10-i10
Author(s):  
Lyne Gagnon ◽  
Kathy Hince ◽  
François Sarra-Bournet ◽  
Liette Gervais ◽  
Alexandra Felton ◽  
...  
Keyword(s):  
Mouse Model ◽  
Kidney Function ◽  
Anti Inflammatory

The therapeutic potential of resveratrol in a mouse model of melanoma lung metastasis

2020 ◽  
Vol 88 ◽  
pp. 106905 ◽  
Author(s):  
Amirhossein Davoodvandi ◽  
Maryam Darvish ◽  
Sarina Borran ◽  
Majid Nejati ◽  
Samaneh Mazaheri ◽  
...  
Keyword(s):  
Mouse Model ◽  
Lung Metastasis ◽  
Therapeutic Potential

scholarly journals Empagliflozin Improves Metabolic and Hepatic Outcomes in a Non-Diabetic Obese Biopsy-Proven Mouse Model of Advanced NASH

2021 ◽  
Vol 22 (12) ◽  
pp. 6332
Author(s):  
Nikolaos Perakakis ◽  
Pavlina Chrysafi ◽  
Michael Feigh ◽  
Sanne Skovgard Veidal ◽  
Christos S. Mantzoros
Keyword(s):  
Mouse Model ◽  
Cell Activation ◽  
Stellate Cell ◽  
Liver Steatosis ◽  
Tolerance Test ◽  
The Body ◽  
Oral Glucose ◽  
Alcoholic Fatty Liver ◽  
Metabolic Outcomes ◽  
Anti Inflammatory

Empagliflozin, an established treatment for type 2 diabetes (T2DM), has shown beneficial effects on liver steatosis and fibrosis in animals and in humans with T2DM, non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH). However, little is known about the effects of empagliflozin on liver function in advanced NASH with liver fibrosis and without diabetes. This study aimed to assess the effects of empagliflozin on hepatic and metabolic outcomes in a diet-induced obese (DIO) and insulin-resistant but non-diabetic biopsy-confirmed mouse model of advanced NASH. Male C57BL/6JRj mice with a biopsy-confirmed steatosis and fibrosis on AMLN diet (high fat, fructose and cholesterol) for 36-weeks were randomized to receive for 12 weeks: (a) Empagliflozin (10 mg/kg/d p.o.), or (b) vehicle. Metabolic outcomes, liver pathology, markers of Kupffer and stellate cell activation and lipidomics were assessed at the treatment completion. Empagliflozin did not affect the body weight, body composition or insulin sensitivity (assessed by intraperitoneal insulin tolerance test), but significantly improved glucose homeostasis as assessed by oral glucose tolerance test in DIO-NASH mice. Empagliflozin improved modestly the NAFLD activity score compared with the vehicle, mainly by improving inflammation and without affecting steatosis, the fibrosis stage and markers of Kupffer and stellate cell activation. Empagliflozin reduced the hepatic concentrations of pro-inflammatory lactosylceramides and increased the concentrations of anti-inflammatory polyunsaturated triglycerides. Empagliflozin exerts beneficial metabolic and hepatic (mainly anti-inflammatory) effects in non-diabetic DIO-NASH mice and thus may be effective against NASH even in non-diabetic conditions.

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