Arteannuin-B and its spiro-isoxazoline derivative inhibits LPS induced pro-inflammatory responses in RAW 264.7 macrophages and BALB/c mice via down-regulation of NF-$κ$$β$/P38 MAPK mediated stress signalling. Sawhney, G., Ozturk, M., Parihar, S., Brombacher, F., Ahmad, B., Bhagat, A., Ali, A., & Ahmed, Z. Research Square, jul, 2022. ![Arteannuin-B and its spiro-isoxazoline derivative inhibits LPS induced pro-inflammatory responses in RAW 264.7 macrophages and BALB/c mice via down-regulation of NF-$κ$$β$/P38 MAPK mediated stress signalling [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex Amongst the most significant scientific findings in the last two decades has been the role of inflammatory processes in protecting the host against the causative agents of injury. In this work, we examined the anti-inflammatory activities of Arteannuin-B (1) and its novel spirocyclic-2-isoxazoline derivative (2). Various anti-inflammatory assays were performed in lipopolysaccharide (LPS) induced RAW 264.7 macrophages using enzyme-linked immunosorbent assay, flow cytometric analysis, and western blotting. As a result, treatment with (2) decreased LPS-stimulated inducible nitric oxide synthase protein expression (iNOS), as well as production of nitric oxide (NO), tumor necrosis factor-alpha (TNF-$α$), and interleukin-6 (IL-6) in LPS induced RAW 264.7 cells. Additionally, the effects of (1) and (2) in an acute inflammatory condition were investigated in-vivo by using models like carrageenan-induced paw edema assay, acetic acid-induced writhing and tail immersion model in experimental mice, suggesting that (2) is a more potent anti-inflammatory candidate as compared to (1) with very low cell toxicity. In addition, biocomputational studies and histopathological analysis were also performed to validate the efficiency of (2) as compared to (1).
@article{Sawhney2022,
abstract = {Amongst the most significant scientific findings in the last two decades has been the role of inflammatory processes in protecting the host against the causative agents of injury. In this work, we examined the anti-inflammatory activities of Arteannuin-B (1) and its novel spirocyclic-2-isoxazoline derivative (2). Various anti-inflammatory assays were performed in lipopolysaccharide (LPS) induced RAW 264.7 macrophages using enzyme-linked immunosorbent assay, flow cytometric analysis, and western blotting. As a result, treatment with (2) decreased LPS-stimulated inducible nitric oxide synthase protein expression (iNOS), as well as production of nitric oxide (NO), tumor necrosis factor-alpha (TNF-$\alpha$), and interleukin-6 (IL-6) in LPS induced RAW 264.7 cells. Additionally, the effects of (1) and (2) in an acute inflammatory condition were investigated in-vivo by using models like carrageenan-induced paw edema assay, acetic acid-induced writhing and tail immersion model in experimental mice, suggesting that (2) is a more potent anti-inflammatory candidate as compared to (1) with very low cell toxicity. In addition, biocomputational studies and histopathological analysis were also performed to validate the efficiency of (2) as compared to (1).},
author = {Sawhney, Gifty and Ozturk, Mumin and Parihar, Suraj and Brombacher, Frank and Ahmad, Bilal and Bhagat, Asha and Ali, Asif and Ahmed, Zabeer},
doi = {10.21203/RS.3.RS-1881315/V1},
file = {:C$\backslash$:/Users/01462563/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Sawhney et al. - 2022 - Arteannuin-B and its spiro-isoxazoline derivative inhibits LPS induced pro-inflammatory responses in RAW 264.7 m.pdf:pdf},
journal = {Research Square},
keywords = {Innammation,Interleukin-6 (IL-6),Lipopolysaccharide (LPS),Nitric oxide (NO),OA,RAW 2647 cells,Tumor necrosis factor-alpha (TNF-$\alpha$),fund{\_}not{\_}ack,original},
mendeley-tags = {OA,fund{\_}not{\_}ack,original},
month = {jul},
pages = {https://doi.org/10.21203/rs.3.rs--1881315/v1},
title = {{Arteannuin-B and its spiro-isoxazoline derivative inhibits LPS induced pro-inflammatory responses in RAW 264.7 macrophages and BALB/c mice via down-regulation of NF-$\kappa$$\beta$/P38 MAPK mediated stress signalling}},
url = {https://www.researchsquare.com https://www.researchsquare.com/article/rs-1881315/v1},
year = {2022}
}
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