2-Chloroadenosine (2-CADO) treatment modulates the pro-inflammatory immune response to prevent acute lung inflammation in BALB/c mice suffering from Klebsiella pneumoniae B5055-induced pneumonia

Kumar, Vijay; Harjai, Kusum; Chhibber, Sanjay

doi:10.1016/j.ijantimicag.2010.01.014

Cited by 8 publications

(5 citation statements)

References 9 publications

(7 reference statements)

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“…Drugs that block all inflammation links could be used to treat delayed damage caused by cerebral ischemia (26,27). So far, the drugs that resist inflammatory activation of MG after cerebral ischemia are pro-inflammatory factor inhibitors: a non-selective adenosine receptor agonist 2-Cado can effectively suppress the expression of TNF-α in ischemia-injured tissue and cells, and brazilein has been shown to effectively protect brain tissue by inhibiting TNF-α and IL-6 expressions (28,29). Mechanistic studies have shown that NF-κB, a classical regulator of inflammatory response, plays a dominant role in ischemia-reperfusioninduced MG activation.…”

Section: Discussionmentioning

confidence: 99%

Sinomenine relieves oxygen and glucose deprivation-induced microglial activation via inhibition of the SP1/miRNA-183-5p/IÎºB-Î± signaling pathway

Qin

Zhao

Wang

et al. 2018

Cell Mol Biol (Noisy-le-grand)

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Studies have shown that the inflammatory activation of miroglia (MG) and nuclear factor kappa B ( NF-κB ) play a dominant role in inflammatory response. Previous studies have shown that sinomenine, an anti-inflammatory agent extracted from Sinomenium acutum, can directly protect neurons against cerebral ischemia injury. However, there are no reports on its effect on ischemia/reperfusion-induced inflammatory activation of MG. In the present study, an in vitro ischemia/reperfusion model was developed with mouse BV-2 microglia cells, a model of oxygen-glucose deprivation/reperfusion (OGD/R), and the inhibitory effect of sinomenine pretreatment on inflammatory activation was confirmed through measurement of inflammatory indicators. Mechanistically, sinomenine suppressed OGD/R-induced inflammatory activation through the SP1/miRNA-183-5p/IκB-α pathway. In conclusion, this study shows that sinomenine effectively inhibits OGD/R-induced inflammatory activation in MG by suppressing the activation of transcription specificity protein 1 (SP 1). This finding is of significance for the clinical use of sinomenine in treating cerebral ischemia/reperfusion injury.

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Section: Discussionmentioning

confidence: 99%

Sinomenine relieves oxygen and glucose deprivation-induced microglial activation via inhibition of the SP1/miRNA-183-5p/IÎºB-Î± signaling pathway

Qin

Zhao

Wang

et al. 2018

Cell Mol Biol (Noisy-le-grand)

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“…2-Chloro (7) 19 and 2-fluoroadenosine (8) 20 show interesting activities in several biological systems. Thus, the development of simple and efficient ways to construct these compounds is highly desirable.…”

Section: Resultsmentioning

confidence: 99%

Diversity-Oriented Synthesis of 2-Substituted Purine Nucleosides from Available Nucleosides via the Late-Stage Nitration/Derivatization

Ran¹,

Chen²,

Liu³

et al. 2022

HETEROCYCLES

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A practical synthesis of 2-substituted purine nucleosides was developed in good to excellent yields from readily available nucleosides, such as adenosine, vidarabine and 2′-deoxyadenosine, via the late-stage nitration/derivatization. The C(2)-H bonds of purines were nitrated by 2,2,2-trifluoroacetic anhydride/Bu4NNO3, followed by nucleophilic substitution or hydrogenolysis reduction converting C(2)-NO2 to C(2)-Cl, C(2)-F, C(2)-N, C(2)-O and C(2)-S bonds. This system could tolerate arabinofuranosyl, ribosyl, deoxyribosyl, -OH or -NH2 groups. The clinical drugs, Regadenoson, Cladribine and Fludarabine, and the important naturally occurring nucleosides, spongosineand crotonoside, could be obtained successfully even on 20 g scales, which made this route more attractive for industrial applications.

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“…For all we know, K. pneumoniae is a pathogen of clinical relevance and can induce the inflammatory response of lung, 64 while in vivo experiments revealed that KLA significantly reduced the bacterial load and levels of inflammatory cytokine in the lungs of mice with pneumonia and reduced the degree of lesions and the accumulation of neutrophils in the lung tissues, indicating that KLA could reduce inflammatory response to protect lung cells by destroying K. pneumoniae . It has been pointed out that the in vitro activity of antimicrobial peptides usually cannot be translated into in vivo efficacy due to the interference of the host microenvironment on peptide stability/efficacy.…”

Section: Discussionmentioning

confidence: 99%

Exploration of Antimicrobial Peptides in the Treatment of Gentamicin-Resistant Klebsiella pneumoniae Infection

Chen,

Zhang,

et al. 2024

IDR

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2-Chloroadenosine (2-CADO) treatment modulates the pro-inflammatory immune response to prevent acute lung inflammation in BALB/c mice suffering from Klebsiella pneumoniae B5055-induced pneumonia

Cited by 8 publications

References 9 publications

Sinomenine relieves oxygen and glucose deprivation-induced microglial activation via inhibition of the SP1/miRNA-183-5p/IÎºB-Î± signaling pathway

Sinomenine relieves oxygen and glucose deprivation-induced microglial activation via inhibition of the SP1/miRNA-183-5p/IÎºB-Î± signaling pathway

Diversity-Oriented Synthesis of 2-Substituted Purine Nucleosides from Available Nucleosides via the Late-Stage Nitration/Derivatization

Exploration of Antimicrobial Peptides in the Treatment of Gentamicin-Resistant Klebsiella pneumoniae Infection

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