International immunopharmacology
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Int. Immunopharmacol. · Sep 2019
Dexmedetomidine ameliorates LPS induced acute lung injury via GSK-3β/STAT3-NF-κB signaling pathway in rats.
Acute lung injury (ALI) is a serious complication of sepsis and an important cause of death in intensive care. Studies have shown that DEX can inhibit inflammation. However, the anti-inflammatory effect and protective mechanism of DEX in lipopolysaccharide (LPS) induced ALI are still unclear. ⋯ What's more, NSC74859 inhibited the phosphorylation of STAT3 and reversed the protect effect of DEX on LPS. SB216763 inhibited the phosphorylation of NF-κB and reversed the damage effect of LPS and plays the same anti-inflammatory effect as DEX. In summary, our data demonstrated that DEX can ameliorate ALI induced by LPS through GSK-3β/STAT3-NF-κB pathway.
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Int. Immunopharmacol. · Aug 2019
PIM1 inhibitor SMI-4a attenuated lipopolysaccharide-induced acute lung injury through suppressing macrophage inflammatory responses via modulating p65 phosphorylation.
PIM kinase is involved in the cellular processes of growth, differentiation and apoptosis. However, the role of PIM1 in lipopolysaccharide (LPS)-induced acute lung injury (ALI) remains largely unknown. A trend of PIM1 in the lung tissue of LPS-induced ALI at different time points was detected. ⋯ The PIM1 inhibitor SMI-4a suppressed the production of cytokines in LPS-treated RAW264.7 cell supernatants and BALF. Furthermore, LPS administration upregulated the levels of nuclear p65 and phosphorylated p65 (p-p65) at Ser276, whereas pretreatment with the PIM1 inhibitor SMI-4a reduced p65 upregulation in the nucleus and p-p65 at Ser276. Taken together, these data indicate that the PIM1 inhibitor SMI-4a may serve as a promising therapeutic strategy for LPS-induced ALI by suppressing macrophage production of cytokines via a reduction of p65 activities.
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Int. Immunopharmacol. · Jul 2019
ReviewBibliometric analysis of global research on PD-1 and PD-L1 in the field of cancer.
To identify the cooperation of authors, countries, and institutions and explore the hot topics and future prospects regarding programmed cell death protein 1 (PD-1) and programmed cell death 1 ligand 1 (PD-L1) research. ⋯ PD-1 and PD-L1 studies have significantly increased after 2014. The USA contributed the most publications. There were active cooperations between authors, countries, and institutions. Further research should expand and develop new topics such as those likely to boost therapeutic strategies for cancer.
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Int. Immunopharmacol. · Jul 2019
Doxycycline alleviates paraquat-induced acute lung injury by inhibiting neutrophil-derived matrix metalloproteinase 9.
Paraquat (PQ), a highly toxic herbicide, selectively accumulates in the lungs and causes pulmonary damage through oxidative and inflammatory processes after intentional or accidental poisoning. The resulting acute lung injury (ALI) is characterized by neutrophil infiltration and extensive inflammation with rapid respiratory failure. However, effective therapies are lacking. ⋯ Consistently, oral delivery of DOX to mice decreased the overexpression of MMP9 that was activated by PQ and phenocopied the resolution of PQ-induced ALI observed after neutrophil depletion. Taken together, our results show for the first time that DOX is involved in the resolution of PQ-induced ALI via a mechanism involving reducing the activity of neutrophil-derived MMP9. We speculate that DOX may represent a novel therapeutic strategy for PQ-induced ALI.
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Int. Immunopharmacol. · Jun 2019
UCP2 ameliorates mitochondrial dysfunction, inflammation, and oxidative stress in lipopolysaccharide-induced acute kidney injury.
UCP2 is involved in the maintenance of mitochondrial function, immune response and regulation of oxidative stress under physiological or pathological conditions. The aim of this study was to investigate the effects of UCP2 on mitochondrial dysfunction, inflammation, and oxidative stress in septic acute kidney injury (AKI). ⋯ UCP2 may protect LPS-induced AKI by ameliorating mitochondrial dysfunction, anti-inflammation, and antioxidative activities, ultimately inhibiting tubule epithelial cell apoptosis, and that increasing the UCP2 content in mitochondria constitutes a new therapeutic approach for septic AKI.