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• Research Paper Volume 13, Issue 11 pp 15511-15522

  Propofol ameliorates renal ischemia/reperfusion injury by enhancing macrophage M2 polarization through PPARγ/STAT3 signaling

  Relevance score: 16.473232

  Zhaohui Liu, Yanli Meng, Yu Miao, Lili Yu, Qianjie Wei, Yuqing Li, Bing Zhang, Qiannan Yu

  Keywords: renal ischemia/reperfusion injury, propofol, peritoneal macrophage, inflammatory response

  Published in Aging on June 10, 2021

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  Propofol (Pro) confers protection against renal ischemia/reperfusion (rI/R) injury through incompletely characterized mechanisms. Since Pro has shown net anti-inflammatory properties as part of its beneficial effects, we examined the potential role of Pro in the modulation of macrophage polarization status during both rI/R injury in vivo and exposure of cultured peritoneal macrophages (PMs) to hypoxia/reoxygenation (H/R). Rats were subjected to 45-min r/IR surgery or a sham procedure and administered PBS (vehicle) or Pro during the ischemia stage. Pro administration attenuated rI/R-induced kidney damage and renal TNF-α, IL-6, and CXCL-10 expression. Enhanced macrophage M2 polarization, evidenced by reduced iNOS and increased Arg1 and Mrc1 mRNA levels, was further detected after Pro treatment both in the kidney, after rI/R in vivo, and in H/R-treated PMs. Pro administration also repressed phosphorylated signal transducer and activator of transcription 1 (p-STAT1) and increased p-STAT3, p-STAT6, and peroxisome proliferator-activated receptor-γ (PPARγ) mRNA levels in H/R-exposed PMs. Importantly, siRNA-mediated PPARγ silencing repressed Pro-mediated STAT3 activation in PMs and restored proinflammatory cytokine levels and prevented macrophage M2 marker expression in both rI/R-treated rats and cultured PMs. These findings suggest that Pro confers renoprotection against rI/R by stimulating PPARγ/STAT3-dependent macrophage conversion to the M2 phenotype.

• Research Paper Volume 11, Issue 7 pp 2031-2044

  Exogenous biological renal support ameliorates renal pathology after ischemia reperfusion injury in elderly mice

  Relevance score: 15.839151

  Dong Liu, Zhiwei Yin, Qi Huang, Yi Ren, Diangeng Li, Linna Wang, Shaoyuan Cui, Ying Zhang, Yichun Ning, Lide Lun, Guangyan Cai, Xueyuan Bai, Xuefeng Sun, Xiangmei Chen

  Keywords: aged, renal ischemia reperfusion injury, parabiosis model, exogenous biological renal support, cytokines

  Published in Aging on April 12, 2019

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  We established an exogenous biological renal support model through the generation of parabiotic mice. At 72 hours after ischemia reperfusion injury (IRI), the aged mice that received exogenous biological renal support showed significantly higher levels of renal cell proliferation and dedifferentiation, lower levels of renal tubular injury, improved renal function, and a lower mortality than those that did not receive exogenous biological renal support. Using the Quantibody Mouse Cytokine Antibody Array, we found that aged IRI mice that received exogenous biological renal support had an up-regulation of multiple inflammatory related cytokines compared to the group that did not receive exogenous biological renal support. We suggest that the exogenous biological renal support might promote renal tubular epithelial cell proliferation and dedifferentiation and improve the prognosis of aged IRI mice. Exogenous biological renal support may play an important role in the amelioration of renal IRI by regulating the expression of multiple cytokines.

  

  Exogenous biological renal support improved renal IRI and decreased mortality and serum Cr, BUN levels in old IRI mice. (A) Survival curves for the old IRI mice at 72 hours. (B) Cr levels in the old mice. (C) BUN levels in the old mice. (D) Representative photographs of kidney sections from the old mice stained with periodic acid–Schiff (400× magnification). (E) Renal tubular injury score. (F) The levels of Kim1 in kidney extracts from the old mice, as measured by western blotting. Gels were performed under the same experimental conditions. (G) Quantitative analyses of the band densities of Kim1 expression. Values are presented as means ± SDs. ▲P < 0.05, ▲▲P < 0.01 vs. O: sham; *P < 0.05, **P < 0.01 vs. O: IRI. BUN, blood urea nitrogen Cr, serum creatinine; SD, standard deviation.

  
  
  

  

  Exogenous biological renal support increased renal cell proliferation in old IRI mice. (A) Representative images of renal EdU-positive cells in independent groups (600× magnification; red, EDU; green, LTL; blue, DAPI). (B) The percentages of EdU-positive cells in the kidneys of the old mice at 72 hours after IRI. The mice in the O: IRI group displayed more EdU-positive cells than in O: sham group. The percentage of EdU-positive cells was higher in the O-O: IRI group and the Y-O: IRI group than in the O: IRI group. No significant difference was found between the O-O: IRI group and the Y-O: IRI group. (C) Representative images of renal PCNA-positive tubular cells in independent groups (400× magnification). (D) The percentages of PCNA-positive tubular cells in the kidneys of the old mice at 72 hours after IRI. The mice in the O: IRI group had more PCNA-positive tubular cells than the O: sham group. The percentages of PCNA-positive tubular cells were higher in the O-O: IRI group and the Y-O: IRI group than in the O: IRI group. No significant difference was found between the O-O: IRI group and the Y-O: IRI group. (E) The levels of cyclin D1 and cyclin E1 in kidney extracts of the old IRI mice as measured by western blotting. Gels were performed under the same experimental conditions. (F, G) Quantitative analyses of the band densities of cyclin D1 and cyclin E1 protein expression. Data are presented as means ± SDs. ▲P < 0.05, ▲▲P < 0.01 vs. O: sham; *P < 0.05, **P < 0.01 vs. O: IRI. SD, standard deviation.

  
  
  

  

  Exogenous biological renal support increased dedifferentiation in old IRI mice kidney. (A) The levels of Pax2, vimentin, and ERK1/2 in kidney extracts of the old IRI mice as measured by western blotting. Gels were performed under the same experimental conditions. (B–D) Quantitative analyses of the band densities of Pax2, vimentin, and ERK1/2 expressions. Data are presented as means ± SDs. ▲P < 0.05, ▲▲P < 0.01 vs. O: sham; *P < 0.05, **P < 0.01 vs. O: IRI. SD, standard deviation.

  
  
  

  

  The impact of serum cytokines on the prognosis of the old IRI mice. (A) The canonical serum cytokines between the O-O: IRI to the old: IRI group and the Y-O: IRI to the old: IRI group. (B) Heat map of the O-O: IRI to the old: IRI group. (C) Heat map of the Y-O: IRI to the old: IRI group. (D) Gene Ontology Annotation was used to identify the molecular function of the differentially expressed cytokines (E) Gene Ontology Annotation was used to identify the cellular components of the differentially expressed cytokines (F) Gene Ontology Annotation was used to identify the biological process of differentially expressed cytokines (G) The KEGG pathways that changed significantly were those related to differentially expressed cytokines. (H) The protein-protein interaction network among the differentially expressed cytokines.

  
  
  

• Research Paper pp undefined-undefined

  Protective effect of fluoxetine against oxidative stress induced by renal ischemia-reperfusion injury via the regulation of miR-450b-5p/Nrf2 axis

  Relevance score: 15.10333

  Zhiqiang Qin, Hao Wang, Quanliang Dou, Luwei Xu, Zheng Xu, Ruipeng Jia

  Keywords: renal ischemia-reperfusion injury, fluoxetine, miR-450b-5p, Nrf2, oxidative stress

  Published in Aging on Invalid Date

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  The present study was performed to assess the protective effect of fluoxetine (FLX) on renal ischemia-reperfusion injury (IRI) via the regulation of miR-450b-5p/Nrf2 axis in male rats. In vivo, these male rats were randomly divided into different treatment groups. The rats were administered with FLX (20 mg/kg, intraperitoneally) once daily for 3 days before operation. The pathomorphological changes of renal tissues were assessed by histological examination and Masson staining. In vitro, HK-2 cells was used to detect the activity by CCK-8 assay in Hypoxia/Reoxygenation (H/R) group and Hypoxia/Reoxygenation+Fluoxetine (H/R+FLX) group. In addition, the oxidative stress biomarkers were evaluated. Subsequently, Nrf2, NF-κB, and Nrf2-dependent antioxidant enzymes, were detected by Western blot assay. In vivo, the pathological changes and serological renal function were significantly relieved in the rats with the pre-treatment of FLX, compared to IRI group. After FLX stimulation, the expression levels of oxidative stress indices significantly decreased, while tissue antioxidant indices significantly increased, compared to IRI group. The differently expressed miRNAs on renal IRI in male rats were screened out by miRNA microarray, especially showing that miR-450b-5p was selected as the target miRNA. Following miR-450b-5p agomir injection, the pathological changes and oxidative stress biomarkers significantly aggravated, whether in IRI group or IRI+FLX group. Bioinformatics analysis and double-luciferase reporter assay demonstrated that miR-450b-5p directly targeted Nrf2. The expression level of NF-κB significantly increased, while the expression levels of Nrf2 and Nrf2-dependent antioxidant enzymes significantly decreased after miR-450b-5p agomir injection. Furthermore, the expression levels of Nrf2 and it-dependent antioxidant enzymes were apparently increased in ischemic kidney after the transfection of miR-450b-5p mimic+recombination protein Nrf2, as well as the decreased expression levels of intracellular ROS and iNOS. In vitro, FLX significantly increased HK-2 cell viability, and relieved H/R HK-2 cell oxidative injury via down-regulating ROS and iNOS. In addition, H/R-induced oxidative damage was recovered with miR-450b-5p mimic and recombination protein Nrf2. Consequently, FLX played an important protective role in renal IRI-induced oxidative damage by promoting antioxidation via targeting miR-450b-5p/Nrf2 axis.