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Träfflista för sökning "WFRF:(Zhu Ning) ;pers:(Wei Jiang)"

Sökning: WFRF:(Zhu Ning) > Wei Jiang

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1.
  • Zhang, Xiaoying, et al. (författare)
  • Expression of MMP-10 in lung cancer
  • 2007
  • Ingår i: Anticancer research. - 1791-7530. ; 27:4C, s. 2791-2795
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Matrix metalloproteinase (MMP)-mediated degradation of the extracellular matrix is a key point in tumor development and expansion. MMP-10 is one of the most important and well-characterized members of the MMP family. In the present study, we examined MMP-10 mRNA and protein levels in non-small cell lung cancer (NSCLC). Patients and Methods: Three endogenous reference genes including GAPDH, beta-actin and 18S rRNA, and MMP-10 mRNA levels were determined using real-time RT-PCR. Immunohistochemical staining was applied to examine MMP-10 protein levels. Both tumor and adjacent normal lung tissues were collected from 32 NSCLC patients. The mRNA levels of GAPDH, beta-actin and 18S rRNA exhibited great differences in tumor tissues and in the adjacent normal tissues. The ratio of mRNA levels in the tumor tissues compared to the adjacent normal tissues followed the pattern GAPDH > beta-actin > 18S rRNA. Thereafter, we chose 18S rRNA as the reference gene for MMP-10 mRNA level determinations. MMP-10 mRNA levels in tumor tissues were significantly lower than those in the adjacent normal tissues (p = 0.0423). However, the MMP- 10 protein levels were higher in the tumor tissues than in the adjacent normal tissues (p=0.0055). The MMP-10 mRNA level was positively-correlated to the MMP-10 protein level in tumor tissues (r=0.4672, p=0.0161), but this correlation was not seen in the adjacent normal tissues (r=-0.0030, p=0.9891). Conclusion: There were no statistical differences in MMP-10 mRNA levels and protein levels in relation to patient's gender, age, tumor stages, tumor size, lymph node metastasis or tumor histological type.
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2.
  • Zhu, Bin, et al. (författare)
  • Apolipoprotein M Protects Against Lipopolysaccharide-Induced Acute Lung Injury via Sphingosine-1-Phosphate Signaling
  • 2018
  • Ingår i: Inflammation. - : Springer Science and Business Media LLC. - 0360-3997 .- 1573-2576. ; 41:2, s. 643-653
  • Tidskriftsartikel (refereegranskat)abstract
    • Abstract: It had been demonstrated that apolipoprotein M (apoM) is an important carrier of sphingosine-1-phosphate (S1P) in blood, and the S1P has critical roles in the pathogenesis of sepsis-induced acute lung injury (ALI). In the present study, we investigated whether apoM has beneficial effects in a mouse model after lipopolysaccharide (LPS)-induced ALI. Forty-eight mice were divided into two groups: male C57BL/6 wild-type (apoM+/+) group (n = 24) and apoM gene-deficient (apoM−/−) group (n = 24) and then randomly subdivided into four subgroups (n = 6 each) according to different intraperitoneal (i.p.) injection: control group, W146 group, LPS group, and LPS + W146 group. Serum levels of interleukin-1 beta (IL-1β) and mRNA levels of IL-1β, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), lung histology, wet/dry weight ratio, and immunohistochemistry were measured at 3 h after the baseline and compared in each group. Our results clearly demonstrated that IL-1β mRNA levels and other inflammatory biomarkers were significantly increased in the lungs of LPS-induced ALI apoM−/− mice compared to those of the apoM+/+ mice. Moreover, when apoM+/+ mice were treated with W146, a S1P receptor (S1PR1) antagonist, these inflammatory biomarkers could be significantly upregulated by LPS-induced ALI. Therefore, it suggests that apoM-S1P-S1PR1 signaling might underlie the pathogenesis of ALI and apoM could have physiological benefits to alleviate LPS-induced ALI.
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3.
  • Zhu, Chunhua, et al. (författare)
  • TO901317 regulating apolipoprotein M expression mediates via the farnesoid X receptor pathway in Caco-2 cells
  • 2011
  • Ingår i: Lipids in Health and Disease. - 1476-511X. ; 10
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Apolipoprotein M (apoM) may have potential antiatherosclerotic properties. It has been reported that apoM expression could be regulated by many intracellar and extracellar factors. In the present study we further investigated regulation of apoM expression in Caco-2 cells stimulated by a liver X receptor (LXR) agonist, TO901317. Materials and methods: Caco-2 cells were cultured in the presence of either TO901317, farnesoid X receptor (FXR) antagonist guggulsterone or TO901317 together with guggulsterone at different concentrations for 24 hrs. The mRNA levels of ATP-binding cassette transporter A1 (ABCA1), apoA1, apoM, liver receptor homologue-1 (LRH-1) and short heterodimer partner 1 (SHP1) were determined by real-time RT-PCR. Results: When Caco-2 cell cultured with TO901317 alone, the mRNA levels of ABCA1, apoA1, apoM, LRH-1 and SHP1 were significantly increased with dose-dependent manners (p < 0.05), whereas when the cells cultured with guggulsterone alone, the mRNA levels of apoM, SHP1 and LRH-1 (p < 0.05) were strongly inhibited. Moreover, guggulsterone could abolish the TO901317 enhanced mRNA levels of apoA1 apoM, SHP1 and LRH-1. Conclusion: The present study demonstrated that LXR agonist TO901317 induced apoM expression in Caco-2 cells might be mediated via the LXR/FXR pathway.
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