N Lin

Renji Hospital, Shanghai, Shanghai Shi, China

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Publications (3)5.3 Total impact

  • N Lin, H Zhang, Q Su
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    ABSTRACT: This study evaluated the direct effects of advanced glycation end-products (AGEs) on pancreatic β cells, including cellular viability, generation of reactive oxygen species (ROS) and insulin secretion, and also looked for the main source of ROS in INS-1 cells and the possible molecular mechanism(s) of cell injury by AGEs. INS-1 cells were cultured with 100, 200 and 500 mg/L of AGEs for specific periods of time. Cell apoptosis was determined by ELISA and real-time PCR assays. ROS were detected by DCFH-DA and MitoSOX Red probes with a flow cytometer, NADPH oxidase activity was measured by lucigenin chemiluminescence and MAPK phosphorylation was measured by Western blot tests. Both cell apoptosis and ROS generation increased in AGE-treated cells in a dose-dependent way, and both the mitochondrial electron transport chain and NADPH oxidase pathway participated in ROS generation, although the role of the mitochondrial pathway was earlier and more important. AGEs exerted a toxic effect on insulin secretion that could be largely reversed by inhibiting ROS. AGEs injured INS-1 cells by oxidative stress mainly through the mitochondrial pathway, although the JNK and p38 MAPK signaling pathways were also key modulators in ROS-mediated β-cell death.
    Diabetes & Metabolism 02/2012; 38(3):250-7. · 2.39 Impact Factor
  • S-C DU, Q-M Ge, N Lin, Y Dong, Q Su
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    ABSTRACT: Overproduction of reactive oxygen species (ROS) or exhaustion of antioxidants may cause oxidative stress which is a major factor of defective insulin secretion and increases apoptosis of pancreatic β-cells in diabetes. So there comes a consideration of whether antioxidant strategies can be used to protect deterioration of the β-cells. In this study, we explored the mechanism of oxidative stress mediated lipopolysaccharide (LPS) induced apoptosis in insulin secreting (INS-1) cells from a rat pancreatic β-cell line. ROS was monitored by using intracellular ROS capture dihydroethidium (DHE) and dihydrorhodamine123 (DHR123). Apoptosis rate was measured by flow cytometry (FCM). The pro-apoptotic gene Bax and anti-apoptotic gene Bcl-2 were analysed by Western blot and RT-PCR. The results demonstrate that LPS-stimulated INS-1 cells manifest intensified intracellular fluorescence in both dose- and time- dependent manners. Apoptosis rate of LPS stimulated INS-1 cells is significantly increased by FCM, with a significant increase in Bax/Bcl-2 ratio revealed by Western blot and RT-PCR. Furthermore, α-lipoic acid (α-LA) inhibits LPS-induced apoptosis, but can not restore the function of glucose stimulated insulin secretion (GSIS) in INS-1 cells.
    Cellular and molecular biology (Noisy-le-Grand, France) 01/2012; 58 Suppl:OL1654-9. · 1.46 Impact Factor
  • Q-M Ge, S-C Du, F Bian, N Lin, Q Su
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    ABSTRACT: The aim of the study was to obtain insight into the mechanism of sepsis-induced hyperglycemia, to explore the expression of Toll-like receptor 4 (TLR4) on INS-1 cells, the effects of lipopolysaccharide (LPS) on TLR4 expression and cell viability. The expression of TLR4 on INS-1 was detected by both RT-PCR and Western blot assays. After being intervened by LPS of various concentrations (0.01, 0.1, 1, 5, 10mg/L) for a certain time, the effects of LPS on TLR4 expression and cell viability were detected by quantitative real-time reverse-transcriptase polymerase chain reaction, western blotting and CCK-8 assay. Then INS-1 cells were stimulated by LPS (0.1, 1mg/L) together with anti-TLR4 antibody, cell viability and TLR4 expression were detected again. TLR4 expressed in INS-1 cell line. Its expression was up-regulated by the stimulation of LPS higher than 0.1mg/L for 12h (P<0.05). However, there was a little down-regulation of TLR4 between the LPS treated groups and controls with further LPS treatment for 24 and 48 h (P>0.05). In certain concentrations(0.1~10mg/L), viability of INS-1 cells was inhibited by LPS in a dose dependent manner (P<0.05) These effects could be blocked by anti-TLR4 antibody partially. These results suggest that LPS may act directly on the pancreatic β cells via TLR4 on the β-cell membrane. LPS increased TLR4 expression in the early short period of time and caused injury to INS-1 cells after a certain time. It could be one of the mechanisms that hyperglycemia occurs in the early stage of sepsis.
    Cellular and molecular biology (Noisy-le-Grand, France) 01/2011; 57 Suppl:OL1513-9. · 1.46 Impact Factor