Chai-Yi Lin

Publications (2)3.17 Total impact

• Article: Lipopolysaccharide/adenosine triphosphate-mediated signal transduction in the regulation of NLRP3 protein expression and caspase-1-mediated interleukin-1β secretion.

  Pei-Chun Liao, Louis Kuoping Chao, Ju-Ching Chou, Wei-Chih Dong, Chien-Nan Lin, Chai-Yi Lin, Ann Chen, Shuk-Man Ka, Chen-Lung Ho, Kuo-Feng Hua
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  ABSTRACT: OBJECTIVE: Reactive oxygen species (ROS) plays a critical role in the regulation of NLRP3 inflammasome activation. However, the ROS-mediated signaling pathways controlling NLRP3 inflammasome activation are not well defined. METHODS: Using lipopolysaccharide (LPS) and adenosine triphosphate (ATP) activated murine macrophages as the testing model, cytokine release and protein expression were quantified by enzyme-linked immunosorbent assay and Western blot, respectively. ROS was scavenged by N-acetyl cysteine; NADPH oxidase, the major source of ROS, was inhibited by diphenyliodonium, apocynin or gp91-phox siRNA transfection; and protein kinase was inhibited by its specific inhibitor. RESULTS: LPS-induced NLRP3 protein expression was regulated through the NADPH oxidase/ROS/NF-κB-dependent, JAK2/PI3-kinase/AKT/NF-κB-dependent, and MAPK-dependent pathways, while ATP-induced caspase-1 activation was regulated through the NADPH oxidase/ROS-dependent pathway. CONCLUSIONS: These results demonstrate that ROS regulates not only the priming stage, but also the activation stage, of NLRP3 inflammasome activation in LPS + ATP-activated macrophages.
  Agents and Actions 09/2012; · 1.59 Impact Factor
• Article: High glucose increases nitric oxide generation in lipopolysaccharide-activated macrophages by enhancing activity of protein kinase C-α/δ and NF-κB.

  Kuo-Feng Hua, Szu-Hsuan Wang, Wei-Chih Dong, Chai-Yi Lin, Chen-Lung Ho, Tzu-Hua Wu
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  ABSTRACT: Although several mechanisms by which hyperglycemia modulate inflammation have been proposed, it remains unclear how hyperglycemia regulates inflammation induced by lipopolysaccharide (LPS). We hypothesized that hyperglycemia might interplay with LPS to modulate the generation of an inflammatory mediator. RAW 264.7 macrophages cultured in medium containing either normal glucose (5.5-mM) or high glucose (HG) (15- and 25-mM) were treated with LPS. The nitric oxide (NO) generation, inducible NO synthase (iNOS) expression and cytokine release were then quantified by Griess reaction, western blot, and enzyme-linked immunosorbent assay (ELISA) respectively. The effect of HG on the activation of kinase and Nuclear Factor-Kappa B (NF-κB) were measured by western blot and NF-κB reporter assay respectively. Without LPS stimulation, HG alone did not induce NO generation and cytokine secretion; but LPS-induced NO generation, iNOS expression, and interleukin-1beta (IL-1β) secretion were higher in HG-cultured cells than in normal glucose-cultured cells. In contrast, LPS-induced interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) secretion were lower in HG-cultured cells than in normal glucose-cultured cells. Furthermore, HG increased iNOS expression and NO generation by enhancing phosphorylation levels of protein kinase C-alpha (PKC-α), protein kinase C-delta (PKC-δ), and p38 phosphorylation and NF-κB transcriptional activity. This study revealed a possible role of PKC-α and PKC-δ potentially involved in diabetes-promoted inflammation.
  Agents and Actions 06/2012; 61(10):1107-16. · 1.59 Impact Factor