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18 results on '"Lo, Horng‐Ren"'

17. Effect of Allyl Sulfides from Garlic Essential Oil on Intracellular Ca2+Levels in Renal Tubular Cells

Author

Jan, Chung-Ren, Lo, Horng-Ren, Chen, Chung-Yi, and Kuo, Soong-Yu

Abstract

Diallyl sulfide (1), diallyl disulfide (2), and diallyl trisulfide (3), which are major organosulfur compounds of garlic (Allium sativum), are recognized as a group of potential chemopreventive compounds. In this study, the early signaling effects of 3were examined on Madin-Darby canine kidney (MDCK) cells loaded with the Ca2+-sensitive dye fura-2. It was found that 3caused an immediate and sustained increase of [Ca2+]iin a concentration-dependent manner (EC50= 40 μM). Compound 3also induced a [Ca2+]ielevation when extracellular Ca2+was removed, but the magnitude was reduced by 45%. In Ca2+-free medium, the 3-induced [Ca2+]ilevel was abolished by depleting stored Ca2+with 1 μM thapsigargin (an endoplasmic reticulum Ca2+pump inhibitor). Elevation of [Ca2+]icaused by 3in the Ca2+-containing medium was not affected by modulation of protein kinase C activity. The 3-induced Ca2+influx was inhibited by nifedipine and nicardipine (1 μM). U73122, an inhibitor of phospholipase C, abolished ATP (but not the 3-induced [Ca2+]ilevel). These findings suggest that 3induced a significant [Ca2+]ielevation in MDCK renal tubular cells by stimulating both extracellular Ca2+influx and thapsigargin-sensitive intracellular Ca2+release via as yet unidentified mechanisms. Furthermore, the order of the allyl sulfide-induced [Ca2+]ielevation and cell viability was 1 < 2< 3. The differential effect of allyl sulfides on Ca2+signaling and cell death appears to correlate with the number of sulfur atoms in the structure of these allyl sulfides.

Published
2012
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18. Helicobacter pylori Induces IL-33 Production and Recruits ST-2 to Lipid Rafts to Exacerbate Inflammation.

Author

Kuo, Chia-Jung, Chen, Chun-Ya, Lo, Horng-Ren, Feng, Chun-Lung, Wu, Hui-Yu, Huang, Mei-Zi, Liao, Tung-Nan, Chen, Yu-An, and Lai, Chih-Ho

Subjects
LIPID rafts, HELICOBACTER pylori, INTERLEUKIN-33, GASTRITIS, MEMBRANE lipids, EPITHELIAL cells
Abstract

Helicobacter pylori colonizes human gastric epithelial cells and contributes to the development of several gastrointestinal disorders. Interleukin (IL)-33 is involved in various immune responses, with reported proinflammatory and anti-inflammatory effects, which may be associated with colitis and colitis-associated cancer. IL-33 induces the inflammatory cascade through its receptor, suppression of tumorigenicity-2 (ST-2). Binding of IL-33 to membrane-bound ST-2 (mST-2) recruits the IL-1 receptor accessory protein (IL-1RAcP) and activates intracellular signaling pathways. However, whether IL-33/ST-2 is triggered by H. pylori infection and whether this interaction occurs in lipid rafts remain unclear. Our study showed that both IL-33 and ST-2 expression levels were significantly elevated in H. pylori-infected cells. Confocal microscopy showed that ST-2 mobilized into the membrane lipid rafts during infection. Depletion of membrane cholesterol dampened H. pylori-induced IL-33 and IL-8 production. Furthermore, in vivo studies revealed IL-33/ST-2 upregulation, and severe leukocyte infiltration was observed in gastric tissues infected with H. pylori. Together, these results demonstrate that ST-2 recruitment into the lipid rafts serves as a platform for IL-33-dependent H. pylori infection, which aggravates inflammation in the stomach. [ABSTRACT FROM AUTHOR]

Published
2019
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