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Hsin-Chung Cheng

Researcher at Taipei Medical University Hospital

Publications -  6
Citations -  40

Hsin-Chung Cheng is an academic researcher from Taipei Medical University Hospital. The author has contributed to research in topics: NADPH oxidase & Surfactin. The author has an hindex of 1, co-authored 6 publications receiving 1 citations. Previous affiliations of Hsin-Chung Cheng include Taipei Medical University.

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The potentials of carbon monoxide-releasing molecules in cancer treatment: An outlook from ROS biology and medicine.

TL;DR: In this paper, the authors present a short but crucial view concerning the characteristics of CO and CO-RMs, and identify the possible signaling network by which CORMs can exert their anticancer actions, where reactive oxygen species (ROS) play the central role.
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Carbon Monoxide-Releasing Molecule-2 Ameliorates Particulate Matter-Induced Aorta Inflammation via Toll-Like Receptor/NADPH Oxidase/ROS/NF-κB/IL-6 Inhibition.

TL;DR: In this article, aortic vascular smooth muscle cells (HASMCs) were utilized as in vitro models for the assessment of signaling pathways behind CORM-2 activities against PM-induced inflammatory responses, including Toll-like receptors (TLRs), NADPH oxidase, ROS, nuclear factor-kappa B (NF-κB), and IL-6.
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Surfactin reduces particulate matter-induced VCAM-1-dependent monocyte adhesion in human gingival fibroblasts by increasing Nrf2-dependent HO-1 expression

TL;DR: In this article, the anti-inflammatory effects of surfactin on PM-exposed human gingival fibroblasts (HGFs) and signaling pathways were investigated, and the involvement of Nrf2/HO-1 and ROS signaling pathways was investigated by treating HGFs with specific pathway interventions, genetically or pharmacologically.
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Surfactin induces autophagy, apoptosis, and cell cycle arrest in human oral squamous cell carcinoma.

TL;DR: In this article, the authors investigated the anticancer effects and underlying mechanisms of surfactin on human oral squamous cell carcinoma (OSCC) and showed that it could induce apoptosis, autophagy, and cell cycle arrest in ROS-dependent manner, suggesting a multifaced anticancer agent for OSCC.