| Literature DB >> 27746371 |
Ha Ryong Kim1, Da Young Shin2, Kyu Hyuck Chung3.
Abstract
Polyhexamethylene biguanide (PHMB) is a member of the polymeric guanidine family, which is used as a biocide and preservative in industrial, medicinal, and consumer products. Some studies reported that polyhexamethylene guanidine phosphate, which is also a member of the guanidine family, induced severe inflammation and fibrosis in the lungs. However, limited studies have evaluated the pulmonary toxicity of PHMB associated with inflammatory responses. The aim of this study was to elucidate the inflammatory responses and its mechanisms induced by PHMB in lung cells. A549 cells exposed to PHMB showed decreased viability, reactive oxygen species (ROS) generation, inflammatory cytokine secretion, and nuclear factor kappa B (NF-κB) activation. The cells showed dose-dependent cytotoxicity and slight generation of ROS. PHMB triggered inflammatory cytokine secretion and NF-κB activation by modulating the degradation of IκB-α and the accumulation of nuclear p65. TNF-α plays important roles in IL-8 expression as well as NF-κB activation. Moreover, IL-8 production induced by PHMB was completely suppressed by a NF-κB inhibitor, but not by a ROS scavenger. In conclusion, we suggest that PHMB induces the inflammatory responses via the NF-κB signaling pathway. Copyright ÂEntities:
Keywords: Inflammation; Nuclear factor kappa B; Polyhexamethylene biguanide; Reactive oxygen species; Tumor necrosis factor alpha
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Year: 2016 PMID: 27746371 DOI: 10.1016/j.tiv.2016.10.006
Source DB: PubMed Journal: Toxicol In Vitro ISSN: 0887-2333 Impact factor: 3.500