Effects of Triclosan on Neural Stem Cell Viability and Survival.
10.4062/biomolther.2015.164
- Author:
Bo Kyung PARK
1
;
Edson Luck T GONZALES
;
Sung Min YANG
;
Minji BANG
;
Chang Soon CHOI
;
Chan Young SHIN
Author Information
1. Department of Neuroscience, School of Medicine, and Neuroscience Research Center, SMART-IABS and KU Open Innovation Center, Konkuk University, Seoul 05029, Republic of Korea. chanyshin@kku.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Triclosan;
Apoptosis;
Oxidation;
Rat neural stem cells;
MAPK signaling
- MeSH:
Animals;
Apoptosis;
Brain;
Caspase 3;
Cell Survival;
Embryonic Structures;
Glutathione;
Household Products;
Humans;
Mouthwashes;
Neural Stem Cells*;
Rats;
Soaps;
Toothpastes;
Triclosan*
- From:Biomolecules & Therapeutics
2016;24(1):99-107
- CountryRepublic of Korea
- Language:English
-
Abstract:
Triclosan is an antimicrobial or sanitizing agent used in personal care and household products such as toothpaste, soaps, mouthwashes and kitchen utensils. There are increasing evidence of the potentially harmful effects of triclosan in many systemic and cellular processes of the body. In this study, we investigated the effects of triclosan in the survivability of cultured rat neural stem cells (NSCs). Cortical cells from embryonic day 14 rat embryos were isolated and cultured in vitro. After stabilizing the culture, triclosan was introduced to the cells with concentrations ranging from 1 muM to 50 muM and in varied time periods. Thereafter, cell viability parameters were measured using MTT assay and PI staining. TCS decreased the cell viability of treated NSC in a concentration-dependent manner along with increased expressions of apoptotic markers, cleaved caspase-3 and Bax, while reduced expression of Bcl2. To explore the mechanisms underlying the effects of TCS in NSC, we measured the activation of MAPKs and intracellular ROS. TCS at 50 muM induced the activations of both p38 and JNK, which may adversely affect cell survival. In contrast, the activities of ERK, Akt and PI3K, which are positively correlated with cell survival, were inhibited. Moreover, TCS at this concentration augmented the ROS generation in treated NSC and depleted the glutathione activity. Taken together, these results suggest that TCS can induce neurodegenerative effects in developing rat brains through mechanisms involving ROS activation and apoptosis initiation.
