Effects of triclosan on the biological characteristics of dental pulp stem cells
10.12016/j.issn.2096-1456.202440222
- Author:
WANG Xinxin
1
;
HE Jihui
2
;
LI Gang
3
;
YE Qingsong
4
;
HE Yan
5
Author Information
1. 1.Institute of Regenerative and Translational Medicine, Affiliated Tianyou Hospital, Wuhan University of Science and Technology.2.First Clinical College of the Ministry of Medicine, Wuhan University of Science and Technology
2. 1.Institute of Regenerative and Translational Medicine, Affiliated Tianyou Hospital, Wuhan University of Science and Technology 2First Clinical College of the Ministry of Medicine, Wuhan University of Science and Technology.
3. 1.Institute of Regenerative and Translational Medicine, Affiliated Tianyou Hospital, Wuhan University of Science and Technology 2.Department of Stomatology, Affiliated Tianyou Hospital, Wuhan University of Science and Technology
4. 1.Center of Regenerative Medicine, Renmin Hospital of Wuhan University, Wuhan UniversiDepartment of Stomatology, Renmin Hospital of Wuhan University, Wuhan Universityty 2.
5. 1.Institute of Regenerative and Translational Medicine, Affiliated Tianyou Hospital, Wuhan University of Science and Technology 2.First Clinical College of the Ministry of Medicine, Wuhan University of Science and Technology 3Department of Stomatology, Affiliated Tianyou Hospital, Wuhan University of Science and Technology.
- Publication Type:Journal Article
- Keywords:
triclosan / dental pulp stem cells / proliferation / differentiation / reactive oxygen species / oxidative stress / inflammatory factors / mitochondrial membrane potential / PI3K/Akt/mTOR / dental pulp tissue
- From:
Journal of Prevention and Treatment for Stomatological Diseases
2024;32(11):834-844
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To explore whether the environmental pollutant triclosan (TCS) has negative effects on the various biological characteristics of dental pulp stem cells (DPSCs), as well as the distribution and hazards of TCS in rat dental pulp tissue in vivo, which will provide a basis for the clinical application of DPSCs and the safety of TCS.
Methods : Tooth collection was approved by the Ethics Committee of Tianyou Hospital Affiliated to Wuhan University of Science and Technology. Human DPSCs were extracted, cultured, and identified. Up to 0.08 mmol/L of TCS was added to the in vitro culture medium of DPSCs. The proliferation ability of DPSCs was detected by CCK-8. The migration ability of DPSCs was detected via scratch assay. The differentiation ability of DPSCs was detected by inducing trilineage differentiation. The gene or protein expression levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), inducible nitric oxide synthase (iNOS), and transforming growth factor-β (TGF-β) in DPSCs were detected. The level of reactive oxygen species (ROS) generated by DPSCs was analyzed using fluorescence staining. Changes in mitochondrial membrane potential of DPSCs were detected using a fluorescent probe. The activity of PI3K/Akt/mTOR, p38, and JNK pathways of DPSCs were detected. Animal experiments were approved by the Animal Ethics Committee of Wuhan University of Science and Technology. A rat model of short-term oral exposure to 50 mg/kg/d of TCS for 2 months was established, and the TCS concentration in the liver, brain, and dental pulp tissues of rats was detected through liquid chromatography-mass spectrometry.
Results: TCS at 0.02 mmol/L, 0.04 mmol/L, and 0.08 mmol/L significantly inhibited the proliferation ability of human-derived DPSCs on the 5th and 7th days of contact. TCS at 0.04 mmol/L and 0.08 mmol/L significantly inhibited the migration ability and tri-lineage differentiation ability of DPSCs on the 3rd day of contact. TCS induced the gene or protein expression of proinflammatory factors including TNF-α, IL-1β, IL-6, and iNOS, induced the gene or protein expression of TGF-β, and inhibited the protein expression of anti-inflammatory factor IL-10. On day 1, TCS at 0.04 mmol/L and 0.08 mmol/L induced the production of ROS in DPSCs and reduced the mitochondrial membrane potential of DPSCs. On day 3, TCS at these levels inhibited PI3K/Akt/mTOR pathway activity and enhanced p38 pathway activity of DPSCs, without affecting the pathway activity of JNK. After short-term intragastric exposure of rats to TCS, TCS was detected in liver (430 ng/mL) and brain (41.4 ng/mL) tissues but not in the dental pulp. The TCS concentration was highest in the liver, but no obvious histopathological changes were observed.
Conclusion:TCS inhibits a variety of biological characteristics of DPSCs and poses a potential risk to the organism. No TCS exists in the dental pulp tissue of rats exposed to TCS for a brief period of time, and the health of the rats is not damaged.
