Role of autophagy in lipopolysaccharide-induced apoptosis of odontoblasts.
10.12122/j.issn.1673-4254.2020.12.18
- Author:
Huacui XIONG
1
;
Ke CHEN
1
;
Meimei LI
1
Author Information
1. Stomatological Hospital, Southern Medical University, Guangzhou 510115, China.
- Publication Type:Journal Article
- Keywords:
apoptosis;
autophagy;
lipopolysaccharide
- MeSH:
Animals;
Apoptosis;
Autophagy;
Lipopolysaccharides/pharmacology*;
Mice;
Odontoblasts/metabolism*;
Proto-Oncogene Proteins c-akt/metabolism*;
Signal Transduction
- From:
Journal of Southern Medical University
2020;40(12):1816-1820
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the role of autophagy in lipopolysaccharide (LPS)-induced apoptosis of murine odontoblasts.
METHODS:Murine odontoblasts (mDPC-23 cells) were treated with 5 μg/mL LPS for 6, 12 and 24 h, and the changes in cell viability was examined using CCK8 kit and cell apoptosis was detected by TUNEL staining. The changes in the protein levels of LC3, Beclin1, Atg5, AKT, p-AKT, mTOR and p-mTOR were detected using Western blotting. The effect of 3-MA treatment for 24 h on LPS-induced apoptosis of mDPC-23 cells was evaluated by detecting the expressions of apoptosis-related proteins caspase-3 and Bax using Western blotting.
RESULTS:Stimulation with LPS for 6 and 12 h did not cause significant changes in the proliferation or apoptosis of mDPC-23 cells, but LPS treatment for 24 h significantly suppressed cell proliferation (
CONCLUSIONS:LPS stimulation induces autophagy to promote apoptosis of mDPC-23 cells, and suppression of autophagy attenuates LPS-induced apoptosis. Autophagy may play an important role in the injury of inflamed pulp tissues.
