S-Space College of Dentistry/School of Dentistry (치과대학/치의학대학원) Dept. of Dentistry (치의학과) Theses (Master's Degree_치의학과)
Indole-3-acetic acid prevents human dental pulp stem cells from hydrogen peroxide-induced oxidative toxicity
과산화수소로 인한 인간치수줄기세포의 산화독성에 대한 인돌 3-아세트산의 영향
- Sooyoung Yu
- 치과대학 치의학과B
- Issue Date
- 서울대학교 치의학대학원
- Indole 3-acetic acid (IAA); hydrogen peroxide (H2O2); Antioxidant; Supernumerary tooth; Dental pulp stem cell
- 학위논문 (석사)-- 서울대학교 치의학대학원 : 치과대학 치의학과, 2016. 2. 노상호.
- The purpose of present study was to investigate the effect of Indole-3-acetic acid (IAA) on human dental pulp stem cells (hDPSCs) during hydrogen peroxide (H2O2)-induced oxidative toxicity. To validate this situation, we first assessed the effects of H2O2 on viability in hDPSCs at different concentrations ranging from 1-400 μM. The measurement of viable cells was determined after 24h treatment. To demonstrate the effect of IAA, the experimentation was also conducted same as the H2O2 experiment. Next, we tested the effects of IAA on H2O2-induced cytotoxicity in hDPSCs. To assess the effect of IAA as antioxidant, we tested IAA at various concentrations ranging from 1-400 μM after treatment of H2O2 at 180 μM and the cell cycle was also estimated. As our results, H2O2 at 40 μM did not affect cell viability, whereas the inhibitory effect started at 50 μM H2O2 and maximal performance was at 180 μM for 24 h. On the other hands, the treatment of IAA did not influence on the viability of hDPSCs. TheH2O2-induced cytotoxicity was strikingly inhibited in the presence of IAA and these effects were maximal at 150 μM. By the FACS analysis, the cell cycle in control group was seriously destroyed by H2O2 treatment through whole phase. Moreover, the apoptotic cells in control group were remarkably increased comparing with that in non-treat group. Interestingly, the damaged cell cycle by H2O2-induced cytotoxicity was recovered with the treatment IAA at 150 μM and the apoptotic cells were also decreased. In conclusion, the IAA was able to protect hDPSCs from H2O2-induced cytotoxicity via cell cycle restoration.