Protective effect of resveratrol on apoptosis of human periodontal ligament cells in vitro.
- Author:
Huai-Xiu LU
1
;
Song-Shan LIN
;
Shi-Sen LIU
;
Zhong-Ying NIU
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Cell Survival; drug effects; Flow Cytometry; Humans; Hydrogen Peroxide; In Vitro Techniques; L-Lactate Dehydrogenase; analysis; Malondialdehyde; analysis; Oxidants; Oxidative Stress; drug effects; Periodontal Ligament; cytology; drug effects; Stilbenes; pharmacology; Superoxide Dismutase; analysis; bcl-2-Associated X Protein; analysis
- From: Chinese Journal of Stomatology 2009;44(8):469-473
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of resveratrol (RES) on apoptosis of human periodontal ligament cells (HPLC).
METHODSHPLC were subjected to oxidative injury induced by H2O2 for 24 h after pretreatment with different concentration of RES. HPLC were then divided into the control, model, vector, RES 1, 10, 30, 50 micromol/L treatment group. The viability of the HPLC was determined by methyl thiazolyl tetrazolium (MTT) method. Lactate dehydrogenase (LDH) rate and malondialdehyde (MDA) in the culture medium, superoxide dismutase (SOD) in the HPLC homogenate were evaluated by spectrophotometry. The apoptotic HPLC was detected by flow cytometry (FCM) and calculated by relative apoptosis rate. Bax and Bcl-2 protein levels were detected by Western blotting.
RESULTSRES increased the cell survival rate after H2O2 injury. The survival rate of RES 30 micromol/L group was (86.1 +/- 4.1)% and the model group was (54.6 +/- 4.0)%, which was significantly different between the two groups (P < 0.01). The LDH leakage rate and MDA content of the RES 30 micromol/L group were (32.6 +/- 2.0)% and (1.70 +/- 0.21) micromol/L, which were significantly different with that in the model group (P < 0.01). At the same time RES could remarkably restore the vitality of SOD in the HPLC. RES increased Bcl-2 and reduced the expression of Bax protein. The apoptosis rate of the RES 30 micromol/L group and model group was (14.84 +/- 1.36)% and (64.37 +/- 2.34)%, respectively (P < 0.01). The protective effect of RES on the cell apoptosis was in a dose-dependent manner, reaching peak at a concentration of 30 micromol/L (P < 0.01).
CONCLUSIONSRES reduced oxidative stress and apoptosis in an experimental HPLC injury model induced by H2O2. RES plays a key role in the HPLC protection against oxidative injury.
