학술논문

The Antioxidant Resveratrol Protects against Chondrocyte Apoptosis by Regulating the COX-2/NF-κB Pathway in Created Temporomandibular Osteoarthritis.
Document Type
Article
Source
BioMed Research International. 7/9/2021, p1-7. 7p.
Subject
*CARTILAGE cells
*IN vitro studies
*REVERSE transcriptase polymerase chain reaction
*BIOMARKERS
*MANDIBULAR condyle
*IN vivo studies
*STAINS & staining (Microscopy)
*ANIMAL experimentation
*ANTIOXIDANTS
*APOPTOSIS
*SIGNAL peptides
*RESVERATROL
*CELLULAR signal transduction
*GENE expression
*OSTEOARTHRITIS
*TEMPOROMANDIBULAR disorders
*POLYMERASE chain reaction
*MICE
Language
ISSN
2314-6133
Abstract
Temporomandibular joint osteoarthritis (TMJOA) is characterized by chronic inflammatory degradation of mandibular condylar cartilage (MCC). Studies have found a positive correlation between inflammation and cyclooxygenase- (COX-) 2 in OA pathology. NF-κB is a crucial transcription factor of inflammatory and immune responses in the cause of TMJOA pathology. Resveratrol (RES) plays a critical role in antioxidation and anti-inflammation. But, studies on the effects of RES on TMJOA are very limited. So, the purpose of this study is to investigate the antioxidant and protective effects of RES against MCC degradation through downregulating COX-2/NF-κB expression. In vitro studies, the MCC cells were divided into three groups: the NC group, OA group, and RES group. The optimum dose of RES (10 μM) was determined. The TMJOA model of mice was created by injection of collagenase. And mice were injected with RES (100 μg/10 μl) 3 times one week for 4 weeks in the RES group. The expressions of COX-2, P65, MMP1, MMP13, COL2, and ACAN were measured by RT-PCR. Morphological changes of MCC were studied with HE staining. The results showed that inflammation could induce MCC degradation in vitro and vivo, while RES could reverse the degradation. Meanwhile, RES could downregulate COX-2/NF-κB/MMP expression and increase cartilage markers in vitro and vivo studies. The results indicated that RES treatment had antioxidant effects against chondrocyte apoptosis by downregulating the COX-2/NF-κB pathway in created TMJOA. [ABSTRACT FROM AUTHOR]