Abstract
(-)-Epigallocatechin 3-gallate (EGCG) is the main active green tea catechin and has a wide variety of benefits for health. Post-traumatic osteoarthritis (PTOA) occurs as a consequence of joint injuries that commonly happen in the young population. In this study, we investigated the effects of EGCG on PTOA prevention by using the anterior cruciate ligament transection (ACLT)–OA model and further investigated the roles of autophagy in OA treatment. Our results showed that intra-articular injection of EGCG significantly improved the functional performances and decreased cartilage degradation. EGCG treatment attenuated the inflammation on synovial tissue and cartilage through less immunostained cyclooxygenase-2 and matrix metalloproteinase-13. We further noted EGCG may modulate the chondrocyte apoptosis by activation of the cytoprotective autophagy through reducing the expression of the mTOR and enhancing the expression of microtubule-associated protein light chain 3, beclin-1, and p62. In conclusion, intra-articular injection of EGCG after ACL injury inhibited the joint inflammation and cartilage degradation, thereby increasing joint function. EGCG treatment also reduced the chondrocyte apoptosis, possibly by activating autophagy. These findings suggested that EGCG may be a potential disease-modifying drug for preventing OA progression.
Highlights
Post-traumatic osteoarthritis (PTOA) frequently occurs as a sequela of joint injury.Intra-articular incongruity or joint instability after acute joint injury increases the risk of PTOA
There were no significant differences in serum glutamateoxaloacetate transaminase (SGOT), serum glutamate-pyruvate transaminase (SGPT), blood urea nitrogen (BUN), CRE, and high sensitivity C-reactive protein (hsCRP) between the OA and the Epigallocatechin 3-gallate (EGCG)-treated groups
We suggested that the reduction of chondrocyte apoptosis mediated by activation of autophagy may be a potential mechanism of action of EGCG for OA prevention
Summary
Post-traumatic osteoarthritis (PTOA) frequently occurs as a sequela of joint injury. Intra-articular incongruity or joint instability after acute joint injury increases the risk of PTOA. Despite the advances in surgical techniques and the novel developments of instruments, joint reconstruction surgery has not been shown to reduce the rate of PTOA [1,2,3,4]. The chondrocyte death and extracellular matrix (ECM) breakage caused by a high-energy joint injury triggers a degenerative cascade and has a significant role in the development of PTOA [5,6]. Due to the limited regenerative capacity of chondrocytes, the prevention of chondrocyte death after injury is mandatory for the prevention of PTOA
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
