Abstract
The aim of the study was to assess the effects of therapeutic ultrasound (US) on oxidative stress (OS)-induced changes in cultured human chondrocytes (HCH). For this, monolayer HCH were randomized in three groups: a control group (CG), a group exposed to OS (OS group), and a group exposed to US and OS (US-OS group). US exposure of the chondrocytes was performed prior to OS induction by hydrogen peroxide. Transmission electron microscopy (TEM) was used to assess the chondrocytes ultrastructure. OS and inflammatory markers were recorded. Malondialdehyde (MDA) and tumor necrosis factor (TNF)-α were significantly higher (p < 0.05) in the OS group than in CG. In the US-OS group MDA and TNF-α were significantly lower (p < 0.05) than in the OS group. Finally, in the US-OS group MDA and TNF-α were lower than in CG, but without statistical significance. TEM showed normal chondrocytes in CG. In the OS group TEM showed necrotic chondrocytes and chondrocytes with a high degree of vacuolation and cell organelles damages. In the US-OS group the chondrocytes ultrastructure was well preserved, and autophagosomes were generated. In conclusion, US could protect chondrocytes from biochemical (lipid peroxidation, inflammatory markers synthesis) and ultrastructural changes induced by OS and could stimulate autophagosomes development.
Highlights
Osteoarthritis (OA) is the most common cause of chronic disability in older people [1]
Chondrocytes were divided into three groups (Figure 1): 1. control group—chondrocytes with no treatment; 2. group exposed to oxidative stress (OS) (OS group)—chondrocytes exposed to H2O2; 3. group exposed to US and OS (US—OS group)—chondrocytes exposed to US and H2O2
In the US-OS group, where chondrocytes had been exposed to the US at the frequency of 850 KHz and the intensity of 100 mW/cm2 for 5 min, on 3 consecutive days before H2O2 treatment, MDA (5.0 ± 0.8 nmoL/mg prot) failed to increase
Summary
Osteoarthritis (OA) is the most common cause of chronic disability in older people [1]. An increase in oxidative stress (OS) and a decrease in autophagy in aging cartilage are the main factors involved in OA pathogenesis in the elderly [2]. The entire joint structure may be affected in OA, the main structural changes occur in the cartilage. These changes include extracellular matrix (ECM) damage and chondrocyte death by apoptosis, necrosis, or chondroptosis. Proinflammatory cytokine excess and OS underlie these structural changes, and autophagy deficiency allows chondrocytes and ECM’s defects to accumulate in aging cartilage. In OA cartilage, chondrocytes synthesize reactive oxygen species (ROS) and reactive nitrogen species (RNS) in a large amount and have impaired antioxidant defense, both leading to OS. ROS and RNS promote ECM degradation [6], impair chondrocytes ultrastructure [7], and may induce chondrocytes death [8,9]
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.
