Oxidative stress-induced apoptosis and matrix loss of chondrocytes is inhibited by eicosapentaenoic acid.
نویسندگان
چکیده
Eicosapentaenoic acid (EPA) is an antioxidant and n-3 polyunsaturated fatty acid that reduces the production of inflammatory cytokines. We evaluated the role of EPA in chondrocyte apoptosis and degeneration. Normal human chondrocytes were treated with EPA and sodium nitroprusside (SNP). Expression of metalloproteinases (MMPs) was detected by real-time polymerase chain reaction (PCR) and that of apoptosis-related proteins was detected by western blotting. Chondrocyte apoptosis was detected by flow cytometry. C57BL/6J mice were used for the detection of MMP expression by immunohistochemistry and for investigation of chondrocyte apoptosis. EPA inhibited SNP-induced chondrocyte apoptosis, caspase 3 and poly(ADP-ribose) polymerase cleavage, phosphorylation of p38 MAPK and p53, and expression of MMP3 and MMP13. Intra-articular injection of EPA prevented the progression of osteoarthritis (OA) by inhibiting MMP13 expression and chondrocyte apoptosis. EPA treatment can control oxidative stress-induced OA progression, and thus may be a new approach for OA therapy.
منابع مشابه
Ascorbic acid provides protection for human chondrocytes against oxidative stress.
Oxidative stress is considered to be an important cause of dysfunction in chondrocytes and articular cartilage degradation, which leads to the pathogenesis of osteoarthritis (OA) and cartilage aging. The present study aimed to assess the effects of the widely applied antioxidant, ascorbic acid (AA), on human chondrocytes against hydrogen peroxide (H2O2) in vitro. Using annexin V‑fluorescein iso...
متن کاملPKCa Agonists Enhance the Protective Effect of Hyaluronic Acid on Nitric Oxide-Induced Apoptosis of Articular Chondrocytes in Vitro
Objective(s): Protein kinase C (PKCα) is involved in modulating articular chondrocytes apoptosis induced by nitric oxide (NO). Hyaluronic acid (HA) inhibits nitric oxide-induced apoptosis of articular chondrocytes by protecting PKCα, but the mechanism remains unclear. The present study was performed to investigate the effects and mechanisms of PKCα regulate protective effect of hya...
متن کاملProtective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling
Objective(s): Oxidative stress has been established as a key cause of alcohol-induced hepatotoxicity. Licochalcone B, an extract of licorice root, has shown antioxidative properties. This study was to investigate the effects and mechanisms of licochalcone B in ethanol-induced hepatic injury in an in vitro study. Materials and Methods: An in vitro model of Ethanol-induced cytotoxicity in BRL cel...
متن کاملEffect of Short and Long-Term Treatment with Omega-3 Fatty Acids on Scopolamine-Induced Amnesia
Two omega-3 fatty acids including docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are essential for the physiologic function of neuronal cell membrane. Normal function of neuronal cell membrane requires appropriate composition of fatty in its structure. Present study was designed to compare the effect of short-term and long-term pretreatment with omega-3 fatty acids on scopolamine...
متن کاملEffect of Short and Long-Term Treatment with Omega-3 Fatty Acids on Scopolamine-Induced Amnesia
Two omega-3 fatty acids including docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are essential for the physiologic function of neuronal cell membrane. Normal function of neuronal cell membrane requires appropriate composition of fatty in its structure. Present study was designed to compare the effect of short-term and long-term pretreatment with omega-3 fatty acids on scopolamine...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Journal of orthopaedic research : official publication of the Orthopaedic Research Society
دوره 33 3 شماره
صفحات -
تاریخ انتشار 2015