Notoginsenoside R1 attenuates oxidative stress‐induced osteoblast dysfunction through JNK signalling pathway

Abstract

Oxidative stress (OS)‐induced mitochondrial damage and the subsequent osteoblast dysfunction contributes to the initiation and progression of osteoporosis. Notoginsenoside R1 (NGR1), isolated from Panax notoginseng, has potent antioxidant effects and has been widely used in traditional Chinese medicine. This study aimed to investigate the protective property and mechanism of NGR1 on oxidative‐damaged osteoblast. Osteoblastic MC3T3‐E1 cells were pretreated with NGR1 24 h before hydrogen peroxide administration simulating OS attack. Cell viability, apoptosis rate, osteogenic activity and markers of mitochondrial function were examined. The role of C‐Jun N‐terminal kinase (JNK) signalling pathway on oxidative injured osteoblast and mitochondrial function was also detected. Our data indicate that NGR1 (25 μM) could reduce apoptosis as well as restore osteoblast viability and osteogenic differentiation. NGR1 also reduced OS‐induced mitochondrial ROS and restored mitochondrial membrane potential, adenosine triphosphate production and mitochondrial DNA copy number. NGR1 could block JNK pathway and antagonize the destructive effects of OS. JNK inhibitor (SP600125) mimicked the protective effects of NGR1while JNK agonist (Anisomycin) abolished it. These data indicated that NGR1 could significantly attenuate OS‐induced mitochondrial damage and restore osteogenic differentiation of osteoblast via suppressing JNK signalling pathway activation, thus becoming a promising agent in treating osteoporosis.

In Vitro and Ex Vivo Investigation of the Effects of Polydopamine Nanoparticle Size on Their Antioxidant and Photothermal Properties: Implications for Biomedical Applications

“…Furthermore, several pathologies, such as neurodegenerative disease, are characterized by severe intracellular levels of oxidative stress (OS), mainly associated with failure in ROS scavenging. , PDNPs, thanks to their excellent antioxidant properties, represent suitable agents for the treatment of cells showing an overproduction of ROS. To mimic these particular conditions, the degradation behavior of the eight PDNP classes was assessed in 5% H 2 O 2 . Degradation analysis was performed through spectrophotometric and DLS measurements at different time points (0, 24, 48, and 72 h) during incubation.…”

Exogenous Hydrogen Sulfide Mitigates Oxidative Stress and Mitochondrial Damages Induced by Polystyrene Microplastics in Osteoblastic Cells of Mice

“…Mitochondrial dysfunction and ROS rise induced osteoblast senescence and osteoblast activity [ 21 ] and led to type 2 diabetic osteoporosis [ 22 ]. Proanthocyanidins and notoginsenoside R1 treatments reduced ROS level and weakened mitochondrial dysfunction to improve osteoblast activity [ 23 , 24 ]. These studies suggest that oxidative stress and disturbances in mitochondrial metabolism are targets for improving osteogenic capacity.…”

Notoginsenoside R1-loaded mesoporous silica nanoparticles targeting the site of injury through inflammatory cells improves heart repair after myocardial infarction

“…In a study on diabetic cardiomyopathy, NGR1 pretreatment significantly reduced AGE-induced mitochondrial damage, restricted ROS increase, and reduced apoptosis in H9C2 cells [ 36 ]. In oxidative stress induced osteoporpsis, NGR1 relieve oxidative stress through JNK signalling pathway [ 37 ]. Oxidized low-density lipoprotein induced oxidative stress could be alleviated by NGR1 via lnc RNA X-inactive specific transcript/miR-221 regulation [ 38 ].…”