ArticleJournal of cellular and molecular medicine2021
Notoginsenoside R1 attenuates oxidative stress-induced osteoblast dysfunction through JNK signalling pathway.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- The role of active constituents of in traditional Chinese medicine for primary osteoporosis: a mechanistic review.Frontiers in endocrinology · 2025Pooled it
- Intradiscal Delivery of Notoginsenoside R1-Loaded PLGA Nanoparticles Attenuates Intervertebral Disc Degeneration in Rats.Journal of cellular and molecular medicine · 2026Article
- NGR1 Ameliorates Hepatocyte Steatosis and Mitochondrial Dysfunction Associated with the Restoration of NDUFS2.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Traditional Chinese Medicine for osteoporosis management: from molecular mechanisms to drug discovery.Chinese medicine · 2026Review
- Implications of notoginsenoside R1 in osteoclastogenesis and bone remodeling via nitric oxide modulation.BMC complementary medicine and therapies · 2026Article
- The role and mechanisms of bone microenvironment regulators in osteoporosis: novel intervention strategies for addressing the challenges of aging.Frontiers in endocrinology · 2026Review
- Mitigating mitochondrial dysfunction: a novel strategy for Chinese botanical drugs against osteoporosis.Frontiers in pharmacology · 2026Review
- Therapeutic potential of natural products from Traditional Chinese Medicine in the treatment of osteoporosis.Frontiers in pharmacology · 2026Review
- Spermidine prevents iron overload-induced impaired bone mass by activating SIRT1/SOD2 signaling in senile rat model.Redox report : communications in free radical research · 2025Article
- CXCL1 Promotes Osteoblast Autophagy and Inhibits Ferroptosis Through the Activation of the TGF-β/Smad Signalling Pathway.Journal of cellular and molecular medicine · 2025Article
- Curcumin preserves bone health compromised by diabetes by inhibiting osteoporosis through regulation of the SIRT3/FoxO3a signalling pathway.Scientific reports · 2025Article
- Beyond Bone Loss: A Biology Perspective on Osteoporosis Pathogenesis, Multi-Omics Approaches, and Interconnected Mechanisms.Biomedicines · 2025Review
- Mechanistic Insights into Salvigenin for Glucocorticoid-Induced Femoral Head Osteonecrosis: A Network Pharmacology and Experimental Study.Biomedicines · 2025Article
- Network Pharmacology Unveils Multi-Systemic Intervention ofEndocrine, metabolic & immune disorders drug targets · 2025Article
- Mitochondria: a key regulator of programmed cell death in OP.Frontiers in endocrinology · 2025Review
- Imbalance of Bone Homeostasis Caused by Nrf2 Deficiency Leads to Bone Loss in OVX Rats.Stem cells international · 2025Article
- Interruption of mitochondrial symbiosis is associated with the development of osteoporosis.Frontiers in endocrinology · 2025Review
- Research progress on the mechanism of curcumin anti-oxidative stress based on signaling pathway.Frontiers in pharmacology · 2025Review
- Astaxanthin prevents bone loss in osteoporotic rats with palmitic acid through suppressing oxidative stress.Redox report : communications in free radical research · 2024Article
- Therapeutic Potential of Ginsenosides on Bone Metabolism: A Review of Osteoporosis, Periodontal Disease and Osteoarthritis.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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