ArticleInternational journal of clinical and experimental pathology2015
Tanshinone IIA blocks dexamethasone-induced apoptosis in osteoblasts through inhibiting Nox4-derived ROS production.
Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- The Skeletal Effects of Tanshinones: A Review.Molecules (Basel, Switzerland) · 2021Pooled it
- Regulatory Effect and Mechanism of Tanshinone I on Cell Apoptosis in Steroid-Induced Osteonecrosis of the Femoral Head.The Kaohsiung journal of medical sciences · 2025Article
- Pharmacological Effects and Mechanisms of Tanshinone IIA in Bone Injury Repair.Pharmaceuticals (Basel, Switzerland) · 2025Review
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Pharmacological impacts of tanshinone on osteogenesis and osteoclastogenesis: a review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Mitochondria: a key regulator of programmed cell death in OP.Frontiers in endocrinology · 2025Review
- Tanshinone IIA promotes osteogenic differentiation potential and suppresses adipogenic differentiation potential of bone marrow mesenchymal stem cells.Molecular medicine reports · 2024Article
- Local Application of Tanshinone IIA protects mesenchymal stem cells from apoptosis and promotes fracture healing in ovariectomized mice.Journal of orthopaedic surgery and research · 2024Article
- Salvia miltiorrhiza in osteoporosis: a review of its phytochemistry, traditional clinical uses and preclinical studies (2014-2024).Frontiers in pharmacology · 2024Review
- Expanding the therapeutic potential ofFrontiers in pharmacology · 2023Review
- Therapeutic approach of natural products that treat osteoporosis by targeting epigenetic modulation.Frontiers in genetics · 2023Review
- CORM-3 Attenuates Oxidative Stress-Induced Bone Loss via the Nrf2/HO-1 Pathway.Oxidative medicine and cellular longevity · 2022Article
- Total flavonoids ofMolecular medicine reports · 2021Article
- The Use of Herbal Medicines for the Prevention of Glucocorticoid-Induced Osteoporosis.Frontiers in endocrinology · 2021Review
- NADPH oxidases and HIF1 promote cardiac dysfunction and pulmonary hypertension in response to glucocorticoid excess.Redox biology · 2020Article
- CSF-1 in Osteocytes Inhibits Nox4-mediated Oxidative Stress and Promotes Normal Bone Homeostasis.JBMR plus · 2020Article
- Crocin protects against dexamethasone‑induced osteoblast apoptosis by inhibiting the ROS/Ca2+‑mediated mitochondrial pathway.Molecular medicine reports · 2019Article
- Decrease of GSK3β Ser-9 Phosphorylation Induced Osteoblast Apoptosis in Rat Osteoarthritis Model.Current medical science · 2019Article
- Therapeutic Anabolic and Anticatabolic Benefits of Natural Chinese Medicines for the Treatment of Osteoporosis.Frontiers in pharmacology · 2019Review
- Dexamethasone-induced production of reactive oxygen species promotes apoptosis via endoplasmic reticulum stress and autophagy in MC3T3-E1 cells.International journal of molecular medicine · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis of osteoblasts caused by glucocorticoids has been identified as an important contributor to the development of osteoporosis. Tanshinone IIA (Tan), an active ingredient extracted from the rhizome of the Salvia miltiorrhiza Bunge (Danshen), has been reported to cast positive effects on osteoporosis. However, the precise mechanisms accounting this action remain elusive. In this study, by using osteoblastic MC3T3-E1 cells as a model, we confirmed the protective effects of Tan against dexamethasone (Dex)-induced cell apoptosis and further clarified its molecular mechanism of action. Our results showed that treatment with Dex caused cell injury, increased cytosol cytochrome c level and Nox expression, induced apoptosis in caspase-9-dependent manner, and enhanced reactive oxygen species (ROS) production. Tan attenuated these deleterious consequence triggered by Dex. Moreover, Dex-induced ROS production and cell injury were inhibited by antioxidant, NADPH oxidases inhibitors, Nox4 inhibitor, and Nox4 small interfering RNA (siRNA). Overexpression of Nox4 almost abolished the inhibitory effect of Tan on Dex-induced cell injury and apoptosis. The results also demonstrated significant involvement of Nox4 in the Dex-induced apoptosis. Nox4-derived ROS led to apoptosis through activation of intrinsic mitochondrial pathway. Additionally, we evidenced that Tan reversed Dex-induced apoptosis via inactivation of Nox4. The present findings suggest that inhibition of Nox4 may be a novel therapeutic approach of Tan to prevent against glucocorticoids-induced osteoblasts apoptosis and osteoporosis.
Indexed as
Identifiers
26722597PMC4680542W2238790889What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.