ArticleBioengineered2022
Butorphanol tartrate mitigates cellular senescence against tumor necrosis factor -α (TNF-α) in human HC-A chondrocytes.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Chondrocyte Senescence in Osteoarthritis: Potential Targets and Pharmacological Interventions.Cartilage · 2026Article
- Fatty Acid Transporter CD36 Promotes Ox-LDL-Induced Senescence of Vascular Endothelial Cells in Preeclampsia.Journal of inflammation research · 2025Article
- Cross-talk of inflammation and cellular senescence: a new insight into the occurrence and progression of osteoarthritis.Bone research · 2024Review
- Inflammatory and Metabolic Signaling Interfaces of the Hypertrophic and Senescent Chondrocyte Phenotypes Associated with Osteoarthritis.International journal of molecular sciences · 2023Review
- A Bibliometric and Knowledge Map Analysis of Osteoarthritis Signaling Pathways from 2012 to 2022.Journal of pain research · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is an important risk factor for osteoarthritis (OA). Butorphanol is a preoperative sedative and analgesic that possesses anti-inflammatory activity. However, the effect of butorphanol on OA has not been reported. Here we aimed to explore the effect of butorphanol tartrate on the cellular senescence of human chondrocyte-articular (HC-A) cells in response to tumor necrosis factor-α (TNF-α) stimulation. Butorphanol tartrate attenuated the TNF-α-caused cellular senescence of HC-A cells, with decreased positive senescence-associated-β-galactosidase (SA-β-gal) staining and elevated telomerase activity. Butorphanol tartrate prevented TNF-α-caused cell cycle arrest in the G0/G1 phase in HC-A cells and decreased p21 expression. The TNF-α-induced production of interleukin (IL)-6 and IL-8 in HC-A cells were mitigated by butorphanol tartrate. In addition, butorphanol tartrate reduced p-NF-κB p65/total p65 and p-STAT3/STAT3 ratios in HC-A cells cultured with TNF-α. Taken together, butorphanol tartrate protected HC-A cells from TNF-α-caused cellular senescence through inactivation of NF-κB and STAT3. These results imply that butorphanol tartrate might be used as a potential agent for the treatment of aging-related OA.
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