ArticleMolecular medicine reports2020
Effects of botulinum toxin A on endometriosis‑associated pain and its related mechanism.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- A Transdermal Prion-Bionics Supermolecule as a RAB3A Antagonist for Enhancing Facial Youthfulness.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Recent advances in the treatment of pain in endometriosis: A bibliometric analysis of experimental models.Veterinary world · 2023Article
Corrections and comments
- Retraction · 2020-11-09Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · Error in Methods ·
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometriosis (EMS) is a common disease in women aged 25‑45 years, and pain is the main clinical symptom. The primary clinical treatment is surgical excision and drug therapy targeting the ectopic lesions, but these have not been very effective. Botulinum neurotoxin serotype A (BTX‑A) has been reported to be useful in the treatment of pain in a variety of diseases. Based on this, the aim of the present study was to explore the therapeutic effect and mechanism of BTX‑A on EMS. A model of nerve injury induced by oxygen glucose deprivation (OGD) was constructed in PC12 cells and EMS mice. Model cells and mice were treated with different concentrations of BTX‑A to observe the changes in pain behavior, to detect cell viability and the secretion of norepinephrine (NE) and methionine enkephalin (M‑EK) in cells and the spinal cord, and to evaluate the expression of apoptosis‑related molecules in spinal cord nerves. The results revealed that BTX‑A significantly reduced the amount of writhing in model mice, enhanced the activity of PC12 OGD cells, increased the secretion of NE and M‑EK in model cells and the spinal cord of mice, and decreased the apoptosis of neural cells in the spinal cord of the model mice. Therefore, it was hypothesized that BTX‑A may alleviate the pain induced by EMS by increasing the secretion of analgesic substances and promoting the repair of nerve injury. The present study provided a theoretical basis for the treatment of pain induced by EMS.
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