Retracted Article: Ginsenoside Rf alleviates dysmenorrhea and inflammation through the BDNF-TrkB-CREB pathway in a rat model of endometriosis

Qin X , Xuying Qin, Yan Liu, Liu Y , Yanchong Feng, Feng Y , Jie Jiang, Jiang J
Food & function · 2018 · vol. 10(1) , pp. 244–249 · doi:10.1039/c8fo01839a · PMID:30547177 · W2904084998
article OA: closed CC0 RETRACTED ⤵ 7 in-corpus citations
Retraction notice. Marked retracted by OpenAlex; see publisher for the formal retraction notice.
Full text JSON View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Ginsenoside Rf reduced endometriotic implant volume and pain in rats by down-regulating VEGF, inflammatory cytokines, and the BDNF-TrkB-CREB pathway.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-12 · read from full text ⓘ

This retracted study investigated ginsenoside Rf in a surgically induced rat model of endometriosis, using homologous transplantation to generate endometriosis in Wistar rats and comparing sham, estradiol valerate control, untreated endometriosis, and three ginsenoside Rf dose groups. After 7 days, the authors measured endometriotic implant volume and writhing responses, along with inflammatory and angiogenic markers (VEGF, iNOS, IL-6, IL-1β, TNF-α) by ELISA and RT-PCR, and BDNF/TrkB/pCREB expression in implants. They reported that ginsenoside Rf reduced implant volume and writhing responses and down-regulated VEGF and multiple inflammation-related markers in a dose-dependent manner, alongside decreased BDNF–TrkB–pCREB expression. The paper acknowledges as a limitation that it is a retracted article, meaning the findings are not considered reliable. This paper is centrally about endometriosis — it evaluates ginsenoside Rf’s effects on dysmenorrhea and inflammation in a rat endometriosis model and proposes mediation via the BDNF-TrkB-CREB pathway.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

To investigate the effects and the underlying mechanisms of ginsenoside Rf in a surgically induced rat endometriosis model, endometriosis was constructed through homologous transplantation and the Wistar rats were further randomly classified into the sham group, the estradiol valerate (E2V) control group, the endometriosis group, and the ginsenoside Rf groups (1.0, 2.0 and 4.0 mg kg-1, respectively). After 7 days of treatment, the implant volume and writhing responses were recorded. Vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α were analyzed using enzyme-linked immunosorbent assay (ELISA) and reverse transcription polymerase chain reaction (RT-PCR) assay. Brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinases (TrkB), and phosphate-c-AMP-responsive element binding protein (pCREB) were further measured. Compared with the endometriosis group, ginsenoside Rf could decrease the volume of the endometriotic implants and writhing responses. Furthermore, the expression levels of VEGF and inflammation-related iNOS, IL-6, IL-1β, and TNF-α were significantly down-regulated in the ginsenoside Rf groups in a dose-dependent manner. The results also showed that ginsenoside Rf could decrease the expression of BDNF, TrkB, and pCREB in the endometriotic implants. The alleviation of endometriosis-associated dysmenorrhea and inflammation by ginsenoside Rf may be partially mediated by the BDNF-TrkB-CREB pathway.
Full text 1,679 characters · extracted from oa-doi-fallback · click to expand
Retracted Article: Ginsenoside Rf alleviates dysmenorrhea and inflammation through the BDNF-TrkB-CREB pathway in a rat model of endometriosis† Abstract To investigate the effects and the underlying mechanisms of ginsenoside Rf in a surgically induced rat endometriosis model, endometriosis was constructed through homologous transplantation and the Wistar rats were further randomly classified into the sham group, the estradiol valerate (E2V) control group, the endometriosis group, and the ginsenoside Rf groups (1.0, 2.0 and 4.0 mg kg−1, respectively). After 7 days of treatment, the implant volume and writhing responses were recorded. Vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α were analyzed using enzyme-linked immunosorbent assay (ELISA) and reverse transcription polymerase chain reaction (RT-PCR) assay. Brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinases (TrkB), and phosphate-c-AMP-responsive element binding protein (pCREB) were further measured. Compared with the endometriosis group, ginsenoside Rf could decrease the volume of the endometriotic implants and writhing responses. Furthermore, the expression levels of VEGF and inflammation-related iNOS, IL-6, IL-1β, and TNF-α were significantly down-regulated in the ginsenoside Rf groups in a dose-dependent manner. The results also showed that ginsenoside Rf could decrease the expression of BDNF, TrkB, and pCREB in the endometriotic implants. The alleviation of endometriosis-associated dysmenorrhea and inflammation by ginsenoside Rf may be partially mediated by the BDNF-TrkB-CREB pathway.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

⚙ Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback ⓘ

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

dysmenorrheaendometriosis

MeSH descriptors

Brain-Derived Neurotrophic Factor Brain-Derived Neurotrophic Factor Cyclic AMP Response Element-Binding Protein Dysmenorrhea Endometriosis Ginsenosides Receptor, trkB Animals Brain-Derived Neurotrophic Factor Brain-Derived Neurotrophic Factor Cyclic AMP Response Element-Binding Protein Cyclic AMP Response Element-Binding Protein Dysmenorrhea Dysmenorrhea Dysmenorrhea Endometriosis Endometriosis Endometriosis Female Ginsenosides

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (30)

Cited by (7)

Source provenance

europepmc
last seen: 2026-07-29T06:27:48.050232+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:19:25.021412+00:00
unpaywall
last seen: 2026-06-13T06:42:57.164913+00:00
License: CC0 · commercial use OK