Protective role of propofol in endometriosis and its mechanism

Feng, Shuo; Sun, Yingui

doi:10.3892/etm.2018.6648

Cited by 4 publications

(3 citation statements)

References 33 publications

(33 reference statements)

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“…However, the function of propofol in the ectopic lesions of EM has not been investigated, which will be explored in the current study. More interestingly, during the conduction of our study, propofol is found to inhibit cell viability and induce cell apoptosis of EM (Feng and Sun 2018), which further indicated the inhibitory role of propofol in the progression of EM. Consistently, we found the inhibitory effects of propofol in EM, evidenced by the decreased cell proliferation and invasion of ESCs after propofol administration.…”

Section: Discussionsupporting

confidence: 65%

Propofol inhibits proliferation and invasion of endometriotic cells by miR-9-5p/TGFBI axis

Zhou

Song

et al. 2020

All Life

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Endometriosis (EM) is an estrogen-dependent, frequent benign gynecological disease, which reduces the quality of life in EM patients. Propofol regulates the apoptosis of EM. miR-9-5p is decreased in early secretory endometrium, TGFBI is increased in EM, however, their functions in EM remain unclear. This study aimed to investigate the mechanisms underlying the effects of propofol on the proliferation and invasion of EM by regulating miR-9-5p/TGFBI. The proliferation and invasion of ectopic endometrial stromal cells (ESCs) were determined by MTT assay and Transwell assay, respectively. Real-time PCR was applied for the evaluation of miR-9-5p and transforming growth factor-β (TGF-β)-induced gene (TGFBI) mRNA level in ESCs. Western blot was used to examine the protein level of TGFBI protein (TGFBIp) in ESCs. The relation between miR-9-5p and TGFBI was predicted by TargetScan 7.1 and verified by dual luciferase reporter assay. Propofol reduced cell proliferation and invasion, while induced miR-9-5p level and reduced TGFBI/TGFBIp level in ectopic ESCs. Additionally, in ectopic ESCs from patients with EM, miR-9-5p was lower, while TGFBI and TGF-BIp were higher than those from eutopic endometrium and normal endometrium from patients with hysteromyoma. Moreover, propofol reduced proliferation and invasion in ectopic ESCs, which was realized by the regulation of miR-9-5p/TGFBI.

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Section: Discussionsupporting

confidence: 65%

Propofol inhibits proliferation and invasion of endometriotic cells by miR-9-5p/TGFBI axis

Zhou

Song

et al. 2020

All Life

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“…The cells were maintained in DMEM/F12 medium (Gibco; Thermo Fisher Scientific, Inc.) with 10% FBS (Gibco; Thermo Fisher Scientific, Inc.), 100 U/ml penicillinG and streptomycin sulfate (Invitrogen; Thermo Fisher Scientific, Inc.) in a humidified incubator with 5% CO 2 at 37˚C. For drug-toxicity assays, the cells were cultured in 6-well plates and exposed to different concentrations of propofol (0, 1, 5 and 10 µg/ml) for 48 h ( 27 ).…”

Section: Methodsmentioning

confidence: 99%

Protective effect of propofol via the regulation of ovarian granulosa cell proliferation and apoptosis

Ding

Kang

et al. 2021

Exp Ther Med

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Propofol is an anesthetic frequently used in surgery. Accumulating evidence suggests that propofol exhibits an effect on cell viability, apoptosis and invasion in several types of cancer cells. MicroRNAs (miRNAs) have been reported to play pivotal roles in the development of polycystic ovary syndrome (PCOS). However, the diagnostic applications of miR-451a in PCOS remain unknown. The present study aimed to elucidate the effects of propofol on ovarian granulosa cell proliferation and apoptosis and illustrate the specific mechanisms associated with this process. Human ovarian granulosa cell-like KGN cells, which were used as a representative of granulosa cells in the present study, were treated with different concentrations (0, 1, 5 and 10 µg/ml) of propofol for 48 h and cell proliferation and apoptosis were assessed using MTT and flow cytometry assays, respectively. Propofol treatment resulted in significant inhibition of cell viability and induction of apoptosis in KGN cells, which was accompanied with increased cleaved caspase 3 and suppressed pro-caspase 3 expression levels. Furthermore, propofol reduced Wnt3a and β-catenin protein and mRNA expression levels. miR-451a expression in KGN cells was evaluated by reverse transcription-quantitative PCR (RT-qPCR). miR-451a expression was upregulated in propofol-stimulated KGN cells. The data further demonstrated that miR-451a mimics suppressed cell proliferation and increased apoptosis of KGN cells compared with cells transfected with control mimics. Furthermore, the association between miR-451a and propofol was investigated. Rescue experiments were performed to investigate the anti-proliferative mechanism of propofol in ovarian granulosa cells. KGN cells were transfected with miR-451a inhibitor or inhibitor control sequences for 6 h and treated with 10 µg/ml propofol for an additional 48 h. The results from the MTT, RT-qPCR and western blot assays indicated that 10 µg/ml propofol inhibited cell viability, induced apoptosis, enhanced cleaved caspase 3 expression, reduced pro-caspase 3 levels and inhibited the protein and mRNA expression of Wnt3a and β-catenin. However, inhibition of miR-451a demonstrated the opposite effects. In conclusion, the results of the present study revealed that propofol exerted an anti-proliferative and apoptosis-inducing role in ovarian granulosa cells through mediation of miR-451a expression. In addition, the data indicated that miR-451a may be used as an effective therapeutic target for PCOS treatment.

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“…Endometriotic cells could not express surface receptors to trigger proapoptotic proteins; neither apoptotic signals were appropriately transduced, leading to proliferation being triggered instead 188 . GnRH agonists, such as leuprolide acetate or the preclinical nonhormonal drug propofol, increased the levels of proapoptotic proteins, as well as decreased the levels of antiapoptotic proteins and promitogenic cytokines 52,100 . Melatonin is highly effective in amplification of apoptotic activity via regulating MMP‐3 signal, was able to regress EM at either early or late stage.…”

Section: Potential New Pharmaceuticals and Their Target‐signaling Pathwaysmentioning

confidence: 99%

Pharmaceuticals targeting signaling pathways of endometriosis as potential new medical treatment: A review

Hung

Zhang

Tan

et al. 2021

Medicinal Research Reviews

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Endometriosis (EM) is defined as endometrial tissues found outside the uterus. Growth and development of endometriotic cells in ectopic sites can be promoted via multiple pathways, including MAPK/MEK/ERK, PI3K/Akt/mTOR, NF‐κB, Rho/ROCK, reactive oxidative stress, tumor necrosis factor, transforming growth factor‐β, Wnt/β‐catenin, vascular endothelial growth factor, estrogen, and cytokines. The underlying pathophysiological mechanisms include proliferation, apoptosis, autophagy, migration, invasion, fibrosis, angiogenesis, oxidative stress, inflammation, and immune escape. Current medical treatments for EM are mainly hormonal and symptomatic, and thus the development of new, effective, and safe pharmaceuticals targeting specific molecular and signaling pathways is needed. Here, we systematically reviewed the literature focused on pharmaceuticals that specifically target the molecular and signaling pathways involved in the pathophysiology of EM. Potential drug targets, their upstream and downstream molecules with key aberrant signaling, and the regulatory mechanisms promoting the growth and development of endometriotic cells and tissues were discussed. Hormonal pharmaceuticals, including melatonin, exerts proapoptotic via regulating matrix metallopeptidase activity while nonhormonal pharmaceutical sorafenib exerts antiproliferative effect via MAPK/ERK pathway and antiangiogenesis activity via VEGF/VEGFR pathway. N‐acetyl cysteine, curcumin, and ginsenoside exert antioxidant and anti‐inflammatory effects via radical scavenging activity. Natural products have high efficacy with minimal side effects; for example, resveratrol and epigallocatechin gallate have multiple targets and provide synergistic efficacy to resolve the complexity of the pathophysiology of EM, showing promising efficacy in treating EM. Although new medical treatments are currently being developed, more detailed pharmacological studies and large sample size clinical trials are needed to confirm the efficacy and safety of these treatments in the near future.

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Protective role of propofol in endometriosis and its mechanism

Cited by 4 publications

References 33 publications

Propofol inhibits proliferation and invasion of endometriotic cells by miR-9-5p/TGFBI axis

Propofol inhibits proliferation and invasion of endometriotic cells by miR-9-5p/TGFBI axis

Protective effect of propofol via the regulation of ovarian granulosa cell proliferation and apoptosis

Pharmaceuticals targeting signaling pathways of endometriosis as potential new medical treatment: A review

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