piperidines has been researched along with Endometriosis* in 7 studies
1 trial(s) available for piperidines and Endometriosis
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Response Entropy is not more sensitive than State Entropy in distinguishing the use of esmolol instead of remifentanil in patients undergoing gynaecological laparoscopy.
Monitoring of analgesia remains a challenge during general anaesthesia. Activation of Response Entropy (RE) to painful stimuli has been suggested to be a sign of inadequate analgesia. We evaluated the ability of RE to be more sensitive than State Entropy (SE) in measuring nociception in patients undergoing gynaecological laparoscopy. Our hypothesis was that while keeping SE at a predetermined level, RE would be higher in patients receiving a beta-blocking agent (esmolol) instead of an opioid (remifentanil) during a propofol/nitrous oxide anaesthesia.. Fifty-one women aged between 22-53 years were randomly assigned to receive esmolol (n=25) or remifentanil (n=26). SE was kept at 50+/-5. RE and SE were recorded at an interval of 30 s to 2 min and the areas under the RE and SE value-time curves (AUCRE and AUCSE) were calculated during the time of intubation and start of surgery as well as during the entire anaesthesia. The difference between RE and SE recordings in both groups was determined by subtracting the AUCSE from the corresponding AUCRE. Movements of the patients were recorded.. No significant differences were detected in any of the several AUC values between the groups. The difference between RE and SE recordings was similar in both groups. Every patient in the esmolol group moved some time during the procedure interfering with surgery while no one in the remifentanil group moved.. In patients undergoing gynaecological laparoscopic day-case surgery, RE seems not to be more sensitive than SE in guiding the use of opioids during general anaesthesia. Topics: Adrenergic beta-Antagonists; Adult; Ambulatory Surgical Procedures; Anesthesia, General; Anesthetics, Intravenous; Area Under Curve; Electroencephalography; Electromyography; Endometriosis; Female; Gynecologic Surgical Procedures; Humans; Laparoscopy; Middle Aged; Monitoring, Intraoperative; Ovarian Cysts; Pain Measurement; Piperidines; Propanolamines; Propofol; Remifentanil | 2006 |
6 other study(ies) available for piperidines and Endometriosis
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In vitro maturation medium supplementation: utilization of repaglinide, L-carnitine, and mesenchymal stem cell-conditioned medium to improve developmental competence of oocytes derived from endometriosis mouse models.
Endometriosis (EMS) is one of the most prevalent causes for female infertility. Herein, we investigated the effect of the repaglinide (RG), L-carnitine (LC), and bone marrow mesenchymal stem cell-conditioned medium (BMSC-CM) supplementation during in vitro maturation (IVM) on the quality, maturation, and fertilization rates, as well as embryonic quality and development of oocytes derived from normal and EMS mouse model. Immature oocytes were collected from two groups of normal and EMS-induced female NMRI mice at 6-8 weeks of age. Oocytes were cultured in IVM medium unsupplemented (control group), or supplemented with 1 M RG, 0.3 and 0.6 mg/mL LC, and 25 and 50% BMSC-CM. After 24 h of oocyte incubation, IVM rate and antioxidant status were assessed. Subsequently, the rates of fertilization, cleavage, blastulation, and embryonic development were assessed. Our results demonstrated that supplementation of IVM medium with LC and BMSC-CM, especially 50% BMSC-CM, significantly enhanced IVM and fertilization rates, and markedly improved blastocyst development and total blastocyst cell numbers in EMS-induced mice compared to the control group (53.28±0.24 vs 18.09±0.10%). Additionally, LC and BMSC-CM were able to significantly modulate EMS-induced nitro-oxidative stress by boosting total antioxidant capacity (TAC) and mitigating nitric oxide (NO) levels. Collectively, LC and BMSC-CM supplementation improved oocyte quality and IVM rates, pre-implantation developmental competence of oocytes after in vitro fertilization, and enhanced total blastocyst cell numbers probably by attenuating nitro-oxidative stress and accelerating nuclear maturation of oocytes. These outcomes may provide novel approaches to refining the IVM conditions that can advance the efficiency of assisted reproductive technologies in infertile couples. Topics: Animals; Antioxidants; Blastocyst; Carbamates; Carnitine; Culture Media, Conditioned; Dietary Supplements; Endometriosis; Female; Fertilization in Vitro; Humans; In Vitro Oocyte Maturation Techniques; Mesenchymal Stem Cells; Mice; Oocytes; Piperidines; Pregnancy | 2022 |
Tofacitinib alters STAT3 signaling and leads to endometriosis lesion regression.
Endometriosis is a widespread gynecologic condition affecting up to 15% of women of reproductive age. The Janus kinase/signal transducer and activator of transcription (JAK/STAT3) pathway is upregulated in endometriosis and is a therapeutic target. Here we sought to determine the effect of Tofacitinib, a JAK inhibitor in widespread clinical use, on JAK/STAT signaling in endometriosis and lesion growth. Endometriosis was surgically induced in C57BL/6 mice using homologous uterine horn transplantation. Lesions were allowed to form over 4 weeks followed by Tofacitinib (10 mg/kg) or vehicle administered by oral gavage over 4 weeks. Tofacitinib treatment in vivo led to endometriosis lesion regression and reduced adhesion burden compared to vehicle treatment. In vitro studies on Ishikawa cells showed that Tofacitinib reduced hypoxia-inducible factor 1α and vascular endothelial growth factor mRNA levels at 12 and 24 h. Western blot analysis showed that Tofacitinib effectively reduced STAT3 phosphorylation in Ishikawa cells and human primary stromal and epithelial cells from eutopic endometrium of patients with and without endometriosis. This study suggests that the inhibition of JAK/STAT signaling using Tofacitinib may be a viable method for the treatment of endometriosis. Topics: Animals; Endometriosis; Female; Humans; Mice; Mice, Inbred C57BL; Piperidines; Pyrimidines; STAT3 Transcription Factor; Vascular Endothelial Growth Factor A | 2021 |
Possible involvement of crosstalk between endometrial cells and mast cells in the development of endometriosis via CCL8/CCR1.
The density and the activity of mast cells are associated with endometriosis. However, the role of mast cells on the pathogenesis of endometriosis remains unclear. Our study aims to investigate whether endometrial cells interact with mast cells and the involvement of their crosstalk in the development of endometriosis.. The transwell assay was applied to investigate the effect of mast cells on the migratory ability of human primary endometrial cells. Mast cells were cocultured with endometrial epithelial and stromal cells respectively and total RNAs were isolated and subjected to mRNA sequencing. Next, the transwell assay, CCK-8, and tube formation were applied to study the role of CCL8 on the endometrial and endothelial cells in vitro. The mouse model was also established to confirm the role of CCL8 in the development and angiogenesis of endometriosis.. CCL8 was up-regulated in mast cells when cocultured with endometrial cells. CCL8 was highly expressed in the ectopic endometrium and the serum of patients with endometriosis. CCL8 promoted the migratory ability of endometrial epithelial and stromal cells and increased the proliferation, migration, and tube formation of endothelial cells. CCR1, the receptor of CCL8, was over-expressed in the ectopic endometrium and colocalized with blood vessels in ovarian endometriomas. The inhibition of CCR1 suppressed the development and angiogenesis of endometriosis in vivo.. The crosstalk between endometrial cells and mast cells in the development of endometriosis via CCL8/CCR1 was demonstrated, thereby providing a new treatment strategy for endometriosis. Topics: Animals; Case-Control Studies; Cell Communication; Cells, Cultured; Chemokine CCL8; Coculture Techniques; Disease Models, Animal; Endometriosis; Endometrium; Endothelial Cells; Epithelial Cells; Female; Humans; Mast Cells; Mice, Inbred BALB C; Neovascularization, Pathologic; Phenylurea Compounds; Piperidines; Receptors, CCR1; Signal Transduction; Stromal Cells | 2020 |
B lymphocytes inactivation by Ibrutinib limits endometriosis progression in mice.
What are the effects of B lymphocyte inactivation or depletion on the progression of endometriosis?. Skewing activated B cells toward regulatory B cells (Bregs) by Bruton's tyrosine kinase (Btk) inhibition using Ibrutinib prevents endometriosis progression in mice while B cell depletion using an anti-CD20 antibody has no effect.. A polyclonal activation of B cells and the presence of anti-endometrial autoantibodies have been described in a large proportion of women with endometriosis though their exact role in the disease mechanisms remains unclear.. This study included comparison of endometriosis progression for 21 days in control mice versus animals treated with the anti-CD20 depleting antibody or with the Btk inhibitor Ibrutinib that prevents B cell activation.. After syngeneic endometrial transplantation, murine endometriotic lesions were compared between treated and control mice using volume, weight, ultrasonography, histology and target genes expression in lesions. Phenotyping of activated and regulatory B cells, T lymphocytes and macrophages was performed by flow cytometry on isolated spleen and peritoneal cells. Cytokines were assayed by ELISA.. Btk inhibitor Ibrutinib prevented lesion growth, reduced mRNA expression of cyclooxygenase-2, alpha smooth muscle actin and type I collagen in the lesions and skewed activated B cells toward Bregs in the spleen and peritoneal cavity of mice with endometriosis. In addition, the number of M2 macrophages decreased in the peritoneal cavity of Ibrutinib-treated mice compared to anti-CD20 and control mice. Depletion of B cells using an anti-CD20 antibody had no effect on activity and growth of endometriotic lesions and neither on the macrophages, compared to control mice.. N/A.. It is still unclear whether B cell depletion by the anti-CD20 or inactivation by Ibrutinib can prevent establishment and/or progression of endometriosis in humans.. Further investigation may contribute to clarifying the role of B cell subsets in human endometriosis.. This research was supported by a grant of Institut National de la Santé et de la Recherche Médicale and Paris Descartes University. None of the authors has any conflict of interest to disclose. Topics: Adenine; Agammaglobulinaemia Tyrosine Kinase; Animals; B-Lymphocytes; Cytokines; Disease Progression; Drug Evaluation, Preclinical; Endometriosis; Female; Mice, Inbred BALB C; Piperidines; Pyrazoles; Pyrimidines; T-Lymphocytes | 2019 |
[Cannabinoid receptor 1 controls nerve growth in ectopic cyst in a rat endometriosis model].
To investigate whether cannabinoid receptor 1 (CB1R) is involved in nerve growth in endometriosis-associated ectopic cyst.. The effect of CB1R agonist and antagonist on the expression of pan-neuronal marker protein gene product (PGP) 9.5 in ectopic cyst was examined by immunofluorescence and Western blot in endometriosis model of 18 rats.. Immunofluorescence revealed that PGP 9.5 was expressed in the nerve fibers and was mainly distributed in the cyst hilum. Western blot revealed that the protein density of either PGP 9.5 (2 week: 0.38 ± 0.05; 4 week: 0.63 ± 0.03; 8 week: 0.80 ± 0.07, P < 0.01) or CB1R (2 week: 0.48 ± 0.04; 4 week: 0.68 ± 0.01; 8 week: 0.80 ± 0.03, P < 0.01) in the ectopic cyst increased with cyst size. In addition, compared to control group (0.75 ± 0.01), PGP 9.5 expression in the ectopic cyst was promoted by CB1R agonist ACPA (0.81 ± 0.01, P < 0.05), and inhibited by CB1R antagonist AM251 (0.67 ± 0.03, P < 0.01).. CB1R was involved in the nerve growth of ectopic cyst associated with endometriosis. Topics: Animals; Blotting, Western; Cysts; Disease Models, Animal; Endometriosis; Female; Peripheral Nerves; Piperidines; Pyrazoles; Rats; Receptor, Cannabinoid, CB1; Ubiquitin Thiolesterase | 2014 |
Effects of the novel orally active antiestrogen TZE-5323 on experimental endometriosis.
Danazol and gonadotropin-releasing hormone agonists which are used as therapeutic drugs for endometriosis, develop adverse reactions in association with their long-term use. The efficacy of anti-estrogens for endometriosis, an estrogen-dependent disorder, has not been demonstrated. A novel, orally active anti-estrogen, TZE-5323 ((2-cyclohexy-6-hydroxybenzo[b]thien-3-yl)[4-[2-(1- piperidinyl)ethoxy]phenyl] methanone hydrochloride, CAS 150797-71-0; free salt formula) was developed. TZE-5323 showed strong affinity for human estrogen receptor alpha (hER alpha) and beta (hER beta), and dose-dependently inhibited estradiol-stimulated transcriptional activation via hER alpha and hER beta. Furthermore, TZE-5323 dose-dependently reduced estrogen-increased uterine weight in ovariectomized rats. Tamoxifen showed agonistic activity on hER alpha, while TZE-5323 did not show such activity. In the experimental endometriosis model in rats in which endometrial tissue is autotransplanted into the renal subcapsular space, TZE-5323 dose-dependently reduced the volume of the endometrial implant as did danazol and leuprorelin acetate. Furthermore, the long-term administration of TZE-5323 neither showed a decrease in bone mineral density nor did it affect serum estradiol concentrations in intact rats. Therefore, TZE-5323 suggested its potential as a novel therapeutic drug for endometriosis which is effective also in long-term use. Topics: Animals; Bone Density; Chloramphenicol O-Acetyltransferase; Cholesterol; Endometriosis; Endometrium; Estradiol; Estrogen Antagonists; Estrogen Receptor alpha; Estrogen Receptor beta; Female; Ligands; Organ Size; Piperidines; Plasmids; Protein Biosynthesis; Rats; Rats, Wistar; Receptors, Estrogen; Transcription, Genetic; Transcriptional Activation; Uterus | 2003 |