Randomized, Double-blind, Placebo-controlled, Parallel Arm Group Study Evaluating Analgesic Efficacy and Safety of Dexketoprofen Trometamol and Tramadol Hydrochloride on Moderate to Severe Acute Pain in Patients With Acute Low Back Pain

A randomized, double-blind, study to evaluate the analgesic efficacy and safety of Dexketoprofen trometamol and Tramadol hydrochloride combination versus placebo on moderate to severe acute pain in patients with acute low back pain.

Start Date17 Sep 2020

Sponsor / Collaborator

Menarini International Operations Luxembourg SA

NCT04178109 / CompletedPhase 2IIT

EVALUATION OF ORAL USE OF DEXKETOPROFEN/TRAMADOL IN ACUTE POSTOPERATIVE PAIN IN PATIENTS UNDERGOING TOTAL HIP REPLACEMENT WITH A MINIMALLY INVASIVE ANTERIOR APPROACH (AMIS).

Pain is a global public health issue and represents the most common reason for both physician consultation and hospital admissions . When unrelieved or poorly controlled, it is associated with medical complications, poor patient satisfaction and increased risk of developing chronic pain. Dexketoprofen is a new NSAID treating acute postoperative pain and when it combined with tramadol may have a better effect. The purpose of this study is to evaluate the analgesic effect of the oral use of the combination of dexketoprofen/tramadole on the reduction of postoperative pain after total hip arthroplasty with minimal invasive anterior approach (AMIS).

Start Date10 Jan 2019

Sponsor / Collaborator-

100 Clinical Results associated with COX-1 x μ opioid receptor x COX-2

100 Translational Medicine associated with COX-1 x μ opioid receptor x COX-2

0 Patents (Medical) associated with COX-1 x μ opioid receptor x COX-2

Literatures (Medical) associated with COX-1 x μ opioid receptor x COX-2

01 Jan 2022·American journal of translational research

Mechanism of Thunberg Fritillaria in treating endometriosis based on network pharmacology and the effect of Peiminine on the MEK/ERK pathway.

Article

Author: Fan, Limin ; Peng, Xia ; Yu, Chaoqin ; Xie, Jiani ; Xia, Yue ; Ni, Xiaorong ; Liu, Honglin

OBJECTIVETo explore the mechanism of Thunberg Fritillaria in treating endometriosis (EMs) based on network pharmacology and the effect of Peiminine on the MEK/ERK pathway.METHODSWe applied Chinese medicine system pharmacology analysis platform (TCMSP) database and literature search to screen the main chemical components of Fritillaria thunbergii Miq and created a Vanny map from the databases of TCMSP, GENECARDS, Online Mendelian Inheritance in Man (OMIM), and some others. The STRING database was used to construct the protein interaction network of Fritillaria thunbergii Miq and EMs. The overlapping targets and enriched pathways were discovered using the cells of the innate immune annotation database (DAVID) and the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. To test the mechanism of Peiminine, the active ingredients of Fritillaria thunbergii, in the therapy of EMs, we designed cell assays and animal research. EMs mouse models were treated with several therapies, including fibrosis inhibitor in Peiminine by utilizing Hematoxylin-eosin staining (HE staining), MASSON staining, Immunohistochemistry, Immunofluorescence, quantitative real-time PCR (qRT-PCR) experiment, and Western blotting test. We evaluated the anti-endometriotic effects of Peiminine using 12Z human endometriotic cells. Cell Counting Kit 8 was used to assess the vitality of 12z cells (CCK8). We evaluated the migration ability of 12z cells by cell scratch test.RESULTSThe effective active ingredients of Fritillaria thunbergii Miq in the treatment of EMs are Pelargonidin, Beta-sitosterol syringaresinol, Peimisine Pelargonidin-3, 5-diglucoside Ziebeimine Zhebeiresinol Verticine Solatubin OSI-2040 Chaksine Peiminine Peiminoside Peiminoside_qt, and 6-Methoxyl-2-acetyl-3-methyl-1, 4-naphthoquinone-8-O-beta-D-glucopyranoside. The critical targets for Fritillaria thunbergii Miq treating EMs are NOS2/PTGS1/AR/PPARG/PTGS2/NCOA2/RXRA/PGR/NR3C1/NCOA1/SLC6A4/OPRM1/BCL2 and ESR1. The results of GO function and KEGG enrichment analysis showed that the role pathway was estrogen-related signaling and thyroid hormone-related signaling. The expression of E-cadherin was decreased in EMs while MEK1/2, P-ERK, N-cadherin and vimentin were all increased in MASSON, immunofluorescence, Real-time PCR and Western blotting. In epithelial 12Z cells, high concentrations of Peiminine can block cell activity and migration, which is directly related to blocking cell fibrosis.CONCLUSIONOverall, this study partially verified the network pharmacological prediction that Peiminine regulates the MAPK pathway in inhibiting 12Z cell proliferation and migration, and finally protects against EMs.

01 Nov 2012·The Clinical Journal of PainQ3 · MEDICINE

Natural Variation in the μ-opioid Gene OPRM1 Predicts Increased Pain on Third Day After Thoracotomy

Q3 · MEDICINE

Article

Author: Peter A. Kanetsky ; Anil Vachani ; Allan Gottschalk ; Edward Andrew Ochroch

OBJECTIVESThe mechanism whereby acute postsurgical pain can persist and become chronic remains unknown. Thoracotomy is a common procedure with a high incidence of long-term pain for which acute postsurgical pain is an established risk factor. Therefore, the genetic basis of elevations in acute postsurgical pain after thoracotomy was investigated.METHODSA cohort of thoracotomy patients participating in an ongoing trial of outcomes after cancer were enrolled. A standard combined general and epidural anesthetic and surgical approach were used. All patients received a standardized postoperative epidural analgesia regimen. Postoperatively, pain scores were determined and blood was collected for genotyping. Our a priori hypothesis was that variability of genes involved in nociception and analgesic therapy would predict pain score ≥3 of 10 on the third postoperative day.RESULTSNinety patients with pain and genotyping data on postoperative day 3 were examined. We found no association between markers in COMT, COX1, COX2, and TRPV1 and postoperative pain. We demonstrated several statistically significant associations with 4 single nucleotide polymorphism markers in OPRM1 (odds ratio, 95% confidence intervals): rs634479 (0.4, 0.17, 0.97), rs499796 (0.35, 0.13, 0.92), rs548646 (0.47, 0.23, 0.97), and rs679987 (0.1, 0.01, 0.84). From these, we inferred 2 haplotype blocks in OPRM1 where both had a frequency of 9% and P=0.03 and 0.04. Previously published functional single nucleotide polymorphisms in OPRM1 and COMT were not associated with increased pain on the third postoperative day.DISCUSSIONWe identified previously unpublished haplotypes of the OPRM1 receptor that predicted increases in self-reported pain on the third postoperative day after thoracotomy. These findings require replication and further refinement before their impact on patient care can be determined.

01 Apr 1998·British Journal of PharmacologyQ2 · MEDICINE

Enhancement of opioid inhibition of GABAergic synaptic transmission by cyclo‐oxygenase inhibitors in rat periaqueductal grey neurones

Q2 · MEDICINE

Article

Author: Vaughan, C W

Cyclo‐oxygenase (COX) inhibitors potentiate opioid inhibition of GABAergic synaptic transmission in rat periaqueductal grey (PAG) (Vaughan et al., 1997). In the present study, the relative contribution of cyclo‐oxygenase‐1 (COX‐1) and COX‐2 inhibition to this phenomenon was examined by use of whole‐cell patch clamp recordings in brain slices. The μ‐receptor partial agonist morphine (10 μM) had little effect on GABAergic synaptic transmission. Morphine reduced the frequency of spontaneous miniature inhibitory postsynaptic currents (m.i.p.s.cs) by 13%. The nonselective COX inhibitor, indomethacin, produced a dose‐dependent potentiation of the morpine inhibition of m.i.p.s.c. frequency (maximum inhibition 42%, IC50=6 nM). More selective COX‐2 inhibitors produced a similar potentiation of the morphine inhibition of m.i.p.s.c. frequency; however, at greater concentrations (IC50=57 nM piroxicam, 1.7 μM DFU). Maintaining slices in the protein synthesis inhibitor cycloheximide (1 μM), to prevent COX‐2 induction, had no effect on the potentiation action of DFU (10 μM). These results demonstrate that the potentiation of opioid inhibition of GABAergic synaptic transmission in PAG is largely a result of inhibition of COX‐1 activity. These findings suggest that COX‐1, rather than COX‐2 inhibition, mediates the synergistic analgesic actions of opioids and non‐steroidal anti‐inflammatory drugs (NSAIDs) in the midbrain PAG.British Journal of Pharmacology (1998) 123, 1479–1481; doi:10.1038/sj.bjp.0701818

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