Theoretical studies on opioid receptors and ligands. I. Molecular modeling and QSAR studies on the interaction mechanism of fentanyl analogs binding to ?-opioid receptor

2000 ◽  
Vol 78 (4) ◽  
pp. 285-293 ◽  
Author(s):  
Hua Liang Jiang ◽  
Xiao Qin Huang ◽  
Suo Bao Rong ◽  
Xiao Min Luo ◽  
Jian Zhong Chen ◽  
...  
Keyword(s):  
Molecular Modeling ◽  
Opioid Receptor ◽  
Opioid Receptors ◽  
Interaction Mechanism ◽  
Theoretical Studies ◽  
Qsar Studies ◽  
Fentanyl Analogs

Study of Molecular Docking of Mu Opioid Receptor Agonist - Fentanyl and its Analogs Based on Docking

2013 ◽  
Vol 655-657 ◽  
pp. 1931-1934 ◽  
Author(s):  
Ming Liu ◽  
Lei Wang ◽  
Xiao Li Liu ◽  
Wen Xiang Hu
Keyword(s):  
Molecular Docking ◽  
Opioid Receptor ◽  
3D Structure ◽  
Interaction Mechanism ◽  
Mu Opioid Receptor ◽  
Mu Opioid ◽  
Opioid Receptor Agonist ◽  
Fentanyl Analogs ◽  
Fully Automatic ◽  
Surflex Docking

The interaction mechanism of a series of fentanyl analogs are examined using molecular docking to the mu-opioid receptor based on Surflex-Docking. Fully automatic flexible molecular docking (Surflex-Docking) was performed by using the possible active conformations of 70 fentanyl analogs and optimized 3D structure of mu-opioid receptor. The site mainly consist of residues ILE 109, ASP 112, TYR113, MET116, HIS262, TYR291. All these residues take part in interaction between fentanyl and mu-opioid receptor. Meanwhile, the results provide new insight to design of experiments aimed at understanding the structure.

Molecular Modeling and 3D-QSAR Studies on the Interaction Mechanism of Tripeptidyl Thrombin Inhibitors with Human α-Thrombin†

1997 ◽  
Vol 40 (19) ◽  
pp. 3085-3090 ◽  
Author(s):  
Hualiang Jiang ◽  
Kaixian Chen ◽  
Yun Tang ◽  
Jianzhong Chen ◽  
Quan Li ◽  
...  
Keyword(s):  
Molecular Modeling ◽  
Interaction Mechanism ◽  
3D Qsar ◽  
Thrombin Inhibitors ◽  
Qsar Studies

The K+-evoked release of [3H]acetylcholine from slices of rat globus pallidus: modulation by δ-opioid receptors

1991 ◽  
Vol 69 (3) ◽  
pp. 414-418 ◽  
Author(s):  
Bianca B. Ruzicka ◽  
Khem Jhamandas
Keyword(s):  
Globus Pallidus ◽  
Opioid Receptor ◽  
Opioid Receptors ◽  
Cholinergic Neurons ◽  
Receptor Activation ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Release Of Acetylcholine ◽  
Δ Opioid Receptor ◽  
Tritium Release

Previous investigations have shown that the activation of δ-opioid receptors depresses the release of acetylcholine (ACh) in the rat caudate putamen. This finding raised the possibility that the release of ACh is similarly modulated in the globus pallidus, a region containing a distinct population of cholinergic neurons and enriched in enkephalinergic nerve terminals. In the present study the pallidal release of ACh was characterized and the effects of δ-opioid receptor activation on this release were examined. The results show that this release is stimulated by high K+ in a concentration- and Ca2+-dependent manner. D-Pen2,L-Pen5-enkephalin (0.1 – 10 μM), a selective δ-opioid receptor agonist, produced a dose-related inhibition of the 25 mM K+-evoked tritium release. The maximal inhibitory effect, representing a 34% decrease in the K+-induced tritium release, was observed at a concentration of 1 μM. This opioid effect was attenuated by the selective δ-opioid receptor antagonist, ICI 174864 (1 μM). These findings support the role of a δ-opioid receptor in the modulation of ACh release in the rat globus pallidus.Key words: globus pallidus, acetylcholine, enkephalin, release.

Studies on the interaction mechanism between CXS and papain by spectroscopic and molecular modeling methods

2012 ◽  
Vol 39 (3) ◽  
pp. 1257-1267 ◽  
Author(s):  
Xiaoli Xi ◽  
Manman Yang ◽  
Tinggui Cheng ◽  
Liwei Zhang ◽  
Pin Yang
Keyword(s):  
Molecular Modeling ◽  
Interaction Mechanism ◽  
Modeling Methods

kappa-Opioid antagonist improves cellular bioenergetics and recovery after traumatic brain injury

1991 ◽  
Vol 261 (6) ◽  
pp. R1527-R1532 ◽  
Author(s):  
R. Vink ◽  
P. S. Portoghese ◽  
A. I. Faden
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Opioid Receptors ◽  
Neurological Outcome ◽  
Kappa Opioid Receptors ◽  
Kappa Opioid ◽  
Opioid Receptor Antagonist ◽  
Cellular Bioenergetics

Treatment with opioid receptor antagonists improves outcome after experimental brain trauma, although the mechanisms underlying the protective actions of these compounds remain speculative. We have proposed that endogenous opioids contribute to the pathophysiology of traumatic brain injury through actions at kappa-opioid receptors, possibly by affecting cellular bioenergetic state. In the present study, the effects of the kappa-selective opioid-receptor antagonist nor-binaltorphimine (nor-BNI) were examined after fluid percussion brain injury in rats. Metabolic changes were evaluated by 31P magnetic resonance spectroscopy; the same animals were subsequently followed over 2 wk to evaluate neurological recovery. Nor-BNI, administered intravenously as a 10 or 20 mg/kg bolus at 30 min after injury, significantly improved neurological outcome at 2 wk posttrauma compared with controls. Animals treated with nor-BNI showed significantly greater recovery of intracellular free magnesium concentrations and cytosolic phosphorylation potentials during the first 4 h after injury compared with saline-treated controls. The improvement in cytosolic phosphorylation potential was significantly correlated to neurological outcome. These data support the hypothesis that kappa-opioid receptors mediate pathophysiological changes after traumatic brain injury and that the beneficial effects of opioid-receptor antagonist may result from improvement of posttraumatic cellular bioenergetics.

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