scholarly journals The Expression Pattern of Genes Related to Melanogenesis and Endogenous Opioids in Psoriasis

2021 ◽  
Vol 22 (23) ◽  
pp. 13056
Author(s):  
Ulvi Loite ◽  
Liisi Raam ◽  
Ene Reimann ◽  
Paula Reemann ◽  
Ele Prans ◽  
...  
Keyword(s):  
Stress Responses ◽  
Endogenous Opioids ◽  
Psoriatic Skin ◽  
Quantitative Real Time Pcr ◽  
Melanocortin System ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Cutaneous Inflammation ◽  
Lesional Skin ◽  
Healthy Control

The melanocortin system is a major regulator of stress responses in the skin and is responsible for the induction of melanin synthesis through activation of melanogenesis enzymes. The expression of both melanocortin system genes and melanogenesis enzyme genes is altered in psoriasis, and the focus here was on twelve genes related to the signal transduction between them. Additionally, five endogenous opioid system genes that are involved in cutaneous inflammation were examined. Quantitative real-time-PCR was utilized to measure mRNA expression in punch biopsies from lesional and non-lesional skin of psoriasis patients and from the skin of healthy control subjects. Most of the genes related to melanogenesis were down-regulated in patients (CREB1, MITF, LEF1, USF1, MAPK14, ICAM1, PIK3CB, RPS6KB1, KIT, and ATRN). Conversely, an up-regulation occurred in the case of opioids (PENK, PDYN, and PNOC). The suppression of genes related to melanogenesis is in agreement with the reported reduction in pigmentation signaling in psoriatic skin and potentially results from the pro-inflammatory environment. The increase in endogenous opioids can be associated with their involvement in inflammatory dysregulation in psoriasis.

scholarly journals  The role of beta-endorphin in horses: a review

2011 ◽  
Vol 56 (No. 9) ◽  
pp. 423-429 ◽  
Author(s):  
M. Golynski ◽  
W. Krumrych ◽  
K. Lutnicki
Keyword(s):  
Pain Threshold ◽  
Social Activity ◽  
Prognostic Indicator ◽  
Endogenous Opioids ◽  
Oxygen Species ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Beta Endorphin ◽  
Opium Alkaloids

  Opium alkaloids counterparts are secreted by human and animal organisms but the role of endogenous opioid peptides in horses has not yet been fully elucidated. Endogenous opioids are involved in regulating food intake, sexual and social activity, pain relief and pain threshold regulation in horses as well as in regulating the functions of the immune system. The aim of this review is to describe the endogenous opioid system in the horse and its function during stress, illness, reproduction, and its influence on immunity and on the formation of reactive oxygen species (ROS) in horses. What is currently known concerning beta-endorphin suggests that they can be a promising diagnostic or prognostic indicator of many pathologic states in horses.

Opioids in Remote Ischemic Preconditioning-Induced Cardioprotection

2016 ◽  
Vol 22 (2) ◽  
pp. 112-121 ◽  
Author(s):  
Puneet Kaur Randhawa ◽  
Amteshwar Singh Jaggi
Keyword(s):  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Endogenous Opioids ◽  
Remote Ischemic Preconditioning ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Cardioprotective Effects

Remote ischemic preconditioning (RIPC) is an intriguing process whereby transient regional ischemia and reperfusion episodes to remote tissues including skeletal, renal, mesenteric provide protection to the heart against sustained ischemia–reperfusion-induced injury. Clinically, this technique has been used in patients undergoing various surgical interventions including coronary artery bypass graft surgery, abdominal aortic aneurysm repair, percutaneous coronary intervention, and heart valve surgery. The endogenous opioid system is extensively expressed in the brain to modulate pain sensation. Besides the role of opioids in relieving pain, numerous researchers have found their critical involvement in evoking cardioprotective effects. Endogenous opioids including endorphins, enkephalins, and dynorphins are released during RIPC and are critically involved in mediating RIPC-induced cardioprotective effects. It has been suggested that during RIPC, the endogenous opioids may be released into the systemic circulation and may travel via bloodstream that act on the myocardial opioid receptors to induce cardioprotection. The present review describes the potential role of opioids in mediating RIPC-induced cardioprotection.

scholarly journals The aetiology of social deficits within mental health disorders: The role of the immune system and endogenous opioids

2019 ◽  
Author(s):  
Sarah Jane Charles ◽  
Miguel Farias ◽  
R. I. M. Dunbar
Keyword(s):  
Mental Health ◽  
Immune System ◽  
Mental Health Disorders ◽  
Social Bonding ◽  
Endogenous Opioids ◽  
Future Research ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Health Disorders

The American National Institute for Mental Health (NIMH) has put out a set of research goals that include a long-term plan to identify more reliable endogenous explanations for a wide variety of mental health disorders (Insel, 2013). In response to this, we have identified a major symptom that underlies multiple mental health disorders – social bonding dysfunction. We suggest that endogenous opioid abnormalities can lead to altered social bonding, which is a symptom of various mental health disorders, including depression, schizophrenia and ASD. This article first outlines how endogenous opioids play a role in social bonding. Then we show their association with the body’s inflammation immune function, and review recent literature linking inflammation to mental health ‘immunophenotypes’. We finish by explaining how these immunophenotypes may be caused by alterations in the endogenous opioid system. This is the first overview of the role of inflammation across multiple disorders where we provide a biochemical explanation for why immunophenotypes might exist across diagnoses. We propose a novel mechanism of how the immune system may be causing ‘sickness-type’ behaviours (fatigue, appetite change, social withdrawal and inhibited motivation) in those who have these immunophenotypes. We hope that this novel aetiology can be used as a basis for future research in mental health.

Effects of naloxone on the sensation of dyspnea during acute respiratory stress in normal adults

1993 ◽  
Vol 74 (2) ◽  
pp. 590-595 ◽  
Author(s):  
Y. Akiyama ◽  
M. Nishimura ◽  
S. Kobayashi ◽  
A. Yoshioka ◽  
M. Yamamoto ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Endogenous Opioids ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Specific Effects ◽  
Mouth Pressure ◽  
End Tidal ◽  
Visual Analogue Scaling ◽  
The Brain ◽  
Normal Adults

To clarify whether endogenous opioids modulate the dyspnea intensity and, if so, by what mechanism they act on it, we examined 12 healthy male volunteers aged 19–27 yr for ventilatory and peak mouth pressure (Pm) responses to hypoxic progressive hypercapnia with inspiratory flow-resistive loading after the intravenous infusion of 3 mg of naloxone or saline. The intensity of dyspnea was simultaneously assessed by visual analogue scaling every 15 s. Naloxone administration increased both ventilatory and Pm responses to hypoxic progressive hypercapnia (P < 0.05 for both). The increase in dyspnea intensity for a given increase in end-tidal PCO2 was significantly greater after naloxone infusion than after saline (P < 0.05). However, there were no differences in the increase in dyspnea intensity for a given increase in minute ventilation or Pm. These results suggest that the endogenous opioid system suppresses the respiratory output under a strong, acute respiratory stress in normal adults and that this system may relieve the dyspnea sensation secondary to the suppression of the brain stem respiratory center without specific effects on the processing of respiratory sensations in the higher brain.

Stress activates pronociceptive endogenous opioid signalling in DRG neurons during chronic colitis

Gut ◽  
2016 ◽  
Vol 66 (12) ◽  
pp. 2121-2131 ◽  
Author(s):  
Raquel Guerrero-Alba ◽  
Eduardo E Valdez-Morales ◽  
Nestor N Jimenez-Vargas ◽  
Cintya Lopez-Lopez ◽  
Josue Jaramillo-Polanco ◽  
...  
Keyword(s):  
G Protein ◽  
Imaging Techniques ◽  
Stress Hormones ◽  
Endogenous Opioids ◽  
Opioid Use ◽  
Chronic Colitis ◽  
Drg Neurons ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Stress Changes

Aims and backgroundPsychological stress accompanies chronic inflammatory diseases such as IBD, and stress hormones can exacerbate pain signalling. In contrast, the endogenous opioid system has an important analgesic action during chronic inflammation. This study examined the interaction of these pathways.MethodsMouse nociceptive dorsal root ganglia (DRG) neurons were incubated with supernatants from segments of inflamed colon collected from patients with chronic UC and mice with dextran sodium sulfate (cDSS)-induced chronic colitis. Stress effects were studied by adding stress hormones (epinephrine and corticosterone) to dissociated neurons or by exposing cDSS mice to water avoidance stress. Changes in excitability of colonic DRG nociceptors were measured using patch clamp and Ca2+imaging techniques.ResultsSupernatants from patients with chronic UC and from colons of mice with chronic colitis caused a naloxone-sensitive inhibition of neuronal excitability and capsaicin-evoked Ca2+responses. Stress hormones decreased signalling induced by human and mouse supernatants. This effect resulted from stress hormones signalling directly to DRG neurons and indirectly through signalling to the immune system, leading to decreased opioid levels and increased acute inflammation. The net effect of stress was a change endogenous opioid signalling in DRG neurons from an inhibitory to an excitatory effect. This switch was associated with a change in G protein-coupled receptor excitatory signalling to a pathway sensitive to inhibitors of protein kinase A-protein, phospholipase C-protein and G protein βϒ subunits.ConclusionsStress hormones block the inhibitory actions of endogenous opioids and can change the effect of opioid signalling in DRG neurons to excitation. Targeting these pathways may prevent heavy opioid use in IBD.

scholarly journals ENDOGENOUS OPIOID SYSTEM AS A MEDIATOR OF ACUTE AND LONG-TERM ADAPTATION TO STRESS. PROSPECTS FOR CLINICAL USE OF OPIOID PEPTIDES

2012 ◽  
Vol 67 (6) ◽  
pp. 73-82 ◽  
Author(s):  
Yu. B. Lishmanov ◽  
L. N. Maslov ◽  
N. Yu. Naryzhnaya ◽  
J.-M. Pei ◽  
F. Kolar ◽  
...  
Keyword(s):  
Opioid Peptides ◽  
Ischemia Reperfusion ◽  
Antiarrhythmic Effect ◽  
Endogenous Opioids ◽  
Protective Effects ◽  
Adaptive Responses ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Future Clinical Practice ◽  
Thromboxane Production

It has been well established that opioid peptides (OPs) affect various hormonal systems. Opioids exhibit stress-limiting and gastro-protective effects in stressed animals, acting via μ- and δ-opioid receptors (OR). Peripheral μ-OR stimulation by endogenous and exogenous opioids increases cardiac tolerance to pathological consequences of stress. Enhancement of prostacyclin synthesis, decrease of thromboxane production as well as suppression of lipid peroxidation can be directly responsible for cardioprotective effects of OPs in stressed animals. Adaptive responses are accompanied by increased OP levels in blood and tissues. Reduction of ventricular arrhythmias induced by repeated short-term immobilization stress is mediated via μ-OR stimulation by endogenous opioids, while δ-OR account for an antiarrhythmic effect of adaptation to chronic intermittent hypobaric hypoxia. The mechanism of infarct size-limiting effect of continuous normobaric hypoxia involves both μ- and δ-OR stimulation. Peptide OR agonists can be considered in future clinical practice for treatment of withdrawal syndrome, stress-related cardiac disease or myocardial injury caused by ischemia-reperfusion insult. 

Influence of endogenous opioids on the response of selected hormones to exercise in humans

1986 ◽  
Vol 61 (3) ◽  
pp. 1051-1057 ◽  
Author(s):  
P. A. Farrell ◽  
A. B. Gustafson ◽  
T. L. Garthwaite ◽  
R. K. Kalkhoff ◽  
A. W. Cowley ◽  
...  
Keyword(s):  
Venous Blood ◽  
Endogenous Opioids ◽  
Psychological State ◽  
Opioid Antagonist ◽  
Plasma Norepinephrine ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Naltrexone Treatment ◽  
The Difference ◽  
Exercise Induced

To examine the influence of endogenous opioids on the hormonal response to isotonic exercise, eight males were studied 2 h after oral administration of placebo or 50 mg naltrexone, a long-lasting opioid antagonist. Venous blood samples were obtained before, during, and after 30 min of bicycle exercise at 70% VO2max. Naltrexone had no effect on resting cardiovascular, endocrine, or serum variables. During exercise epinephrine was higher [mean 433 +/- 100 (SE) pg/ml] at 30 min with naltrexone than during placebo (207 +/- 26 pg/ml, P less than 0.05). Plasma norepinephrine showed the same trend but the difference (2,012 +/- 340 pg/ml with naltrexone and 1,562 +/- 241 pg/ml with placebo) was not significant. Plasma glucose was higher at all times with naltrexone. However, the difference was significant only 10 min into recovery from exercise (104.7 +/- 4.7 vs. 94.5 +/- 2.8 mg/dl). Plasma growth hormone and cortisol increased during recovery and these elevations were significantly (P less than 0.05) augmented by naltrexone. Plasma vasopressin and prolactin increased with exercise as did heart rate, blood pressure, lactic acid, and several serum components; these increases were not affected by naltrexone. Psychological tension or anxiety was lower after exercise compared with before and this improved psychological state was not influenced by the naltrexone treatment. These data suggest that exercise-induced activation of the endogenous opioid system may serve to regulate the secretion of several important hormones (i.e., epinephrine) during and after exercise.

Naloxone: lack of effect of a very low dose on fluid intake and activity in rats

1991 ◽  
Vol 8 (2) ◽  
pp. 100-108
Author(s):  
Robert Bell ◽  
Sheree Davis
Keyword(s):  
Locomotor Activity ◽  
Open Field ◽  
Water Intake ◽  
Low Dose ◽  
Fluid Intake ◽  
Endogenous Opioids ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Opiate Antagonists ◽  
Reduced Water

AbstractOpiate antagonists, such as naloxone, have been employed to indicate the possible involvement of endogenous opioids in a variety of behaviours including the pathogenesis of schizophrenia. This paper describes two experiments which were performed to determine the effects of naloxone on fluid intake and activity in rats. In experiment 1, the administration of 1mg/kg naloxone significantly (p<0.001) reduced water intake. 10mg/kg naloxone considerably reduced water intake, although this result was not significant. This influence was transient, since water intake was restored to control levels at the end of the 4 hours test period, and not dose related. A low dose of naloxone 0.01mg/kg produced no effect. In experiment 2, doses of 1 and 10mg/kg did not influence locomotor activity, rearing or grooming in the open field. These results suggest that naloxone may exert a primary antidipsogenic action that does not depend upon any suppression of concomitant activity. Furthermore, mechanisms controlling water intake and activity appear to be dissociated. A speculative role for the endogenous opioid system is discussed.

scholarly journals Endogenous Opioids at the Intersection of Opioid Addiction, Pain, and Depression: The Search for a Precision Medicine Approach

2020 ◽  
Vol 43 (1) ◽  
pp. 355-374
Author(s):  
Michael A. Emery ◽  
Huda Akil
Keyword(s):  
Individual Differences ◽  
Mood Disorders ◽  
Sensation Seeking ◽  
The United States ◽  
Opioid Addiction ◽  
Endogenous Opioids ◽  
Opioid Abuse ◽  
Opioid System ◽  
Endogenous Opioid System ◽  
Endogenous Opioid

Opioid addiction and overdose are at record levels in the United States. This is driven, in part, by their widespread prescription for the treatment of pain, which also increased opportunity for diversion by sensation-seeking users. Despite considerable research on the neurobiology of addiction, treatment options for opioid abuse remain limited. Mood disorders, particularly depression, are often comorbid with both pain disorders and opioid abuse. The endogenous opioid system, a complex neuromodulatory system, sits at the neurobiological convergence point of these three comorbid disease states. We review evidence for dysregulation of the endogenous opioid system as a mechanism for the development of opioid addiction and/or mood disorder. Specifically, individual differences in opioid system function may underlie differences in vulnerability to opioid addiction and mood disorders. We also review novel research, which promises to provide more detailed understanding of individual differences in endogenous opioid neurobiology and its contribution to opioid addiction susceptibility.

Impact of Intravenous, Perioperative-Administrated Lidocaine on Postoperative Serum Levels of Endogenous Opioids in Children

2019 ◽  
Vol 25 (30) ◽  
pp. 3209-3215 ◽  
Author(s):  
Barbara Kościelniak-Merak ◽  
Ilona Batko ◽  
Krzysztof Kobylarz ◽  
Krystyna Sztefko ◽  
Magdalena Kocot-Kępska ◽  
...  
Keyword(s):  
Pain Intensity ◽  
Elevated Serum ◽  
Serum Levels ◽  
Pain Scale ◽  
Endogenous Opioids ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Postoperative Serum ◽  
Group A ◽  
Group B

Background: Endogenous opioids are neuropeptides involved in pain-relieving processes. In the periphery, they are synthesised and stored in cells of the immune system. Objective: In the current study, we describe the influence of perioperative, intravenous (i.v.) lidocaine infusion in children on postoperative, serum endogenous opioid concentrations in children. Methods: Forty-four children undergoing major spinal surgery were enrolled in the cohort study. They were divided into two groups: group A (n = 21) generally anesthetised with fentanyl, propofol, rocuronium, a mixture of oxygen/air/sevoflurane and with analgetics and co-analgetics: morphine, acetaminophen, metamizole, gabapentin, dexamethason and group B (n = 23) where, in addition to the above-described general anesthesia, patients were given i.v. lidocaine as a co-analgesic. We also recruited 20 healthy age- and gender-matched children (group C). We measured endogenous opioid levels in serum using immunoenzymatic methods. We evaluated postoperative pain intensity using a numerical or visual pain scale and demand for morphine. Results: The levels of measured endogenous opioids were similar in the control and in the studied groups before surgery. We noted that group B patients had lower pain intensity when compared to group A subjects. In group B, the elevated serum concentrations of β -endorphin, enkephalin and dynorphin in the postoperative period were reported. We also observed that the levels of endogenous opioids negatively correlated with morphine requirements and positively correlated with lidocaine concentration. Conclusion: Multidrug pain management including lidocaine seems to be more efficient than models without lidocaine. The endogenous opioid system should be considered as a novel target for pain relief therapy in children.

Sign in / Sign up

Export Citation Format

Share Document