Role of Immune Processes in Peripheral Opioid Analgesia

Herz, A.

doi:10.1007/978-1-4615-1951-5_27

Cited by 17 publications

(6 citation statements)

References 23 publications

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“…Although these treatments have proper curative effect, they also have some side effects, such as addiction, tolerance, immune suppression, and gastrointestinal reactions; furthermore some of them are not effective, leaving about 45% of cancer patients without pain control [2]. Recent findings indicate that there is a considerable curative effect related to the immune analgesia mechanism in vivo , in which immune cells synthesize and release opioid peptides [3–5], whose activities and expressions are positively correlated. Of these peptides, beta endorphin ( β -END) and its precursor (proopiomelanocortin, POMC) have been identified [6].…”

Section: Introductionmentioning

confidence: 99%

A Study on the Mechanism of Cinobufagin in the Treatment of Paw Cancer Pain by Modulating Localβ-Endorphin ExpressionIn Vivo

Chen

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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Background. Cinobufagin has been widely used in the treatment of carcinoma and plays an important role in the relief of cancer pain. But the involved mechanism remains unknown. Aim. To investigate the changes in thermal and mechanical hyperalgesia in paw cancer pain in mice and the action mechanism of cinobufagin using a paw cancer pain model. Methods. 60 female mice were randomly divided into 5 groups: control group, model group, cinobufagin group, cinobufagin +NAL-M group, and morphine group; except ones in control group, mice were inoculated with H22 hepatoma cells in the right hind paw. From the 9th day after inoculation, mice were administrated drug once daily lasting for 8 days. The pain behavior was determined on the 2nd, 4th, 6th, and 8th days before and after administration. On the last day, they were sacrificed. The levels of β-END, CRF, and IL-1β were analyzed by ELISA; immunohistochemistry was performed to detect the expressions of β-END, POMC, and μ-OR in the tumor and adjacent tissue. Results. The thresholds of thermal pain and mechanical pain were significantly increased by cinobufagin. Moreover, the expressions of β-END, CRF, POMC, and μ-OR were significantly upregulated by cinobufagin. The analgesic effect of cinobufagin was blocked by the peripheral opioid receptor antagonist NAL-M. Conclusions. Cinobufagin significantly relieved cancer pain in mice and raised their pain threshold, mainly upregulating the expression levels of β-END and μ-OR in the hind paw tumor and adjacent tissue.

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Section: Introductionmentioning

confidence: 99%

A Study on the Mechanism of Cinobufagin in the Treatment of Paw Cancer Pain by Modulating Localβ-Endorphin ExpressionIn Vivo

Chen

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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“…Most data were collected during experiments on the elicited paw inflammation in rats and mice (14-19). However, only a few investigations were performed on experimental pulmonary inflammation.…”

Section: Discussionmentioning

confidence: 99%

Effects of Opiate Dependence Through Different Administration Routes on Pulmonary Inflammation and its Severity

Masoomi¹,

Tajoddini²,

Mohammadi³

et al. 2013

Iran Red Crescent Med J

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BackgroundSerious health problems and socioeconomic consequences of the illicit use of opiates have been proved in both developed and developing societiesObjectivesWe aimed to evaluate" The effects of opiate addiction through different administration routes on pulmonary inflammation and its severity."Materials and MethodsOur experiments were performed on eighteen adult male Syrian golden hamsters which were allocated to one of the three groups (n = 6): control group which did not receive opiate; the first study group were administered oral opiate via stomach tube; and another study group were administered inhaled opiate. After four weeks, all hamsters were anesthetized with diethyl ether and their lung tissues were isolated for pathological assessment.ResultsSevere perivascular inflammation was detected in 33.3% of the samples with oral opiate dependence and 20% of the cases addicted to opiate through inhalation. Also, severe peribronchial inflammation was observed in only 20% of the samples addicted to inhaled opiate and was not found in the other groups. No significant differences were found in the severity of perivascular and peribronchial inflammation across the three groups. Although the mean of total inflammation scale in the subjects with oral opiate dependence (3.00 ± 1.79) was numerically higher than that in the inhaled dependence group (1.40 ± 2.60) and the controls (2.25 ± 1.26), this difference was not statistically significant.ConclusionsAdministration did not influence the appearance or severity of pulmonary inflammation in animal models addicted to opiate.

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“…Little is known regarding the this route of administration. This is in agreement with sensory pathways within the central nervous system or the previous studies demonstrating that i.t., s.c. or local chemical mediators that are responsible for the nociceptive administration of morphine into the paw does not sig-nificantly affect baseline mechanical nociceptive thresholds enkephalins, in the spinal dorsal horn, that could then act [21,28], whereas others have demonstrated the morphinesynergistically with exogenously administered morphine to induced anti-allodynia in inflammation pain models. Thus, produce the enhanced effectiveness seen in this study.…”

Section: Discussionmentioning

confidence: 99%

“…It local administration of mu opioid agonists in the rat paw has been well established that antinociceptive synergy inhibited prostaglandin E -induced hyperalgesia [29], and occurs following combined mu and delta opioid receptor 2 s.c. morphine elicited dose-dependent naloxone-reversible activation [45]. antinociception in the paw of monoarthritic rats [21].…”

Section: Discussionmentioning

confidence: 99%

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Enhanced thermal antinociceptive potency and anti-allodynic effects of morphine following spinal administration of endotoxin

2003

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Recently, an animal model of central inflammation characterized by widespread cutaneous hyperalgesia and allodynia following intracerebroventricular (i.c.v.) administration of lipopolysaccharide (LPS) was described. In the present study, we demonstrate that central administration of LPS via intrathecal (i.t.) injection produces bilateral tactile allodynia and thermal hyperalgesia in the rat. Also, the effects of morphine-induced antinociception were determined in this model. Here we demonstrate enhanced thermal antinociceptive potency of i.t. morphine in LPS-treated rats compared to controls. Intrathecal morphine was also effective in alleviating the tactile allodynia induced by LPS. Both the antinociceptive and anti-allodynic effects produced by i.t. morphine were completely antagonized by 21 pretreatment with subcutaneous naloxone (1 mg kg ). This study demonstrates the presence of both heat hyperalgesia and mechanical allodynia following central administration of LPS, and an increased antinociceptive potency of i.t. morphine in this model. 

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Role of Immune Processes in Peripheral Opioid Analgesia

Cited by 17 publications

References 23 publications

A Study on the Mechanism of Cinobufagin in the Treatment of Paw Cancer Pain by Modulating Localβ-Endorphin ExpressionIn Vivo

A Study on the Mechanism of Cinobufagin in the Treatment of Paw Cancer Pain by Modulating Localβ-Endorphin ExpressionIn Vivo

Effects of Opiate Dependence Through Different Administration Routes on Pulmonary Inflammation and its Severity

Enhanced thermal antinociceptive potency and anti-allodynic effects of morphine following spinal administration of endotoxin

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