ArticleJournal of physiology and biochemistry2014
Serum IL-10 involved in morphine tolerance development during adjuvant-induced arthritis.
Article in Journal of physiology and biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Microglial-induced apoptosis is potentially responsible for hyperalgesia variations during CFA-induced inflammation.Inflammopharmacology · 2020Article
- An Experimental Study on Spinal Cord µ-Opioid and α2-Adrenergic Receptors mRNA Expression Following Stress-Induced Hyperalgesia in Male Rats.Iranian journal of medical sciences · 2019Article
- Targeting Cytokines for Morphine Tolerance: A Narrative Review.Current neuropharmacology · 2019Review
- Effects of Post-Weaning Chronic Stress on Nociception, Spinal Cord μ-Opioid, and α2-Adrenergic Receptors Expression in Rats and Their Offspring.Journal of molecular neuroscience : MN · 2018Article
- Long-Term Treatment by Vitamin BBasic and clinical neuroscience · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Opioid receptors play an important role in modulation of hyperalgesia in inflamed tissues, but chronic morphine application induces such side effects as tolerance. There is near communications between cytokines and mu opioid receptor expression. This study was aimed to assess the role of serum IL-10 in morphine tolerance development during adjuvant-induced arthritis. Adjuvant arthritis (AA) was induced on day 0 by single injection of Complete Freund's Adjuvant (CFA) into the rats' hindpaw. Hyperalgesia, edema, and spinal mu opioid receptor (mOR) variations were assessed on 0, 7, 14, and 21 days of the study. For assessment of the morphine tolerance development, morphine effective dose (4 mg/kg) was administered from the 14th day after CFA injection and continued until the morphine post-dose paw withdrawal latency (PWL); it did not significantly differ from the baseline. For assessment of the effects of IL-10 on tolerance induction, a neutralizing dose (ND50) of anti-IL-10 was administered daily during different stages of the study. AA induction in the right hindpaw of rats resulted in unilateral inflammation and hyperalgesia within 21 days of the study. Anti-IL-10 antibody administration in the AA rats induced marked elevation of hyperalgesia compared to the AA control group. Our data also indicated that morphine effective anti-hyperalgesic dose significantly decreased in the AA rats compared to the control group, which this symptom was aligned with spinal mu opioid receptor (mOR) expression increase during AA. Moreover, there was a significant difference in morphine tolerance induction between the AA and control rats, and our results also demonstrated that IL-10 played an important role in tolerance-induction process. It can be concluded that morphine tolerance slowly progressed when administered morphine effective dose was reduced during AA chronic inflammation. On the other hand, it seems that increased level of serum IL-10 may affect morphine tolerance development during inflammation.
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