Serum IL-10 involved in morphine tolerance development during adjuvant-induced arthritis

Zaringhalam, Jalal; Hormozi, A J Kalantar; Tekieh, Elaheh; Razavi, Jafar; Khanmohammad, Ramin; Golabi, Sahar

doi:10.1007/s13105-014-0330-7

Cited by 14 publications

(9 citation statements)

References 20 publications

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“…Inflammation was induced on the day 0 by a single sub-cutaneous injection of 100 μL CFA into the right hindpaw (Zaringhalam et al, 2014). This animal model indicates a rapid primary inflammation response to the adjuvant (Santora, Rasa, Visco, Steinetz, & Bagnell, 2007).…”

Section: Methodsmentioning

confidence: 99%

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Long-Term Treatment by Vitamin B1 and Reduction of Serum Proinflammatory Cytokines, Hyperalgesia, and Paw Edema in Adjuvant-Induced Arthritis

Zaringhalam¹,

Akbari²,

Zali³

et al. 2016

BCN

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Introduction:Immune system is involved in the etiology and pathophysiology of inflammation and vitamins are important sources of substances inducing nonspecific immunomodulatory effects. Given the proinflammatory role of cytokines in the inflammation and pain induction, this study aimed to assess the effects of long-term administration of vitamin B1 on the proinflammatory cytokines, edema, and hyperalgesia during the acute and chronic phases of adjuvant-induced arthritis.Methods:On the first day of study, inflammation was induced by intraplantar injection of complete Freund's adjuvant (CFA) in the hindpaws of rats. Vitamin B1 at doses of 100, 150, and 200 mg/kg was administrated intraperitoneally during 21 days of the study. Antinociceptive and anti-inflammatory effects of vitamin B1 were also compared to indomethacin (5 mg/kg). Inflammatory symptoms such as thermal hyperalgesia and paw edema were measured by radiant heat and plethysmometer, respectively. Serum TNF-α and IL-1β levels were checked by rat standard enzyme-linked immune sorbent assay (ELISA) specific kits.Results:The results indicated that vitamin B1(150 and 200 mg/kg) attenuated the paw edema, thermal hyperalgesia, and serum levels of TNF-α and IL-1β during both phases of CFA-induced inflammation in a dose-dependent manner. Effective dose of vitamin B1(150 mg/kg) reduced inflammatory symptoms and serum levels of TNF-α and IL-1β compare to indomethacin during the chronic phase of inflammation.Conclusion:Anti-inflammatory and antihyperalgesic effects of vitamin B1 during CFA-induced arthritis, more specifically after chronic vitamin B1 administration, suggest its therapeutic property for inflammation.

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Section: Methodsmentioning

confidence: 99%

“…The edema was quantified by measuring the paw volume differences between the day zero and other time points of the study. The paw volumes were shown as the percentage of the day zero (Zaringhalam et al, 2014). …”

Section: Methodsmentioning

confidence: 99%

Long-Term Treatment by Vitamin B1 and Reduction of Serum Proinflammatory Cytokines, Hyperalgesia, and Paw Edema in Adjuvant-Induced Arthritis

Zaringhalam¹,

Akbari²,

Zali³

et al. 2016

BCN

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“…Finally, the blots were visualized with a chemiluminescence detection system (ECL, Amersham, RPN2235). Band intensity was measured densitometrically using Image J and expressed as the ratio of the intensity of the BDNF, pro-BDNF, Iba1, and Caspase-3 band to β-actin [36].…”

Section: Western Blotmentioning

confidence: 99%

Nootropic dipeptide, Noopept can modulate hyperalgesia by effecting on spinal microglia dependent Brain Derived Neurotropic Factor (BDNF) and pro-BDNF expression and apoptosis during persistent inflammation

Taghizadeh

Maghsoudi

Manaheji

et al. 2020

Preprint

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Background: There are largely unknown associations between changes in pain behavior responses during persistent peripheral inflammation and spinal cell alteration such as apoptosis. Some evidence suggests that microglia and microglia related mediators play notable roles in induction and maintenance of central nervous system pathologies and inflammatory pain. By considering those relationships and microglia related nootrophic factors, such as the Brain Derived Neurotrophic Factor (BDNF) in CNS, we attempted to assess the relationship between microglia dependent BDNF and its precursor with pain behavior through spinal cell apoptosis as well as the effect of Noopept on this relationship. Methods: Persistent peripheral inflammation was induced by a single subcutaneous injection of Complete Freund’s Adjuvant (CFA) on day 0. Thermal hyperalgesia, paw edema, microglial activity, microglia dependent BDNF, pro-BDNF expression, and apoptosis were assessed in different experimental groups by confirmed behavioral and molecular methods on days 0, 7, and 21 of the study. Results: Our findings revealed hyperalgesia and spinal cell apoptosis significantly increased during the acute phase of CFA-induced inflammation but was then followed by a decrement in the chronic phase of the study. Aligned with these variations in spinal microglial activity, microglia dependent BDNF significantly increased during the acute phase of CFA-induced inflammation. Our results also indicated that daily administration of Noopept (during 21 days of the study) not only caused a significant decrease in hyperalgesia and microglia dependent BDNF expression but also changed the apoptosis process in relation to microglia activity alteration. Conclusions: It appears that the administration of Noopept can decrease spinal cell apoptosis and hyperalgesia during CFA-induced inflammation due to its direct effects on microglial activity and microglia dependent BDNF and pro-BDNF expression.

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“…As a potent immune-regulatory cytokine, IL-10 exhibits critical impact on modulating inflammation and directing adaptive immune response [98]. Spinal MOR, which has been proved to be involved in the development of morphine tolerance, is related to the regulation of serum anti-inflammatory cytokine IL-10 in adjuvant arthritis (AA) morphine-tolerant rats [99]. The expressions of spinal MOR and serum IL-10 were both increased in AA morphine-tolerant rats.…”

Section: Anti-inflammatory Cytokines and Morphine Tolerancementioning

confidence: 99%

“…The development of morphine tolerance in AA rats occurred markedly later than control group. Additionally, daily administration of anti-IL-10 antibody could significantly enhance the thermal hyperalgesia, decrease the spinal MOR expression and accelerate the development of morphine tolerance in AA rats [99]. These results suggested that the up-regulation of serum IL-10 might inhibit the development of morphine tolerance via modulating spinal MOR expression in AA rats.…”

Section: Anti-inflammatory Cytokines and Morphine Tolerancementioning

confidence: 99%

Targeting Cytokines for Morphine Tolerance: A Narrative Review

Liu

Zhou

Gao

2019

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Serum IL-10 involved in morphine tolerance development during adjuvant-induced arthritis

Cited by 14 publications

References 20 publications

Long-Term Treatment by Vitamin B1 and Reduction of Serum Proinflammatory Cytokines, Hyperalgesia, and Paw Edema in Adjuvant-Induced Arthritis

Long-Term Treatment by Vitamin B1 and Reduction of Serum Proinflammatory Cytokines, Hyperalgesia, and Paw Edema in Adjuvant-Induced Arthritis

Nootropic dipeptide, Noopept can modulate hyperalgesia by effecting on spinal microglia dependent Brain Derived Neurotropic Factor (BDNF) and pro-BDNF expression and apoptosis during persistent inflammation

Targeting Cytokines for Morphine Tolerance: A Narrative Review

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