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1

The involvement of NOS inhibitors in effects of morphine and endomorphine-1 in neuropathic pain

100%
Makuch W., Sieja A., Przewlocka B.
Acta Neurobiologiae Experimentalis
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2005
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tom 65
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nr 3
2

Novel pharmacotherapy of osteoarthritis: TRPV1 and CB1 receptors as targets for pharmacological intervention

88%
Starowicz K., Malek N., Makuch W., Kolosowska N., Przewlocka B.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr Suppl.1
Osteoarthritis (OA) is the most common degenerative joint disease, which leads to pain during joint loading and to chronic physical disability. The management of OA is often frustrating for both patients and physicians as adequate pain relief is difficult to achieve and no treatment modality seems to reverse the disease progression. Clearly, OA is a large, unmet medical need, there is a strong need to develop new treatments for OA. Considerable evidence has uncovered new mechanisms underlying the generation and transduction of pain, many of which represent new targets for pharmacological intervention. The endogenous agonist of cannabinoid receptor 1 (CB1), anandamide (AEA), also stimulates transient receptor potential vanilloid channel-1 (TRPV1) channels, which instead plays a key role in the induction of inflammation and the development of pain associated with OA. AEA degradation by fatty acid amides hydrolase (FAAH) limits its activity. Inhibiting FAAH, and TRPV1 with the same molecule might produce more efficacious anti-hyperalgesic actions than the targeting of FAAH or TRPV1 alone. An update of the relationship CB1 and TRPV1 channels and their possible implications for OA pain will also be provided. Bases for the possible future development of new therapeutic approaches that might be used for the treatment of pain will be suggested.
3

The involvement of giycogen synthase and cyclin dependent kinases in morphine analgesia in rats

76%
Obara I., Wawrzczak-Bargiela A., Rodriguez Parkitna J. M., Makuch W., Przewlocki R., Przewlocka B.
Acta Neurobiologiae Experimentalis
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2005
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tom 65
|
nr 3
4

Expression of opioid genes in neuropathie and inflammatory pain

76%
Korostynski M., Kaminska D., Rodriguez Parkitna J. M., Obara I., Makuch W., Przewlocka B., Przewlocki R.
Acta Neurobiologiae Experimentalis
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2005
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tom 65
|
nr 3
5

Minocycline affects neuropathic pain by regulation of kynurenic pathway – role of microglial cells

76%
Rojewska E., Piotrowska A., Jurga A. M., Makuch W., Przewlocka B., Mika J.
Acta Neurobiologiae Experimentalis
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2017
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tom 77
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nr Suppl.1
The participation of kynurenine system in the pathology of neurodegenerative and autoimmune diseases was studied, but the significance of this pathway in neuropathic pain have been poorly studied. The kynurenine pathway has already been shown to exist mainly in macrophages and microglia. Growing evidence suggests that spinal microglia are crucial in the neuropathic pain. Minocycline, a microglial inhibitor, is a substances with diverse mechanisms of action that modulate the neuroimmune system have been shown to relieve neuropathic pain. The aim of our study was to examine the role of kynurenine 3-monooxygenase (Kmo) in a rat model of neuropathy. Chronic constriction injury (CCI) of the sciatic nerve was performed according to Bennett and Xie (1988). Behavioral studies consisted of the tactile and thermal hypersensitivity measurements, biochemical studies comprised the RT-PCR and/or Western blot analysis in the tissue (spinal cord, DRG) and primary glia cultures. The experiments were carried out according to IASP rules. Using microarray and qRT-PCR methods, we showed that intraperitoneal administration of minocycline decreased neuropathic pain in rats and in parallel the spinal 3-monooxygenase kynurenine expression (Kmo). Further, minocycline administration diminished the lipopolysaccharide (LPS)-induced upregulation of Kmo mRNA in primary microglial cell cultures. Moreover, we verified that not only indirect inhibition of Kmo using minocycline but also direct inhibition using Kmo inhibitors (JM6,Ro61-6048) decreased neuropathic pain intensity. Ro61-6048 administration reduced in the spinal cord and/or the DRG the protein levels of IBA-1, IL-6, IL-1beta and NOS2. Interestingly, Kmo inhibitors potentiated the analgesic properties of morphine. Summing up, our results suggest that the kynurenine pathway is an important mediator of neuropathic pain pathology. FINANCIAL SUPPORT: Supported by National Science Centre grant-Sonata 2015/17/D/NZ4/02284 and statutory funds. AP is a scholarship holder from the KNOW sponsored by Ministry of Science and Higher Education, Republic of Poland.
6

Regulation on spinal nociceptive TRPV1/CB1 processing as therapeutic opportunities in a rat model of neuropathic pain

64%
Starowicz K., Zychowska M., Mrugala M., Makuch W., Korostynski M., Slezak M., Petrosino S., Di Marzo V., Przewlocka B.
Acta Neurobiologiae Experimentalis
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2011
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tom 71
|
nr S
Anandamide (AEA) has emerged as a multifunctional lipid mediator of various stimuli. Latest reports suggest a role for AEA as an endovanilloid ligand, however, no data exist on the potential role of endogenous AEA upregulation in the spinal cord in neuropathic pain model. Rats chronically implanted with intrathecal (i.t.) catheters underwent sciatic nerve ligation (CCI model). The effect of selective inhibitor of AEA enzymatic hydrolysis, URB597 and the involvement of TRPV1 or cannabinoid CB1 receptors, were investigated. Measurements of allodynia and hyperalgesia were made 7 days after CCI and the levels of AEA in the spinal cord of CCI rats were determined. The spinal endovanilloid/endocannabinoid system was studied by means of qRT-PCR and western blott analysis in CCI rats. Finally, the distribution of TRPV1 and endovanilloid degradation enzymes were compared in the rat lumbar spinal cord. Depending on the administered dose, URB597 (10 – 200 μg/rat) reduced pain via CB1 or TRPV1 receptors. URB597 (10 – 100 μg) dose-dependently enhanced spinal AEA levels. Surprisingly those were reduced by 200 μg of URB597 suggesting an indirect effect of an endovanilloid/endocannabinoid AEA action at TRPV1. Alterations in lypoxygenases (LOX) mRNA support the idea of alternative ways of AEA metabolism. LOX-mediated production of hydroperoxides was associated with increased phospholipase A2 acitvity. Finally, baicalein by blocking the 12-LOX activity reduced the URB597 (200 μg) analgesic effect in CCI rats. We suggest that i.t. AEA reduces neuropathic pain by acting as an endovanilloid, on the he spinal cord TRPV1/ CB1 neurons. When endogenously up-regulated with URB597, AEA exerts analgesia via both receptors. Dependent on efficiency of FAAH a secondary route of AEA metabolism plays a role in CCI model. Moreover spinal lipoxygenase metabolites contribute to the AEA-mediated nociception in CCI model suggesting a complex interplay these systems in vivo. Supported by 0152/B/2008/35.
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