Articles: neuralgia.
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Recently, microRNAs are reported to be participated in the development of pain and persistence of neuropathic and inflammatory pain in animal models. Here, we characterized the functional role of miR-129-5p in pain processing in chronic constriction injury (CCI) rat models. Bilateral CCI operation was used to generate neuropathic pain rat model. ⋯ Interestingly, downregulation of miR-129-5p in CCI rats was correlated with increased proinflammatory cytokine expression and pain-related behaviors. Furthermore, we found that miR-129-5p alleviated neuropathic pain through downregulating high mobility group protein B1 (HMGB1) expression in CCI rats as overexpression of miR-129-5p suppressed expression of both HMGB1 and proinflammatory cytokine and alleviated pain sensation in CCI rats. In summary, our results show that alteration in miR-129-5p expression contributes to pain processing in our CCI pain rat model, suggesting miR-129-5p could be a causal factor in neuropathic pain and serve as a promising potential biomarker and therapeutic target for neuropathic pain.
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Neuropathic pain with complex mechanisms has become a major public health problem that greatly impacts patients' quality of life. Therefore, novel and more effective strategies against neuropathic pain need further investigation. Electroacupuncture (EA) has an ameliorating effect on neuropathic pain following spared nerve injury (SNI), but the underlying mechanism remains to be fully clarified. Interferon regulatory factor 8 (IRF8), a critical transcription factor, was reported to be involved in the modulation of neuropathic pain. Here, we focused on exploring whether 2 Hz EA stimulation exerts an inhibitory action on spinal IRF8 in SNI rats. ⋯ This experiment highlighted that 2 Hz EA can inhibit IRF8 expression and microglial activation in the spinal cord of SNI rats. Hence, targeting IRF8 may be a promising therapeutic strategy for 2 Hz EA treatment of neuropathic pain.
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This updated systematic review evaluated the efficacy, tolerability and safety of opioids compared to placebo in chronic non-cancer neuropathic pain. ⋯ Some opioids (buprenorphine, morphine, oxycodone, tramadol, tapentadol) provide substantial pain relief compared to placebo in postherpetic neuralgia and peripheral neuropathies of different aetiologies for 4-12 weeks. There is insufficient evidence to support or refute the suggestion that these drugs are effective in other neuropathic pain conditions. The safety of opioids with regards to abuse and deaths in the studies analysed cannot be extrapolated to routine clinical care.
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Chemotherapy-induced peripheral neuropathy (CIPN) is a major, dose-limiting side effect of treatment with neurotoxic cancer treatments which can result in long-term impairment. Deficits often reflect a large fiber polyneuropathy, however small fiber involvement resulting in neuropathic pain and autonomic dysfunction can occur. Quantification of both CIPN and small fiber neuropathy (SFN) remains a challenge. ⋯ Accurately identifying subgroups of patients with neuropathic symptoms which may respond to existing pain medication may reduce the impact of CIPN and improve long-term quality of life as well as provide better categorization of patients for future clinical trials of neuroprotective and treatment strategies for CIPN. PERSPECTIVE: This review provides a critical analysis of SFN associated with neurotoxic cancer treatments and the assessment tools for evaluating small fiber dysfunction in cancer patients. Quantification of small fiber involvement in CIPN will assist in identifying subgroups of patients with neuropathic symptoms which may respond to existing pain medications.
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Chemotherapy-induced neuropathic pain (CINP) in both sexes compromises many current chemotherapeutics and lacks an FDA-approved therapy. We recently identified the sphingosine-1-phosphate receptor subtype 1 (S1PR1) and A3 adenosine receptor subtype (A3AR) as novel targets for therapeutic intervention. Our work in male rodents using paclitaxel, oxaliplatin, and bortezomib showed robust inhibition of CINP with either S1PR1 antagonists or A3AR agonists. ⋯ Thus, alternative mechanisms beyond receptor expression may account for sex differences in response to S1PR1 antagonists. Morphine and duloxetine, both clinical analgesics, reversed BINP in female mice, demonstrating that the lack of response is specific to S1PR1 and A3AR agents. Our findings suggest that A3AR- and S1PR1-based therapies are not viable approaches in preventing and treating BINP in females and should inform future clinical trials of these drugs as adjuncts to chemotherapy.