Suppression of interleukin-6 by minocycline in a rat model of neuropathic pain

Minocycline modulates neuropathic pain behaviour and cortical M1–M2 microglial gene expression in a rat model of depression

“…In comparison, microglial activation has been reported as essential for the development of neuropathic pain behaviour, while astrocytes are responsible for the maintenance of this chronic pain state . Acute pre-treatment with minocycline prevented the development of SNL-induced mechanical allodynia in sham rats, correlating with previous data in several nerve-injury models (Zanjani et al, 2006, Raghavendra et al, 2003, Pu et al, 2013, an effect also observed in OB rats.…”

“…Systemic administration of minocycline has been shown to prevent the development of nerve-injury induced allodynia when administered prior to injury (Raghavendra et al, 2003, Zanjani et al, 2006, without affecting basal nociceptive responding (Mika et al, 2009, Padi andKulkarni, 2008) or locomotor activity (Zhang et al, 2007 Water bottles were weighed daily to determine fluid intake. Fresh drug stock was prepared and replaced every 3-4 days based on data indicating minimal degradation of minocycline in solution at room temperature over 7 days (Pearson and Trissel, 1993).…”

“…Furthermore, minocycline has been shown to be beneficial in pain states such as rheumatoid arthritis (Langevitz et al, 2000) and sciatica (Sumracki et al, 2012). Both systemic and central administration of minocycline has been shown to prevent microglial activation and release of pro-inflammatory cytokines/mediators, and consequently the development of nerve injury-induced allodynia in several models (Raghavendra et al, 2003, Zanjani et al, 2006, Guasti et al, 2009, Pu et al, 2013, LeBlanc et al, 2011, Wei et al, 2008.…”

Neural - Glial Interaction in Neuropathic Pain

“…IL-6 is an important cytokine for transitioning between acute and chronic inflammation and is involved in different stages of arthritis (Nishimoto & Kishimot, 2006). In another study we revealed an increase in the serum level of IL-6 in CCI animals which was blocked by minocyline and produced antinocicepion (Zanjani et al, 2006). These results suggest that the stages of inflammation in arthritis and the pain behaviors in CCI must be considered to achieve effective anti-hyperalgesic and anti-inflammatory intervention via anti-IL-6 antibody and analgesic effect of minocycline treatment respectively.…”

“…‫٭٭٭‬ P < 0.001 indicate a statistically significant difference when compared to CCI saline -treated rats. M10 = minocycline 10 mg/kg, M20 = minocycline 20 mg/kg, M40 = minocycline 40 mg/kg It seems that minocycline could have an anti-inflammatory and analgesic effect in some chronic pain states (Zanjani et al, 2006). As chronic morphine activates spinal cord glia, glial activation causes morphine tolerance, and both neuropathic pain and morphine tolerance share the same mechanism (Mayer et al, 1999), we sought to understand the role of microglia in the morphine tolerance observed following the administration of glial inhibitors (pentoxifylline and minocycline) after glial cells have already been activated.…”