Activation of Microglial Cells: the Bridge between the Immune System and Pain in Central Nervous System
Journal of Cellular & Molecular Anesthesia,
Vol. 1 No. 4 (2016),
26 August 2016
Background: Pain is one of the main protests of inflammatory diseases, hence, understanding the mechanisms which involved in the induction and persistence of pain is essential. Microglia is a contributing factor in the onset and maintenance of inflammation. Increased microglial activation increases the level of central pro-inflammatory cytokines and the development of central sensitization following inflammation. The aim of this study was evaluate the relation of spinal microglia activity with pain related behaviors during Complete Freund’s adjuvant (CFA)-induced inflammation.
Materials and Methods: Inflammation caused by subcutaneous injection of Complete Freund’s adjuvant (CFA) in a single dose to the animals right hind paw. The edema and hyperalgesia caused by inflammation, respectively are measured by Plethysmometer and Radiant Heat, on days 0,7,14 and 21. Spinal Iba-1 protein expression was detected by Western blotting. Minocycline hydrochloride (Sigma, U.S.A) was administered i.p. at a dose of 40mg/kg daily.
Results: Our study findings indicated that CFA injection to right hindpaw of rats increased paw volume and hyperalgesia significantly during different stages of study, while Minocycline treatment significantly reduced paw volume and hyperalgesia. CFA injection into the right hindpaw of the rat increases the expression of molecules Ionized calcium binding adaptor molecule -1 (Iba-1) on different days of study, while Minocycline administration reduced spinal Iba-1 expression significantly compared to the CFA group.
Conclusion: The results of this study indicated the significant roles of microglia activation in deterioration of pain related behaviors during different stages of CFA-induced inflammation. The steady injection of Minocycline (as a microglia inhibitor) could reduce the inflammatory symptoms.
- immune system
How to Cite
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