Document Type : Original Article
Authors
1
Cellular and Molecular Research Center, Department of Physiology and Pharmacology, Faculty of Medicine, Sabzevar University of Medical Sciences, Sabzevar, Iran
2
Department of Pharmacodynamics and Toxicology, Pharmaceutical Research Center, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
3
Targeted Drug Delivery Research Center, Department of Pharmacodynamy and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
Abstract
Objective
We examined the protective effects of ethanolic extract of Lippia citriodora (L. citriodora) on rats subjected to chronic constriction injury (CCI) of sciatic nerve and possible mechanisms of actions.
Materials and Methods
In this experimental study, the extract was administered 50, 100 and 200 mg/kg, Intraperitoneally (I.P) from the surgery time for 14 consecutive days. The changes in the spinal cord levels of apoptotic factors, microglia and astroglia markers during the time course of study were assessed by western blotting on days 3, 7 and 14 post-CCI.
Results
CCI rats developed neuropathy evident from a marked mechanical allodynia, cold allodynia and thermal hyperalgesia on days 3, 5, 7, 10 and 14 post-CCI. A significant increase in the levels of Iba (a marker of microglia activation) and Bax (a proapoptotic factor) was observed three days after nerve injury. The levels of Iba remained high on day 7. In contrast, there was no difference in glial fibrillary acidic protein (GFAP) contents between sham and CCI animals. Treatment with the extract significantly attenuated behavioral changes associated with neuropathy. Bax/Bcl-2 and Iba1 were decreased in CCI animals treated with the extract.
Conclusion
The results support the evidence that microglial activation and apoptosis are correlated with pain behaviors. It is suggested that anti-allodynic and anti-hyperalgesic effects, elicited by L. citriodora, might have some degrees of association with the inhibition of microglia activation and apoptotic pathways.
Keywords
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