Amelioration of chronic relapsing experimental autoimmune encephalomyelitis (cr-eae) using thymoquinone - biomed 2009

Axonal damage, demylination and inflammation of the central nervous system are the major pathological features of the human multiple sclerosis (MS). MS is thought to be due to abnormal T cell mediated immune response. Oxidative stress plays an important role in the advancement of MS. The management...

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Bibliographic Details
Published inBiomedical sciences instrumentation Vol. 45; p. 274
Main Authors Mohamed, Adel, Waris, H M, Ramadan, H, Quereshi, M, Kalra, J
Format Journal Article
LanguageEnglish
Published United States 2009
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Summary:Axonal damage, demylination and inflammation of the central nervous system are the major pathological features of the human multiple sclerosis (MS). MS is thought to be due to abnormal T cell mediated immune response. Oxidative stress plays an important role in the advancement of MS. The management of oxidative stress by outlining central role of reduced glutathione. In our experiment we used Experimental autoimmune encephalomyelitis (EAE) animal model that mimic human MS and tested the effect of Thymoquinone (TQ), an oil constituent of Nigella Sativa also known as black seed. Thirty female mice of strain C57BL/6J and aged between 6 to 12 weeks were placed into 3 groups of 10 and were given Myelin Oligodendrocyte Glycoprotein (MOG) subcutaneously (SC) to induce EAE. Group A was the control group. Group B received MOG (SC) and TQ intraperiotoneally (IP) from day 1 till day 50. Group C received MOG (SC) and TQ (IP) on the appearance of first sign and symptoms of chronic relapsing EAE (CR-EAE). All Mice were examined daily for behavioral deficits and all euthanized and sacrificed on day 50. Preliminary result showed that TQ due to its antioxidant effect is almost 90% preventive and 50% curative in CR-EAE. This result could assist further studies on the mechanism of action of TQ in CR-EAE and explore the possibility of treating the human chronic relapsing multiple sclerosis phase.
ISSN:0067-8856