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Protective effect of thymoquinone versus platelet rich plasma derived lyophilized growth factors against cuprizone induced corpus callosum demyelination in multiple sclerosis rat model

Research Authors
Ahmed, Raghdaa Galal, Ahmed Mubarak, Wafaa Fahmy, Hossam Shenouda, Merry
Research Date
Research Department
Research Journal
The Egyptian Journal of Histology
Research Member
Research Abstract

Background Multiple sclerosis (MS) is the commonest demyelinating degenerative disease causing adult neurological disability. The cuprizone (CPZ) model is suitable for studying MS induced demyelination. Thymoquinone (TQ) and Platelet rich plasma derived lyophilized growth factors (PRP d. LGFs) showed neuroprotective activity and had been successfully applied in degenerative conditions.
Aim of the work to determine and compare the possible neuroprotective activities for TQ and LGFs against CPZ induced demyelination in rat corpus callosum (CC).
Material and methods 40 male adult albino rats were randomly and equally assorted in 4 groups; Group I (Control group): The rats received nothing. Group II (CPZ group): The rats fed standard rodent chow mixed with 0.6% CPZ/ day (0.6 g of Cuprizone was added to 100 g of chow) for 4 weeks. ‏Group III (CPZ + TQ): The rats were given 0.6% CPZ and TQ daily (20 mg/ kg body weight) dissolved in corn oil (0.5 ml/ rat) orally by intragastric tube for 4 weeks. Group IV (CPZ + PRP d. LGF): The rats received 0.6% CPZ and LGF (250 μL dissolved in distilled water, by intraperitoneal injection) 2 times every week in 4 weeks. At the distend time, light microscopic, electron microscopic, immunohistochemical and morphometric studies were used to study myelination and demyelination in rat CC.
Results: Cuprizone induced oligodendrocytes damage or loss in the rat CC with a subsequent loss of myelin, axonal degeneration and astrogliosis. Both LGFs and TQ attenuated the CPZ induced CC demyelination, but it was more obvious in the LGFs treated group.
Conclusion: Simultaneous administration of LGF or TQ with CPZ improved CC architecture in CPZ model of demyelination with higher protective efficacy for LGF over TQ.