Staff Members - Benha University
Impact of Thymoquinone on Memory Deficit-associated with Global Cerebral Ischemia-Reperfusion Injury in Rats; Possible Role of PPAR-γ.
• 2020
Publication Information
Authors
Noha I Hussien, Moataz A Elawady, Mohammed M Elmaghrabi, Marwa H Muhammad
Keywords
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Journal
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Publisher
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Volume
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Issue
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Pages
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publication.type
International
Paper Link
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Supplementary Materials
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Abstract
Context:
Cerebrovascular insults contribute significantly to morbidity and mortality statistics worldwide. More than half of the ischemic stroke survivors experience residual memory deficits. Thymoquinone (TQ) effect on the hippocampus has gained more attention.
Objective:
To clarify the impact of TQ administration on memory status-associated with global cerebral ischemia/reperfusion (I/R)-injury in rats and to illustrate the potential role of peroxisome proliferator-activated receptor gamma (PPAR-γ) as a novel suggested mechanism.
Method:
Sham, Sham+ TQ, I/R, I/R+ TQ, and I/R+ BADGE (selective PPAR-γ antagonist)+ TQ groups were assigned. Memory status was assessed by the novel object recognition test. Hippocampal content of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), in addition to the expression levels of PPAR-ɣ, brain-derived neurotrophic factor (BDNF), and nuclear factor-κB (NF-κB) were evaluated.
Results:
Global cerebral I/R impaired the memory functions and increased hippocampal levels of oxidative stress and inflammatory biomarkers. TQ administration to ischemic rats significantly improved the previous parameters with uprising PPAR-ɣ and BDNF but, lowering NF-κB levels. The prior treatment with PPAR-γ antagonist significantly attenuated the TQ effect.
Conclusion:
TQ exerted nootropic effect against ischemic stroke associated-memory deficits through antioxidant, anti-inflammatory, and neurotrophic mechanisms with PPAR-γ contributes, partly at least, toward TQ-mediated protection.
Cerebrovascular insults contribute significantly to morbidity and mortality statistics worldwide. More than half of the ischemic stroke survivors experience residual memory deficits. Thymoquinone (TQ) effect on the hippocampus has gained more attention.
Objective:
To clarify the impact of TQ administration on memory status-associated with global cerebral ischemia/reperfusion (I/R)-injury in rats and to illustrate the potential role of peroxisome proliferator-activated receptor gamma (PPAR-γ) as a novel suggested mechanism.
Method:
Sham, Sham+ TQ, I/R, I/R+ TQ, and I/R+ BADGE (selective PPAR-γ antagonist)+ TQ groups were assigned. Memory status was assessed by the novel object recognition test. Hippocampal content of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), in addition to the expression levels of PPAR-ɣ, brain-derived neurotrophic factor (BDNF), and nuclear factor-κB (NF-κB) were evaluated.
Results:
Global cerebral I/R impaired the memory functions and increased hippocampal levels of oxidative stress and inflammatory biomarkers. TQ administration to ischemic rats significantly improved the previous parameters with uprising PPAR-ɣ and BDNF but, lowering NF-κB levels. The prior treatment with PPAR-γ antagonist significantly attenuated the TQ effect.
Conclusion:
TQ exerted nootropic effect against ischemic stroke associated-memory deficits through antioxidant, anti-inflammatory, and neurotrophic mechanisms with PPAR-γ contributes, partly at least, toward TQ-mediated protection.