• 검색 결과가 없습니다.

D. ROS production and neuronal damage in the cerebral cortex of APP/PS1

Ⅴ. CONCLUSION

This study showed that the activated microglia surrounding plaques induced excessive expression of pro-inflammatory mediators such as IL-1β, TNF-α, iNOS and ROS, leading to neuronal damage in the cerebral cortex of APP/PS1 mice. Our previous study demonstrated that LPS-induced endogenous expression of IL-10 in microglia down-regulated brain inflammation and neuronal damage in the rat cerebral cortex. However, in the present study, we did not find of an association between IL-10 expression and down-regulation of brain inflammation. Therefore, further understanding the mechanisms of IL-10 expression in chronic brain inflammation may be an important point to comprehend the pathogenesis of Alzheimer’s disease.

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- 국문요약 -

현이 Iba1-면역양성을 보이는 마이크로글리아에서 대부분 배치됨을 관찰하였 다. 활성산소종 (ROS) 생성은 8개월부터 나타나며 14개월과 17개월 사이에서 두드러지게 증가되었다. NADPH oxidase의 주요 구성물질인 gp91phox 단백질 은 Iba1-면역양성을 보이는 마이크로글리아에서 대부분 배치됨을 관찰하였다.

또한, 14개월과 17개월의 대뇌피질에서 NeuN-양성적 뉴론과 MAP2-면역반 응적인 수지상 돌기가 상당히 감소되어 있음을 관찰하였다. 이 결과들은 알츠 하이머병 뇌조직에서 섬유성 아밀로이드 베타 (fibrillar β-amyloid)의 축적에 따라, 활성화된 마이크로글리아가 염증성 매개물질의 과도한 발현과 NADPH oxidase 활성화에 의한 활성산소종 생성을 유도하여 뉴론의 손상을 야기시킬 수 있음을 보여준다.

핵심어: 알츠하이머 질병, 인터루킨-10, 마이크로글리아, IL-1β, TNF-α, iNOS, 활성산소종

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