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논문 기본 정보

자료유형
학위논문
저자정보

정다혜 (제주대학교, 제주대학교 대학원)

지도교수
김재훈
발행연도
2020
저작권
제주대학교 논문은 저작권에 의해 보호받습니다.

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Albeit two-thirds of dementia people suffer from Alzheimer’s disease, there has been no perfect cure from side effects. Therefore, it is required to find candidates for low-risk and efficient treatments from natural substances. In the early stages of Alzheimer''s disease, the cholinergic and glutamatergic damage factors occur so substances suppress these factors can be important candidates for treatment. We screened 75 species of plant extracts to find acetylcholine esterase inhibitors and the leaves of ethanol extracted Styrax japonica (EESJ) was selected. It was also confirmed by MTT assay and annexin-V/PI staining assay that EESJ inhibited glutamate-induced apoptosis in the HT22 mouse hippocampal cells. Subsequently, EESJ suppressed glutamate-mediated ROS production. In addition, western blot revealed that EESJ attenuated the phosphorylation levels of MAPK members including ERK, JNK, and p38 kinases. Therefore, the leaves of S. japonica are suitable for a candidate substance of Alzheimer’s disease treatment.

목차

ABSTRACT. 1
1. INTRODUCTION. 2
2. MATERIALS AND METHODS 5
2.1. Materials 5
2.2. Acetylcholinesterase inhibitory assay. 5
2.3. Preparation of Ethanol Extracted Styrax japonica (EESJ) 5
2.4. Cell Culture and reagents. 6
2.5. Cell Viability Assay. 6
2.6. Cell Apoptosis Assay. 7
2.7. Intracellular ROS production. 7
2.8. Western Blot Analysis. 7
2.9. Statistical Analysis. 8
3. RESULTS. 9
3.1. Screening of 75 plant species for the acetylcholine esterase inhibitory activity 9
3.2. Ethanol extracted Styrax japonica (EESJ) reduced cell glutamate-induced cell death in HT22 cells. 10
3.3. Treatment with EESJ showed inhibition of apoptosis induced by glutamate 12
3.4. EESJ reversed the expression levels of apoptotic regulators Bax and Bcl-2 14
3.5. EESJ suppressed glutamate-induced intracellular ROS production in HT22 cells 16
3.6. EESJ attenuated glutamate-induced neuronal cell death via regulating MAPK signaling pathway 18
4. DISCUSSION 20
5. REFERENCES 22
6. ACKNOWLEDGEMENTS 25

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