臺灣博碩士論文加值系統

PART 1:
Background: The study aimed to investigate the anti-apoptotic and pro-survival effects of Epigallocatechin-3-gallate (EGCG) on the cerebral cortex in spontaneously hypertensive rats.
Materials and methods: Twenty-four 36 weeks old rats were allocated into a control Wistar Kyoto group (WKY, n=8), a spontaneously hypertensive group (SHR, n=8), and a hypertension with EGCG treatment group (SHR-EGCG, n=8; daily oral EGCG 200mg/kg (94%), 12 weeks). Blood pressures were evaluated, and cerebral cortexes were isolated at 48 weeks old for the measurement of TUNEL assay and Western blotting.
Results: Systolic, diastolic, and mean blood pressure levels in the SHR-EGCG group were reduced compared to the SHR group after twelve-week treatment. The percentage of neural apoptotic cells, the levels of Endonuclease G (EndoG) and Apoptosis-inducing factor (AIF) (Caspase-independent apoptotic pathway), Fas, Fas Ligand, FADD, Caspase-8 (Fas-mediated apoptotic pathway), t-Bid, Bax/Bcl-2, Bak/Bcl-xL, Cytochrome C, Apaf-1, Caspase-9 (Mitochondrial-mediated apoptotic pathway), and Caspase-3 (Fas & Mitochondrial) were reduced in the SHR-EGCG group compared to the SHR group. Contrary, the levels of Bcl-2, Bcl-xL, p-Bad, 14-3-3, Bcl-2/Bax, Bcl-xL/Bak, and p-Bad/Bad (Bcl-2 family-related pro-survival pathway), as well as p-PI3K/PI3K and p-AKT/AKT (PI3K/AKT-related pro-survival pathway), were enhanced in the SHR-EGCG group compared to the SHR group.
Conclusion: EGCG might prevent EndoG-AIF-related Caspase-independent, Fas-mediated Caspase-dependent, Mitochondrial-mediated Caspase-dependent apoptotic pathways as well as activate Bcl-2-related and PI3K/AKT-related pro-survival pathways in hypertension. Our findings might suggest the therapeutic effects of EGCG on hypertension-induced cerebral cortex neural apoptosis.
PART 2:
Background: This systematic review sought to determine the effects of treadmill exercise on the neural mitochondrial respiratory deficiency and neural mitochondrial quality-control dysregulation in Parkinson’s disease.
Methods: PubMed, Web of Science, and EMBASE databases were searched by keywords through March 2020. The English-published animal studies that mentioned the effects of treadmill exercise on neural mitochondria in Parkinson’s disease were included. The methodological quality of the included studies was assessed by using the CAMARADES checklist. Two assessors independently conducted the pre-designed protocols of study searching, study selection, and study quality assessment.
Results: Eleven controlled-trials were included (median CAMARADES score = 5.5/10) with various treadmill exercise durations (1-18 weeks). Seven studies analyzed the neural mitochondrial respiration, showing that treadmill training attenuated complex I deficits, cytochrome c release, ATP depletion, and complexes II-V abnormalities in Parkinson’s disease. Ten studies analyzed the neural mitochondrial quality-control, reporting that treadmill exercise improved mitochondrial biogenesis, mitochondrial fusion, and mitophagy in Parkinson’s disease.
Conclusion: The review findings supported the hypothesis that treadmill training could attenuate both neural mitochondrial respiratory deficiency and neural mitochondrial quality-control dysregulation in Parkinson’s disease, suggesting that treadmill training might provide the therapeutic effects to slow down the progression of Parkinson’s disease.
PROSPERO registration ID: CRD42020164122.

PART 1:
Background: The study aimed to investigate the anti-apoptotic and pro-survival effects of Epigallocatechin-3-gallate (EGCG) on the cerebral cortex in spontaneously hypertensive rats.
Materials and methods: Twenty-four 36 weeks old rats were allocated into a control Wistar Kyoto group (WKY, n=8), a spontaneously hypertensive group (SHR, n=8), and a hypertension with EGCG treatment group (SHR-EGCG, n=8; daily oral EGCG 200mg/kg (94%), 12 weeks). Blood pressures were evaluated, and cerebral cortexes were isolated at 48 weeks old for the measurement of TUNEL assay and Western blotting.
Results: Systolic, diastolic, and mean blood pressure levels in the SHR-EGCG group were reduced compared to the SHR group after twelve-week treatment. The percentage of neural apoptotic cells, the levels of Endonuclease G (EndoG) and Apoptosis-inducing factor (AIF) (Caspase-independent apoptotic pathway), Fas, Fas Ligand, FADD, Caspase-8 (Fas-mediated apoptotic pathway), t-Bid, Bax/Bcl-2, Bak/Bcl-xL, Cytochrome C, Apaf-1, Caspase-9 (Mitochondrial-mediated apoptotic pathway), and Caspase-3 (Fas & Mitochondrial) were reduced in the SHR-EGCG group compared to the SHR group. Contrary, the levels of Bcl-2, Bcl-xL, p-Bad, 14-3-3, Bcl-2/Bax, Bcl-xL/Bak, and p-Bad/Bad (Bcl-2 family-related pro-survival pathway), as well as p-PI3K/PI3K and p-AKT/AKT (PI3K/AKT-related pro-survival pathway), were enhanced in the SHR-EGCG group compared to the SHR group.
Conclusion: EGCG might prevent EndoG-AIF-related Caspase-independent, Fas-mediated Caspase-dependent, Mitochondrial-mediated Caspase-dependent apoptotic pathways as well as activate Bcl-2-related and PI3K/AKT-related pro-survival pathways in hypertension. Our findings might suggest the therapeutic effects of EGCG on hypertension-induced cerebral cortex neural apoptosis.
PART 2:
Background: This systematic review sought to determine the effects of treadmill exercise on the neural mitochondrial respiratory deficiency and neural mitochondrial quality-control dysregulation in Parkinson’s disease.
Methods: PubMed, Web of Science, and EMBASE databases were searched by keywords through March 2020. The English-published animal studies that mentioned the effects of treadmill exercise on neural mitochondria in Parkinson’s disease were included. The methodological quality of the included studies was assessed by using the CAMARADES checklist. Two assessors independently conducted the pre-designed protocols of study searching, study selection, and study quality assessment.
Results: Eleven controlled-trials were included (median CAMARADES score = 5.5/10) with various treadmill exercise durations (1-18 weeks). Seven studies analyzed the neural mitochondrial respiration, showing that treadmill training attenuated complex I deficits, cytochrome c release, ATP depletion, and complexes II-V abnormalities in Parkinson’s disease. Ten studies analyzed the neural mitochondrial quality-control, reporting that treadmill exercise improved mitochondrial biogenesis, mitochondrial fusion, and mitophagy in Parkinson’s disease.
Conclusion: The review findings supported the hypothesis that treadmill training could attenuate both neural mitochondrial respiratory deficiency and neural mitochondrial quality-control dysregulation in Parkinson’s disease, suggesting that treadmill training might provide the therapeutic effects to slow down the progression of Parkinson’s disease.
PROSPERO registration ID: CRD42020164122.

Acknowledgments ........................................i
Abstract (PART 1)......................................ii
Abstract (PART 2).....................................iii
List of contents.......................................iv
Index of tables and figures............................vi
PART 1: Anti-apoptotic and pro-survival effects of Epigallocatechin-3-gallate (EGCG) on cerebral cortex in hypertensive rats
I. Introduction........................................ 2
II. Materials and methods.............................. 5
III. Results........................................... 8
Experimental animal characteristics.................... 8
Neural apoptotic activities............................ 8
EndoG and AIF-related Caspase-independent apoptotic pathway................................................ 8
Upstream components of Fas-mediated Caspase-dependent apoptotic pathway...................................... 9
Upstream components of mitochondrial-mediated Caspase-dependent apoptotic pathway and Bcl2 family-related pro-survival pathway....................................... 9
Downstream components of Fas-mediated and mitochondrial-mediated Caspase-dependent apoptotic pathway.......... 10
PI3K/AKT-related pro-survival pathway................. 10
IV. Discussion........................................ 11
References............................................ 17
Table and figures..................................... 21
PART 2: Effects of treadmill exercise on neural mitochondrial functions in Parkinson’s disease: A systematic review of animal studies
I. Introduction....................................... 36
II. Methods........................................... 38
Protocol and registration............................. 38
Eligibility criteria.................................. 38
Information sources and search strategy............... 39
Data collection process............................... 39
Study quality evaluation.............................. 40
Data synthesis and presentation....................... 40
III. Results.......................................... 41
Search results........................................ 41
Study characteristics................................. 41
Outcome summary....................................... 42
Study quality evaluation.............................. 45
IV. Discussion........................................ 46
References............................................ 54
Tables and figures.................................... 58

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PART 2:
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