| Alzheimer's Disease (AD), also known as Senile Dementia, is primary degenerative disease dominated by the central nervous system. The number of the AD patients increases year by year because of the growing global aging population. Currently, it has regarded as the third killer among other diseases of human beings, with the patient number only less than those of the cancer and heart disease. Due to the current situation, studies on AD have become a research focus in the medical and the biological field. However, the pathogenesis of AD has not yet fully understood by now. This paper tentatively studied the EGCG in tea's protective effect on Alzheimer's disease based on the protein aggregation level, and results were obtained as follows:1. BSA/MDA stress system was built by the in-vitro experiment, and the BSA monomer structure is proved to be damaged to protein aggregation by scanning TEM, ThT fluorescence detection, SDS-PAGE, Native-PAGE,silver staining, NBT dyeing and dot blot, ?-sheet structure(A11+) which rarely exists in natural has been found in the protein aggregation, and the structure contains cytotoxic. While the poisonous aggregation is inhibited to some extent in the other group which has been added into the EGCG with concentration 75-375?M. The EGCG turns into quinoid structure modified on the protein thus changes the protein aggregation conformation and restrains the toxicity.2.PC12 neuronal cell model was built by added BSA,the protein aggregation generated by BSA/MDA stress or EGCG system. The LDH experiment shows that EGCG can reduce the cell toxicity caused by aggregates. PCR results showed that the aggregate of BSA/ MDA stress system regulated expression of aging related gene of p21, RAGE and BACE1 the key enzyme about A?42 formed. Western-blot results showed that, the aggregates promote P-APP, RAGE and p62 protein expression of nerve cell.It also made the content of 4-HNE, A11 increase in cells.By PCR and western blot experiments proved that the EGCG to nerve cell damage caused by protein aggregation has prevention and protection.It is safe to draw a conclusion that EGCG has a medical value.3. SAMP8 mice were chosen as the animal model for Alzheimer's Disease. The controlled mouse group was gavaged with EGCG (10 mg·kg-1 d-1) for 3 months. Through brain histopathological examination, blood and various issues' protein aggregation content measurement, SOD and GSH-Px enzyme activity and MDA content measurement, the results showed that, mice's hippocampus and cortical neurons of model group were lost or damaged to different degree. Slice of Congo red staining the typical aggregate has formed on P8's cortex and hippocampus. A?42 content in serum and other amyloid proteins in spleen, pancreas, kidney, and liver was obviously higher than that in the normal mice of controlled group, enzyme activity test also showed that both SOD and GSH-Px activity reduced while the MDA content increased in the tissues of serum, spleen, pancreas, kidney, and liver. Compared to the model group, the EGCG group showed quite different results:each index can recover to the normal group level, which indicates an alleviative aging effect. This result clearly demonstrates that EGCG can restrain ?-amyloid protein forming and aggregating on different tissues and organs, and delay the nervous system and organs'aging process. EGCG'S protective effect on AD model can be derived from AD mechanism which is caused by the A? cascade hypothesis and oxidative stress theory. |
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