In this study, an Aβ25-35-induced PC12 cell damage model was established to investigate the neuroprotective effects and underlying mechanisms of aged Liupao tea (ALPT), with green tea (GT) as a reference. The results show that Aβ25-35 significantly reduced PC12 cell viability, induced mitochondrial dysfunction, and promoted the formation of toxic aggregates and related pathways. ALPT markedly improved cell survival, increased mitochondrial membrane potential, and significantly inhibited the accumulation of toxic aggregates and the formation of related pathways. Furthermore, transcriptome analysis reveals that the overall gene expression pattern in the ALPT treatment group was the opposite to that in the Aβ25-35 group, with upregulated genes involved in mitophagy, glycolysis and glycerophospholipid metabolism, and downregulated genes associated with cell cycle regulation, ribosomal function, ubiquitin-mediated proteolysis and cellular senescence. Overall, both GT and ALPT exhibited significant protective effects against Aβ25-35-induced PC12 cell damage, though transcriptomic differences suggest that ALPT may have superior bioavailability due to its active components. This study provided experimental evidence for the potential application of ALPT in the prevention and treatment of neurodegenerative diseases.
NIE Qing
,
PANG Yuelan
,
WU Huan
,
DING Shuqia
,
ZHONG Keyu
,
LIU Zhonghua
,
CAI Shuxian
. Neuroprotective Mechanisms of Aged Liupao Tea against Aβ25-35-induced PC12 Cell Damage[J]. Journal of Tea Science, 2024
, 44(6)
: 1005
-1013
.
DOI: 10.13305/j.cnki.jts.20241203.001
[1] 余锋, 贾芳芳. 饮食干预肠道微生物调控认知和神经退行性疾病的作用机制[J]. 中国食品学报, 2022, 22(6): 403-413.
Yu F, Jia F F.Mechanism of dietary intervention gut microbiota in regulating cognition and neurodegenerative diseases[J]. Journal of Chinese Institute of Food Science and Technology, 2022, 22(6): 403-413.
[2] 曹雨欣, 张彦青, 戚务勤, 等. 食源性天然产物调控线粒体自噬预防神经退行性疾病的研究进展[J]. 食品科学, 2024, 45(1): 301-312.
Cao Y X, Zhang Y Q, Qi W Q, et al.Food-derived natural products prevent neurodegenerative diseases by regulating mitophagy: a review of research progress[J]. Food Science, 2024, 45(1): 301-312.
[3] Chao A C, Chen C H, Wu M H, et al.Roles of Id1/HIF-1 and CDK5/HIF-1 in cell cycle reentry induced by amyloid-beta peptide in post-mitotic cortical neuron[J]. Biochimica et Biophysica Acta, 2020, 1867(4): 118628. doi: 10.1016/j.bbamcr.2019.118628.
[4] Hidalgo F J, Delgado R M, Zamora R.Protective effect of phenolic compounds on carbonyl-amine reactions produced by lipid-derived reactive carbonyls[J]. Food Chemistry, 2017, 229: 388-395.
[5] Pan H B, Gao Y, Tu Y Y.Mechanisms of body weight reduction by black tea polyphenols[J]. Molecules, 2016, 21(12): 1659. doi: 10.3390/molecules21121659.
[6] Schimidt H L, Garcia A, Martins A, et al.Green tea supplementation produces better neuroprotective effects than red and black tea in Alzheimer-like rat model[J]. Food Research International, 2017, 100(Part1): 442-448.
[7] Deb S, Dutta A, Phukan B C, et al.Neuroprotective attributes of L-theanine, a bioactive amino acid of tea, and its potential role in Parkinson's disease therapeutics[J]. Neurochemistry International, 2019, 129: 104478. doi: 10.1016/j.neuint.2019.104478.
[8] Zhao T T, Li C, Wang S, et al.Green tea (Camellia sinensis): a review of its phytochemistry, pharmacology, and toxicology[J]. Molecules, 2022, 27(12): 3909. doi: 10.3390/molecules27123909.
[9] 李玥, 王屹豪, 张静聿, 等. 茶叶功能成分治疗阿尔茨海默病分子作用机制的研究进展[J]. 中国当代医药, 2023, 30(31): 19-23.
Li Y, Wang Y H, Zhang J Y, et al.Research progress on the molecular mechanism of functional components of tea in the treatment of Alzheimer's disease[J]. China Modern Medicine, 2023, 30(31): 19-23.
[10] Cai S X, Yang H, Wen B B, et al.Inhibition by microbial metabolites of Chinese dark tea of age-related neurodegenerative disorders in senescence-accelerated mouse prone 8 (SAMP8) mice[J]. Food & Function, 2018, 9(10): 5455-5462.
[11] Pan W J, Li W S, Wu H, et al.Aging-accelerated mouse prone 8 (SAMP8) mice experiment and network pharmacological analysis of aged Liupao tea aqueous extract in delaying the decline changes of the body[J]. Antioxidants, 2023, 12(3): 685. doi: 10.3390/antiox12030685.
[12] Wan J, Feng M Y, Pan W J, et al.Inhibitory effects of six types of tea on aging and high-fat diet-related amyloid formation activities[J]. Antioxidants, 2021, 10(10): 1513. doi: 10.3390/antiox10101513.
[13] Li B Y, Mao Q Q, Xiong R G, et al.Preventive effects of different black and dark teas on obesity and non-alcoholic fatty liver disease and modulate gut microbiota in high-fat diet fed mice[J]. Foods, 2022, 11(21): 3457. doi: 10.3390/foods11213457.
[14] Song Y X, Li P, Liu L, et al.Nanostructural differentiation and toxicity of amyloid-β25-35 aggregates ensue from distinct secondary conformation[J]. Scientific Reports, 2018, 8(1): 765. doi: 10.1038/s41598-017-19106-y.
[15] Tikhonova L A, Kaminsky Y G, Reddy V P, et al.Impact of amyloid β25-35 on membrane stability, energy metabolism, and antioxidant enzymes in erythrocytes[J]. American Journal of Alzheimer's Disease and Other Dementias, 2014, 29(8): 685-695.
[16] Couly S, Denus M, Bouchet M, et al.Anti-amnesic and neuroprotective effects of fluoroethylnormemantine in a pharmacological mouse model of Alzheimer's disease[J]. The International Journal of Neuropsychopharmacology, 2021, 24(2): 142-157.
[17] Pang Q Q, Kim J H, Choi J M, et al.Cirsium japonicum var. Maackii improves cognitive impairment under amyloid β25-35-induced Alzheimer's disease model[J]. BioMed Research International, 2022: 4513998. doi: 10.1155/2022/4513998.
[18] Zhang Y Y, Bao H L, Dong L X, et al.Silenced lncRNA H19 and up-regulated microRNA-129 accelerates viability and restrains apoptosis of PC12 cells induced by Aβ25-35 in a cellular model of Alzheimer's disease[J]. Cell Cycle, 2021, 20(1): 112-125.
[19] 郑新. 茶黄素延缓细胞衰老效应研究[D]. 长沙: 湖南农业大学, 2021.
Zheng X.Study on the effect of theaflavins in delaying cell senescence[D]. Changsha: Hunan Agricultural University, 2021.
[20] Crouch P J, Harding S M, White A R, et al.Mechanisms of Aβ mediated neurodegeneration in Alzheimer's disease[J]. The International Journal of Biochemistry & Cell Biology, 2008, 40(2): 181-198.
[21] Strope T A, Birky C J, Wilkins H M.The role of bioenergetics in neurodegeneration[J]. International Journal of Molecular Sciences, 2022, 23(16): 9212. doi: 10.3390/ijms23169212.
[22] Fan X L, Huang T T, Tong Y D, et al.p62 works as a hub modulation in the ageing process[J]. Ageing Research Reviews, 2022, 73: 101538. doi: 10.1016/j.arr.2021.101538.
[23] Tóbon-Velasco J C, Cuevas E, Torres-Ramos M A. Receptor for AGEs (RAGE) as mediator of NF-κB pathway activation in neuroinflammation and oxidative stress[J]. CNS & Neurological Disorders Drug Targets, 2014, 13(9): 1615-1626.
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