Protective Effects of Heat-Killed Ruminococcus albus against β-Amyloid-Induced Apoptosis on SH-SY5Y Cells
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A high level of β-amyloid (Aβ) in the brains of patients with Alzheimer’s disease (AD) generates reactive oxygen species that induce neuronal death and DNA damage. The interaction between the gut microbiota and brain health has attracted attention in recent years. Heat-killed Ruminococcus albus (hkRA) reportedly protects neurons against damage induced by oxidative stress. However, whether hkRA can inhibit Aβ-induced apoptosis and thus alleviate AD remains unclear. Hence, we aimed to evaluate the protective effects of hkRA against Aβ-induced apoptosis on the human neuroblastoma SH-SY5Y cell. HkRA treatment (108 cells/ml) significantly decreased the Aβ-induced cytotoxicity and DNA damage in the SH-SY5Y cells. It also showed a significant increase of the bax/ bcl-2 ratio in the Aβ-treated SH-SY5Y cells. Moreover, hkRA treatment stimulated the expression of antioxidation-related genes HO-1, Nrf2, and PKC-δ and increased the expression of brain-derived neurotrophic factor (BDNF). Meanwhile, it significantly decreased the activity of caspase-3 and protein expression of cleaved caspase-3 in the Aβ-treated SH-SY5Y cells. Additionally, the protein levels of mitochondrial and cytosolic cytochrome c increased and decreased, respectively, in the cells. These results suggest that hkRA protects human neuroblastoma cells from Aβ-induced apoptosis and oxidative stress. Thus, hkRA may be developed into a health-promoting paraprobiotic (the inactivated microbial cells of probiotics) for patients with AD.
Abstract
A high level of β-amyloid (Aβ) in the brains of patients with Alzheimer’s disease (AD) generates reactive oxygen species that induce neuronal death and DNA damage. The interaction between the gut microbiota and brain health has attracted attention in recent years. Heat-killed Ruminococcus albus (hkRA) reportedly protects neurons against damage induced by oxidative stress. However, whether hkRA can inhibit Aβ-induced apoptosis and thus alleviate AD remains unclear. Hence, we aimed to evaluate the protective effects of hkRA against Aβ-induced apoptosis on the human neuroblastoma SH-SY5Y cell. HkRA treatment (108 cells/ml) significantly decreased the Aβ-induced cytotoxicity and DNA damage in the SH-SY5Y cells. It also showed a significant increase of the bax/ bcl-2 ratio in the Aβ-treated SH-SY5Y cells. Moreover, hkRA treatment stimulated the expression of antioxidation-related genes HO-1, Nrf2, and PKC-δ and increased the expression of brain-derived neurotrophic factor (BDNF). Meanwhile, it significantly decreased the activity of caspase-3 and protein expression of cleaved caspase-3 in the Aβ-treated SH-SY5Y cells. Additionally, the protein levels of mitochondrial and cytosolic cytochrome c increased and decreased, respectively, in the cells. These results suggest that hkRA protects human neuroblastoma cells from Aβ-induced apoptosis and oxidative stress. Thus, hkRA may be developed into a health-promoting paraprobiotic (the inactivated microbial cells of probiotics) for patients with AD.
참고문헌 (39)
- Barage SH, "Amyloid cascade hypothesis : pathogenesis and therapeutic strategies in Alzheimer's disease", Neuropeptides, 52, pp.1~18 (2015)
- Gouras GK, "β-Amyloid peptides and amyloid plaques in Alzheimer’s disease", Neurotherapeutics, 12, pp.3~11 (2015)
- Rajasekhar K, "Function and toxicity of amyloid beta and recent therapeutic interventions targeting amyloid beta in Alzheimer's disease", Chem. Commun, 51, pp.13434~13450 (2015)
- Minter MR, "The contribution of neuroinflammation to amyloid toxicity in Alzheimer's disease", J. Neurochem, 136, pp.457~474 (2016)
- Aleksis R, "Structural studies of amyloid-β peptides : unlocking the mechanism of aggregation and the associated toxicity", Biochimie, 140, pp.176~192 (2017)
- Huang WJ, "Role of oxidative stress in Alzheimer's disease", Biomed. Rep, 4, pp.519~522 (2016)
- Das M, "Dihydroactinidiolide regulates Nrf2", HO-1 expression and inhibits caspase-3, Neurotoxicology, pp.2021, 84[DOI]
- Balez R, "Neuroprotective effects of apigenin against inflammation, neuronal excitability and apoptosis in an induced pluripotent stem cell model of Alzheimer’s disease", Sci. Rep, 6, pp.31450~ (2016)
- Hwang S, "Inhibitory effect of lycopene on amyloid-β-induced apoptosis in neuronal cells", Nutrients, 9, pp.883~ (2017)
- Chen G-f, "Amyloid beta : structure, biology and structure-based therapeutic development", Acta Pharmacol. Sin, 38, pp.1205~1235 (2017)
- Carabotti M, "The gut-brain axis : interactions between enteric microbiota, central and enteric nervous systems", Ann. Gastroenterol, 28, pp.203~209 (2015)
- Kohler CA, "The gut-brain axis, including the microbiome, leaky gut and bacterial translocation : mechanisms and pathophysiological role in Alzheimer’s disease", Curr. Pharm. Des, 22, pp.6152~6166 (2016)
- Xu R, "Towards understanding brain-gut-microbiome connections in Alzheimer’s disease", BMC Syst. Biol, 10, pp.277~285 (2016)
- Jiang C, "The gut microbiota and Alzheimer’s disease", J. Alzheimers Dis, 58, pp.1~15 (2017)
- Zhao Y, "Microbial sources of amyloid and relevance to amyloidogenesis and Alzheimer’s disease(AD)", J. Alzheimers Dis. Parkinsonism, 5, pp.177~ (2015)
- Minter MR, "Antibiotic-induced perturbations in gut microbial diversity influences neuro-inflammation and amyloidosis in a murine model of Alzheimer’s disease", Sci. Rep, 6, pp.30028~ (2016)
- Birks JS, "Donepezil for dementia due to Alzheimer's disease", Cochrane Database Syst. Rev, 6, pp.CD001190~ (2018)
- Mendiola-Precoma J, "Therapies for prevention and treatment of Alzheimer’s disease", Biomed Res. Int, 2016, pp.2589276~ (2016)
- Naomi R, "Probiotics for Alzheimer's disease : a systematic review", Nutrients, 14, pp.20~ (2022)
- Guo L, "Effects of gut microbiota and probiotics on Alzheimer's disease", Transl. Neurosci, 12, pp.573~580 (2021)
- Lee CC, "Different impacts of heat-killed and viable Lactiplantibacillus plantarum TWK10 on exercise performance, fatigue, body composition, and gut microbiota in humans", Microorganisms, 10, pp.2181~ (2022)
- Poaty Ditengou JIC, "Are heat-killed probiotics more effective than live ones on colon length shortness, disease activity index, and the histological score of an inflammatory bowel disease-induced murine model? A metaanalysis", J. Appl. Microbiol, 134, pp.lxad008~ (2023)
- Adams CA, "The probiotic paradox : live and dead cells are biological response modifiers", Nutr. Res. Rev, 23, pp.37~46 (2010)
- Warda AK, "Heat-killed lactobacilli alter both microbiota composition and behaviour", Behav. Brain Res, 362, pp.213~223 (2019)
- Noh H-J, "Immunostimulatory effect of heat-killed probiotics on RAW264.7macrophages", J. Microbiol. Biotechnol, 32, pp.638~644 (2022)
- Park J, "Neuroprotective effect of Ruminococcus albus on oxidatively stressed SH-SY5Y cells and animals", Sci. Rep, 7, pp.14520~ (2017)
- Kabiraj P, "An 11-mer amyloid beta peptide fragment provokes chemical mutations and Parkinsonian biomarker aggregation in dopaminergic cells : a novel road map for"transfected"Parkinson’s", ACS Chem. Neurosci, 7, pp.1519~1530 (2016)
- Abarikwu SO, "Atrazine induces apoptosis of SH-SY5Y human neuroblastoma cells via the regulation of Bax", Bcl-2 ratio and caspase-3-dependent pathway, 2015, pp.118, 90~98
- Beeri MS, "Brain BDNF expression as a biomarker for cognitive reserve against Alzheimer disease progression", Neurology, 86, pp.702~703 (2016)
- Lattanzio F, "Treatment with the neurotoxic Aβ(25–35)peptide modulates the expression of neuroprotective factors Pin1, Sirtuin 1, and brain-derived neurotrophic factor in SH-SY5Y human neuroblastoma cells", Exp. Toxicol. Pathol, 68, pp.271~276 (2016)
- Dinkova-Kostova AT, "The role of Nrf2 signaling in counteracting neurodegenerative diseases", FEBS J, 285, pp.3576~3590 (2018)
- Han XJ, "Amyloid β-42 induces neuronal apoptosis by targeting mitochondria", Mol. Med. Rep, 16, pp.4521~4528 (2017)
- Swerdlow RH, "Mitochondria and mitochondrial cascades in Alzheimer’s disease", J. Alzheimers Dis, 62, pp.1403~1416 (2018)
- Cosentino K, "Mitochondrial alterations in apoptosis", Chem. Phys. Lipids, 181, pp.62~75 (2014)
- Hu Q, "Elevated cleaved caspase-3 is associated with shortened overall survival in several cancer types", Int. J. Clin. Exp. Pathol, 7, pp.5057~5070 (2014)
- Li RM, "Overexpression of fibroblast growth factor 13 ameliorates amyloid-β-induced neuronal damage", Neural Regen. Res, 18, pp.1347~1353 (2023)
- Choudhary GS, "Caspase-3 activation is a critical determinant of genotoxic stress-induced apoptosis", Apoptosis Cancer, 1219, pp.1~9 (2015)
- Kang S, "Dysbiosis of fecal microbiota in Crohn's disease patients as revealed by a custom phylogenetic microarray", Inflamm. Bowel. Dis, 16, pp.2034~2042 (2010)
- Mohandas S, "Differences in gut microbiome in hospitalized immunocompetent vs. immunocompromised children, including those with sickle cell disease", Front. Pediatr, 8, pp.583446~ (2020)