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rBTI reduced β-amyloid-induced toxicity by promoting autophagy-lysosomal degradation via DAF-16 in Caenorhabditis elegans.
Exp Gerontol. 2017 03; 89:78-86.EG

Abstract

Alzheimer's disease (AD) is an age-related neurodegenerative disease, of which β-amyloid (Aβ) induced toxicity was suggested as a main cause. Some substances with prolongevity effects have been shown to be protective against AD. In a previous study we demonstrated that a recombinant buckwheat trypsin inhibitor (rBTI) could prolonge the lifespan in Caenorhabditis elegans (C. elegans). Here, we investigated whether rBTI may benefit to mitigate the AD symptom by feeding the AD model C. elegans CL4176. CL4176 is a transgenic C. elegans expressing human Aβ3-42 in muscle tissue. The results showed that rBTI not only could extend lifespan but also could reduce Aβ toxicity-triggered body paralysis in AD worms. Further study found the accumulation of Aβ was decreased and autophagy-lysosomal degradation pathway was activated in AD worms treated with rBTI. Moreover, the inhibition of autophagy reduced rBTI-mediated paralysis delay. Genetic analyses showed rBTI increased the transcriptional activity of dauer formation abnormal-16 (DAF-16) and the disruption of daf-16 abolished rBTI-mediated protective effect in AD worms. Taken together, these data indicated that rBTI promoted the autophagy-lysosomal degradation pathway to reduce the Aβ-induced toxicity via DAF-16 in an AD model C. elegans, implying that BTI has the potential to protect against AD.

Authors+Show Affiliations

Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Institute of Biotechnology, Shanxi University, Taiyuan 030006, PR China.Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Institute of Biotechnology, Shanxi University, Taiyuan 030006, PR China.College of Life Science, Shanxi University, Taiyuan 030006, PR China.College of Life Science, Shanxi University, Taiyuan 030006, PR China. Electronic address: zhwang@sxu.edu.cn.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

28119052

Citation

Li, Jiao, et al. "RBTI Reduced Β-amyloid-induced Toxicity By Promoting Autophagy-lysosomal Degradation Via DAF-16 in Caenorhabditis Elegans." Experimental Gerontology, vol. 89, 2017, pp. 78-86.
Li J, Cui X, Ma X, et al. RBTI reduced β-amyloid-induced toxicity by promoting autophagy-lysosomal degradation via DAF-16 in Caenorhabditis elegans. Exp Gerontol. 2017;89:78-86.
Li, J., Cui, X., Ma, X., & Wang, Z. (2017). RBTI reduced β-amyloid-induced toxicity by promoting autophagy-lysosomal degradation via DAF-16 in Caenorhabditis elegans. Experimental Gerontology, 89, 78-86. https://doi.org/10.1016/j.exger.2017.01.018
Li J, et al. RBTI Reduced Β-amyloid-induced Toxicity By Promoting Autophagy-lysosomal Degradation Via DAF-16 in Caenorhabditis Elegans. Exp Gerontol. 2017;89:78-86. PubMed PMID: 28119052.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - rBTI reduced β-amyloid-induced toxicity by promoting autophagy-lysosomal degradation via DAF-16 in Caenorhabditis elegans. AU - Li,Jiao, AU - Cui,Xiaodong, AU - Ma,Xiaoli, AU - Wang,Zhuanhua, Y1 - 2017/01/22/ PY - 2016/11/09/received PY - 2017/01/17/revised PY - 2017/01/20/accepted PY - 2017/1/26/pubmed PY - 2017/10/27/medline PY - 2017/1/26/entrez KW - Alzheimer's disease KW - Autophagy KW - DAF-16 KW - rBTI KW - β-Amyloid SP - 78 EP - 86 JF - Experimental gerontology JO - Exp. Gerontol. VL - 89 N2 - Alzheimer's disease (AD) is an age-related neurodegenerative disease, of which β-amyloid (Aβ) induced toxicity was suggested as a main cause. Some substances with prolongevity effects have been shown to be protective against AD. In a previous study we demonstrated that a recombinant buckwheat trypsin inhibitor (rBTI) could prolonge the lifespan in Caenorhabditis elegans (C. elegans). Here, we investigated whether rBTI may benefit to mitigate the AD symptom by feeding the AD model C. elegans CL4176. CL4176 is a transgenic C. elegans expressing human Aβ3-42 in muscle tissue. The results showed that rBTI not only could extend lifespan but also could reduce Aβ toxicity-triggered body paralysis in AD worms. Further study found the accumulation of Aβ was decreased and autophagy-lysosomal degradation pathway was activated in AD worms treated with rBTI. Moreover, the inhibition of autophagy reduced rBTI-mediated paralysis delay. Genetic analyses showed rBTI increased the transcriptional activity of dauer formation abnormal-16 (DAF-16) and the disruption of daf-16 abolished rBTI-mediated protective effect in AD worms. Taken together, these data indicated that rBTI promoted the autophagy-lysosomal degradation pathway to reduce the Aβ-induced toxicity via DAF-16 in an AD model C. elegans, implying that BTI has the potential to protect against AD. SN - 1873-6815 UR - https://www.unboundmedicine.com/medline/citation/28119052/rBTI_reduced_β_amyloid_induced_toxicity_by_promoting_autophagy_lysosomal_degradation_via_DAF_16_in_Caenorhabditis_elegans_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0531-5565(16)30500-9 DB - PRIME DP - Unbound Medicine ER -