Therapeutic activity of plant-derived alkaloid conophylline on metabolic syndrome and neurodegenerative disease models

Increasing metabolic syndromes including type-2 diabetes mellitus, obesity, and steatohepatitis are serious problems in most countries in the world. Neurodegenerative diseases such as Alzheimer, Parkinson’s, and Huntington’s diseases are increasing in many countries. However, therapy for these disea...

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Bibliographic Details
Published in:Human cell : official journal of Human Cell Research Society 2018-04, Vol.31 (2), p.95-101
Main Authors: Umezawa, Kazuo, Kojima, Itaru, Simizu, Siro, Lin, Yinzhi, Fukatsu, Hitomi, Koide, Naoki, Nakade, Yukiomi, Yoneda, Masashi
Format: Article
Language:English
Subjects:
Animal models
Autophagy
Beta cells
Biomedical and Life Sciences
Cell Biology
Cell death
Chemotherapy
Cirrhosis
Diabetes
Diabetes mellitus
Fibrosis
Gynecology
Life Sciences
Liver
Liver cirrhosis
Metabolic syndrome
Metabolism
Neurodegenerative diseases
Oncology
Oral administration
Pancreas
Phagocytosis
Plants
Protein interaction
Reproductive Medicine
Review Article
Rodents
Stem Cells
Surgery
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Summary:Increasing metabolic syndromes including type-2 diabetes mellitus, obesity, and steatohepatitis are serious problems in most countries in the world. Neurodegenerative diseases such as Alzheimer, Parkinson’s, and Huntington’s diseases are increasing in many countries. However, therapy for these diseases is not sufficient yet. Thus, effective chemotherapy for these diseases is being expected. Conophylline is an alkaloid isolated from the leaves of Ervatamia microphylla and related plants. It was found to induce beta-cell differentiation in the precursor pancreatic cells. Oral administration of this compound ameliorated type-2 diabetes mellitus model in mice and rats. Later, fibrosis of the pancreatic islets was found to be greatly reduced by conophylline in the pancreatic islets. It also inhibited chemically induced liver cirrhosis. Further study indicated that conophylline inhibited non-alcoholic steatohepatitis in the model mice. On the one hand, loss of autophagy often causes protein aggregation to give neural cell death. Conophylline was found to activate autophagy in cultured neural cells. Activation of autophagy ameliorated cellular models of Parkinson’s and Huntington’s diseases. Thus, conophylline is likely to be useful for the development of chemotherapy for metabolic and neurodegenerative diseases.
ISSN:1749-0774
0914-7470
1749-0774
DOI:10.1007/s13577-017-0196-4