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Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation with Modulation of Autophagy and Inflammation

Authors Zhang Y, Tian Z, Wan H, Liu W, Kong F, Ma G

Received 20 August 2019

Accepted for publication 6 January 2020

Published 31 March 2020 Volume 2020:16 Pages 871—879


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Yuping Ning

Yi Zhang,1 Zhiming Tian,1 Hongyan Wan,1 Wen Liu,1 Fanping Kong,2 Guoping Ma3

1Cerebral Vascular Center, Zhongda Hospital, Southeast University, Nanjing City, Jiangsu Province 210044, People’s Republic of China; 2Department of Neurology, Fu-Ning People’s Hospital, Yancheng City, Jiangsu Province 224400, People’s Republic of China; 3Department of Neurology, Tian-Shui First People’s Hospital, Tianshui City, Gansu Province 741000, People’s Republic of China

Correspondence: Fanping Kong
Department of Neurology, Fu-Ning People’s Hospital, No. 111 Bucheng Street, Yancheng City, Jiangsu Province 224400, People’s Republic of China

Guoping Ma
Department of Neurology, Tian-Shui First People’s Hospital, No. 105 Jianshe Road, Tianshui City, Gansu Province 741000, People’s Republic of China

Introduction: Deltonin, an active component extracted from Dioscorea zingiberensis C.H. WRIGHT, was widely utilized in traditional Chinese medicines. It has been shown to have anti-cancer functions such as colon cancer, breast cancer, and head and neck squamous carcinoma. Herein, we will investigate the role of deltonin in cerebral ischemia/reperfusion injuries.
Methods: Ly294002 and anisomycin were used as inhibitors to monitor the effects of deltonin. Middle cerebral artery occlusion I/R model was constructed. Infarct volumes, neurological deficits and brain water contents were evaluated under different conditions. Rotarod test, ELISA, and Western blotting were carried to investigate the effects in vitro.
Results: We found that deltonin in ischemia/reperfusion (I/R) rats greatly enhanced brain damages as well as neurological functions through up-regulating p-Akt and p-mTOR as well as inhibiting the expressions of LC3-II/LC3-I, Beclin-1, IL-1, TLR4, and p-p38. Deltonin exerted neuroprotection effect through relieving autophagy activity by regulating PI3K/Akt/mTOR signaling. Deltonin suppressed inflammation reactions through modulation TLR4/p38/MAPK signaling as well.
Conclusion: Overall, our data suggested that deltonin could suppress ischemic brain injury by regulating autophagy and inflammation during I/R. Deltonin can be a potential therapeutic method for patient with I/R.

Keywords: deltonin, cerebral I/R, MCAO/R, autophagy, inflammation

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