Send to

Choose Destination
Mol Med Rep. 2018 Jan;17(1):1963-1969. doi: 10.3892/mmr.2017.8085. Epub 2017 Nov 15.

Curcumin improves diabetes mellitus‑associated cerebral infarction by increasing the expression of GLUT1 and GLUT3.

Author information

Vascular Ultrasonography Department, Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China.
Structural Heart Disease Department, Fuwai Hospital, Chinese Academy of Medical Sciences, Beijing 100037, P.R. China.
Radiology Department, Daqing Longnan Hospital, Daqing, Heilongjiang 163453, P.R. China.
Traditional Chinese Medicine Department, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, P.R. China.


Curcumin is characterized by anti‑inflammatory, anti‑oxidative, antiviral, antifibrotic, anticoagulation and glucose regulatory functions. However, whether it is protective in diabetes mellitus‑associated cerebral infarction remains to be fully elucidated. In the present study, it was demonstrated for the first time, to the best of our knowledge, that curcumin markedly improved neurological deficits, cerebral infarct volume and brain edema rate following middle cerebral artery occlusion (MCAO) surgery. It was also shown that the expression levels of glucose transporter (GLUT)1 and GLUT3 were reduced in the MCAO group. However, following curcumin treatment, the levels of GLUT1 and GLUT3 were markedly increased. In addition, curcumin markedly decreased cell apoptosis, indicating an anti‑apoptotic role of curcumin in the brain. To further evaluate whether curcumin prevented cell apoptosis by modulating the expression of GLUT1 and GLUT3, small interfering RNAs targeting GLUT1 and GLUT3 were selected. It was found that the knockdown of GLUT1 and GLUT3 inhibited the abundance of GLUT1, GLUT3 and B‑cell lymphoma 2, even following incubation with curcumin. These data showed that curcumin protected brain cells from apoptosis and cerebral infarction, predominantly by upregulating GLUT1 and GLUT3.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Spandidos Publications
Loading ...
Support Center