- Author:
Lu GAN
1
,
2
,
3
;
Zhen Hua WANG
4
;
Hong ZHANG
1
;
Rong ZHOU
1
;
Chao SUN
1
;
Yang LIU
1
;
Jing SI
1
;
Yuan Yuan LIU
1
;
Zhen Guo WANG
5
Author Information
- Publication Type:Letter
- MeSH: Animals; Antioxidants; pharmacology; Brain Injuries; prevention & control; Catalase; metabolism; Heavy Ion Radiotherapy; Male; Malondialdehyde; metabolism; Mice; Naphthoquinones; pharmacology; Protein Carbonylation; Radiation Injuries, Experimental; prevention & control; Radiation-Protective Agents; pharmacology; Random Allocation; Specific Pathogen-Free Organisms; Superoxide Dismutase; metabolism
- From: Biomedical and Environmental Sciences 2015;28(2):148-151
- CountryChina
- Language:English
- Abstract: Radiation encephalopathy is the main complication of cranial radiotherapy. It can cause necrosis of brain tissue and cognitive dysfunction. Our previous work had proved that a natural antioxidant shikonin possessed protective effect on cerebral ischemic injury. Here we investigated the effects of shikonin on carbon ion beam induced radiation brain injury in mice. Pretreatment with shikonin significantly increased the SOD and CAT activities and the ratio of GSH/GSSG in mouse brain tissues compared with irradiated group (P<0.01), while obviously reduced the MDA and PCO contents and the ROS levels derived from of the brain mitochondria. The shikonin also noticeably improved the spatial memory deficits caused by carbon ion beam irradiation. All results demonstrated that shikonin could improve the irradiated brain injury which might resulted from its modulation effects on the oxidative stress induced by the 12C6+ ion beam.