Cerebrolysin reduces amyloid-beta deposits, apoptosis and autophagy in the thalamus and improves functional recovery after cortical infarction

作者：Xing Shihui; Zhang Jian; Dang Chao; Liu Gang; Zhang Yusheng; Li Jingjing; Fan Yuhua; Pei Zhong; Zeng Jinsheng^*

来源：Journal of the Neurological Sciences, 2014, 337(1-2): 104-111.

DOI：10.1016/j.jns.2013.11.028

• Cerebrolysin
• Amyloid-beta
• Apoptosis
• Autophagy
• Thalamus
• Cerebral infarction

Focal cerebral infarction causes amyloid-beta (A beta) deposits and secondary thalamic neuronal degeneration. The present study aimed to determine the protective effects of Cerebrolysin on A beta deposits and secondary neuronal damage in thalamus after cerebral infarction. At 24 h after distal middle cerebral artery occlusion (MCAO), Cerebrolysin (5 ml/kg) or saline as control was once daily administered for consecutive 13 days by intraperitoneal injection. Sensory function and secondary thalamic damage were assessed with adhesive-removal test, Nissl staining and immunofluorescence at 14 days after MCAO. A beta deposits, activity of beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1), apoptosis and autophagy were determined by TUNEL staining, immunofluorescence and immunoblot. The results showed that Cerebrolysin significantly improved sensory deficit compared to controls (p < 0.05). A beta deposits and BACE1 were obviously reduced by Cerebrolysin, which was accompanied by decreases in neuronal loss and astroglial activation compared to controls (all p < 0.05). Coincidently, Cerebrolysin markedly inhibited cleaved caspase-3, conversion of LC3-II, downregulation of Bcl-2 and upregulation of Bax in the ipsilateral thalamus compared to controls (all p < 0.05). These findings suggest that Cerebrolysin reduces A beta deposits, apoptosis and autophagy in the ipsilateral thalamus, which may be associated with amelioration of secondary thalamic damage and functional recovery after cerebral infarction.

• 单位
  2; 中山大学; 1