期刊
ACTA HISTOCHEMICA
卷 122, 期 3, 页码 -出版社
ELSEVIER GMBH
DOI: 10.1016/j.acthis.2020.151514
关键词
Andrographolide; Chronic cerebral hypoperfusion; Neuronal damage; PTEN/AKT signaling; Mechanism
类别
资金
- National Nature Science Foundation of China [81974207, 81771410]
- Priority of Shanghai key discipline of medicine [2017ZZ02020]
- Key Research and Development Program of Hunan Province [2016JC2073]
To explore the potential effects of andrographolide on chronic cerebral hypoperfusion (CCH)-induced neuronal damage as well as the underlying mechanisms. Rat CCH model was established by 2-vessel occlusion (2VO). The CCH rats received andrographolide treatment for 4 weeks. The neuron loss was detected by using neuronal nuclei (NeuN) immunofluorescent staining. The expression levels of phospho-phosphatase and tensin homolog deleted on chromosome ten (p-PTEN), protein kinase B (AKT), p-AKT, and cysteinyl aspartate specific proteinase-3 (Caspase-3) proteins were accessed by Western blotting. Moreover, the neuronal apoptosis of hippocampus tissues was detected via terminal deoxynucleotidyl transferase- mediated dUTP nick end labeling (TUNEL) staining. CCH reduced the number of NeuN-positive cells, while the number was significant increased after andrographolide treatment. CCH increased the proteins expression level of p-PTEN, Caspase-3, and decreased the p-AKT, which were reversed by andrographolide treatment. Furthermore, andrographolide treatment also down-regulated CCH-induced TUNEL-apoptosis rate. Our results suggest that the PTEN/AKT pathway may be modulated by andrographolide and the damaging effects of CCH on hippocampus may be ameliorated by andrographolide treatment. Andrographolide may act as a potential therapeutic approach for chronic ischemic insults.
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