Effect of Schisandra chinensis lignans on neuronal apoptosis and p-AKT expression of rats in cerebral ischemia injury model.
- Author:
En-Ping JIANG
;
Shuai-Qun WANG
;
Zhuo WANG
;
Chun-Rong YU
;
Jian-Guang CHEN
;
Chun-Yan YU
- Publication Type:Journal Article
- MeSH: Administration, Oral; Animals; Apoptosis; drug effects; Blotting, Western; Brain Ischemia; metabolism; pathology; prevention & control; Disease Models, Animal; Dose-Response Relationship, Drug; Immunohistochemistry; Lignans; administration & dosage; pharmacology; Male; Neurons; drug effects; metabolism; pathology; Phosphatidylinositol 3-Kinases; metabolism; Phosphorylation; Phytotherapy; Proto-Oncogene Proteins c-akt; metabolism; Proto-Oncogene Proteins c-bcl-2; metabolism; Rats; Rats, Sprague-Dawley; Schisandra; chemistry; Signal Transduction; drug effects; bcl-2-Associated X Protein; metabolism
- From: China Journal of Chinese Materia Medica 2014;39(9):1680-1684
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of Schisandra chinensis lignans (SCL) on neuronal apoptosis and PI3K/AKT signaling pathway of rats in the cerebral ischemia injury model, and study its possible mechanism.
METHODRats were orally administered SCL high, middle and low dose groups (100, 50, 25 mg x kg(-1)) for 14 days. The cerebral ischemia injury model was established by using the suture-occluded method to rate the neurological functions. The cerebral infarction area was observed by TTC staining. The pathological changes in brain tissues were determined by HE staining. Bcl-2 and Bax expressions were detected by immunohistochemical assay. The protein expressions of p-AKT and AKT were assayed by Western blotting.
RESULTCompared with the model group, SCL high, middle and low dose groups showed reduction in the cerebral infarction area to varying degrees, improve the pathological changes in brain tissues, promote the expression of apoptin Bcl-2 and p-AKT, and inhibit the expression of apoptin Bax.
CONCLUSIONSCL shows a protective effect on rats with cerebral ischemia injury. Its mechanism may be related to the increase in p-AKT ability and antiischemic brain injury capacity and the inhibition of nerve cells.