Effect of Modified Ditantang on Autophagy and Relevant Proteins in Brain Cells of Rats with Cerebral Ischemia Reperfusion Injury / 中国实验方剂学杂志
Chinese Journal of Experimental Traditional Medical Formulae
; (24): 64-69, 2019.
Article
en Zh
| WPRIM
| ID: wpr-802335
Biblioteca responsable:
WPRO
ABSTRACT
Objective:To investigate the effect of modified Ditantang on autophagy and relevant proteins in brain cells of rats with cerebral ischemia reperfusion injury. Method:The cerebral ischemic reperfusion (CIR) injury model in rats was built by reversible middle cerebral artery occlusion artery suture of middle cerebral embolism method, and randomly divided into sham group, model group, high-dose modified Ditantang group(H-dose), low-dose modified Ditantang group (L-dose, 0.384 g·kg-1) and PLXT group (0.1 g·kg-1). Sham and model groups were given normal saline by gastric perfusion, H-dose and L-dose groups were given modified Ditantang, and the PLXT group were given Piracetam tablets, intragastric volume 10 mL·kg-1. The treatment lasted for 7 d. Within 24 hours after administration, the histopathological examination was performed, the volume of cerebral infarction, neuronal apoptosis and serum levels of inflammatory factors were compared, and the expressions of autophagy related microtuble-associated protein 1 light chain 3(LC3)Ⅱ, Beclin1, B-cell lymphoma-2(Bcl-2) and p62 in brain tissues were determined. Result:Cells and blood vessel necrosis, neuron swelling and interstitial edema were observed in model group, a few neurons died, edema was reduced, swelling of nerve cells was alleviated in H-dose, L-dose and PLXT groups. The volume of cerebral infarction and neuronal apoptosis in H-dose, L-dose and PLXT groups were lower than those in model group (Pα, intedeukin (IL)-2 and IL-8 in H-dose, L-dose and PLXT groups were lower than those in model group (PPConclusion:Modified Ditantang can improve brain injury and interfere with autophagy after MCAO/R, alleviate inflammation, and regulate autophagic activity, which may be related to the down-regulation of expressions of LC3 Ⅱ, Beclin1 and the up-regulation of expression of p62.
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Banco de datos:
WPRIM
Tipo de estudio:
Prognostic_studies
Idioma:
Zh
Año:
2019
Tipo del documento:
Article