Study on neuroprotective mechanism of salidroside after ischemic stroke based on TGF-β1/Smad3 signaling pathway / 中草药

ABSTRACT

Objective: To investigate the neuroprotective mechanism of salidroside after ischemic stroke and its regulation mechanism in TGF-β1/Smad3 signaling pathway. Methods: A total of 48 SPF SD male rats aged 12-15 weeks were randomly divided into four groups (n = 12) Sham-operated group (sham group), model group, salidroside group (treatment group), and signaling pathway-enhanced intervention group (TGF-β1 group). In the model group, treatment group, and TGF-β1 group, a permanent focal cerebral ischemia rat model was established by suture method, and the sham group was not inserted with nylon thread. 48 h before the modeling operation, the treatment group and the TGF-β1 group were given drug intervention at a fixed time every morning the treatment group was administered with 10 mg/kg salidroside ventricle, and the TGF-β1 group was treated with 20 mg/kg TGF-β1. The intraventricular injection was administered, and the sham group and the model group were given an equal volume of physiological saline. After 14 d of continuous administration, each group of rats was sacrificed by decapitation. TTC staining, Nissl staining, TUNEL staining, immunofluorescence, and Western blot were used to determine the infarct volume, the number of intact neurons, the cell apoptosis, the expression of Bax and Bcl-2 expression, the expression levels of Bax, Bcl-2, TGF-β1, and p-Smad3. The ultrastructural changes of brain tissue were observed by electron microscopy. Results: Compared with the sham group, the cerebral infarction volume of the model group was significantly increased, the number of intact neurons in the brain tissue was significantly reduced, the apoptosis rate of nerve cells was significantly increased, and the expression of Bax was significantly increased, the expression of Bax was significantly decreased. The expression of TGF-β1 and p-Smad3 was significantly increased, and the difference was statistically significant (P 0.05). Conclusion: Salidroside can activate the TGF-β1/Smad3 signaling pathway after ischemic stroke, thereby alleviating neurological damage and exerting protective effects on nerve cells.