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Modulation of autophagy in ischemic penumbra by hydroxysafflor yellow A after cerebral ischemia/reperfusion injury / 中国病理生理杂志
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-510781
Responsible library: WPRO
ABSTRACT

AIM:

To clarify the modulation of autophagy in ischemic penumbra by hydroxysafflor yellow A ( HSYA) after cerebral ischemia/reperfusion ( I/R) injury.

METHODS:

Male SD rats subjected to transient middle cere-bral artery occlusion for 90 min were randomly divided into 4 groupssham-operation (sham) group, cerebral I/R (I/R) group, I/R+HSYA group and sham+HSYA group.Modified neurological severity score (mNSS) was used to evaluate the neurological deficits of the rats at 6 h, 1 d, 3 d and 7 d after reperfusion , accompanied by the detection of autophagy , apoptosis and mRNA expression of IFN-βin ischemic penumbra .

RESULTS:

Compared with sham group , upregulation of LC3-Ⅱand degradation of SQSTM1/P62 were observed in I/R group, indicating the activation of autophagy after I/R.The activation of autophagy in I/R+HSYA group was significantly enhanced by HSYA on day 1 and day 3, and inhibited on day 7, as compared with I/R group (P<0.05).Besides, the mRNA expression of IFN-βin I/R group was significantly upregulated at 6 h, then downregulated on day 1 and day 3, and returned to basal level on day 7, as compared with sham group (P<0.05).In I/R+HSYA group, the mRNA expression of IFN-βwas significantly upregulated on day 1 and day 3, accompanied by the inhibition of apoptosis on day 3 and the significantly decreased mNSS from day 4, as compared with I/R group (P<0.05).

CONCLUSION:

HSYA alleviates cerebral I/R injury by dynamically modulating the activation of autophagy and the expression of IFN-βin ischemic penumbra .

Full text: Available Database: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2017 Document type: Article
Full text: Available Database: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2017 Document type: Article
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