Reduction in Ischemic Cerebral Infarction is Mediated through Golgi Phosphoprotein 3 and Akt/mTOR Signaling Following Salvianolate Administration
Hong You, Ting Li, Jinnan Zhang, Qiang Lei, Xi Tao, Pinghui Xie and Wei Lu
Affiliation: Department of Neurology, The Second Xiangya Hospital, Central South University, Changsha, 410011, P.R. China.
Salvianolate has been reported to possess protective properties. However, its specific mechanisms have yet to
be identified. Our study aimed to identify the molecular mechanism of antioxidative stress function of salvianolate on rat
ischemia and reperfusion brain tissues. Rats were randomly distributed into three experimental groups: sham, model and
intervention . All animal neurobehavioral tests were performed at the end of 72-h reperfusion per Longa’s method, and
rats with a score of 0 (no neurological deficit) or 4 (severe neurological deficit with impaired consciousness) were
excluded. Brain slices were obtained after 72 h of reperfusion and stained with triphenyltetrazolium chloride. Western blot
analysis and quantitative real-time polymerase chain reaction (qRT–PCR) were used to determine levels of GOLPH3,
Akt/p-Akt, and mTOR/p-mTOR expressions in ischemic cortex. Salvianolate (18mg/kg intraperitoneal injection)
significantly decreased the neurological deficit scores of rats in groups of 72 h I/R and reduced the number of TUNELpositive
cells in the cerebral cortex when given at onset and at 24 and 48 h after reperfusion, leading to decreased cerebral
infarction in rats after ischemia/reperfusion injury. Results of Western blot and qRT-PCR showed that salvianolate could
significantly upregulate the expression of Golgi phosphoprotein-3 as well as the phosphorylation of Akt and mTOR.
Above findings indicate that salvianolate exerts potent and long-term neuroprotective effects in the model of cerebral I/R,
and Golgi phosphoprotein-3 and its downstream activation of Akt/mTOR signaling pathway may provide a new insight
for the antioxidative effect of salvianolate.
Keywords: Apoptosis, cerebral ischemia- reperfusion injury, , mammalian target of rapamycin;
neuroprotection, protein kinase B, salvianolate, salvianolic acid B.
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