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Injury of hippocampal neurons in status epilepticus (SE) SD rats kindled by pentylenetetrazol (PTZ) were studied, and the changes of apoptosis neurons, protein expression of Bad and Bcl-2 alone and combined application of phosphatidyl inositol 3-kinase (PI3K) inhibitor LY294002 and recombinant human erythropoietin (rHuEpo) were evaluated for the possible mechanisms of rHuEpo. The SE rats kindled by the PTZ were randomly divided into normal control group [normal saline (NS)], model group (PTZ + NS), rHuEpo treated group (PTZ + rHuEpo), LY294002 treated group (PTZ + LY294002 + rHuEpo) and LY294002 control group (rHuEpo + PTZ + DMSO). Apoptosis of hippocampal neurons was detected by TUNEL method; expression of phosphorylation protein kinase B (p-PKB/p-Akt), Bcl-2 and Bad were detected by immunohistochemistry; the expression of Bcl-2 mRNA, Bad mRNA in hippocampal neurons of rats were detected through reverse transcription polymerase chain reaction (RT-PCR); the expression of Akt, p-Akt and Bcl-2, Bad protein in hippocampal neurons of rats were detected by western blotting. The amount of apoptotic neurons was less in the rHuEpo treated group and the LY294002 control group than in the LY294002 treated group (P<0.05). The expression of p-Akt protein and Bcl-2 protein increased while the Bad protein decreased significantly in the rHuEpo treated group and the LY294002 control group compared with the LY294002 treated group (P<0.05). The expression of Bad protein and Bad mRNA in hippocampus increased while the p-Akt, Bcl-2, Bcl-2 mRNA decreased significantly in the LY294002 treated group compared with the rHuEpo treated group (P<0.05). The PI3K/Akt signaling pathway is one of the pathways of rHuEpo neuroprotective effects and was confirmed from both the of positive and negative aspects. rHuEpo regulates the expression of mitochondrial apoptotic pathway related factors Bad and Bcl-2 to inhibit apoptosis and promotes neuronal survival.

Background- In-stent restenosis (ISR) is a critical issue of endovascular therapy. The predictors for ISR are not fully explored. We aimed to investigate the predictors for ISR, especially the effect of collateral circulation on ISR after cerebral large artery stenting. Methods- From June, 2015 to June, 2018, a total of 312 patients, who performed stenting, with severe cerebral anterior circulation stenosis (≥ 70%), were enrolled. According to the flow velocity indicated by carotid artery ultrasound or Transcranial Doppler, the patients were divided into the ISR and no-ISR groups. Clinical data were collected, including age, sex, cerebrovascular risk factors, preoperative serum lipid, inflammatory markers, and platelet count, stent site, residual stenosis rate, drug therapy after stenting. The collateral circulation was graded according to digital subtraction angiography (DSA). Univariable and multivariable logistic regression analyses were performed to assess the potential risk factors related to restenosis in such patients. Results- Higher residual stenosis rate (median 11% vs 10%, p = 0.040), fewer patients received standard drug therapy ( 73.3% vs 89.4%, p = 0.001), more patients with poor collateral circulation (70.0% vs 41.0%, p = 0.007) were found in ISR group. Residual stenosis rate increased by 10% was associated with a 19.1% increase in restenosis risk. Good collateral circulation (OR 0.16, [95%CI, 0.04–0.49]; p = 0.002) and receiving standard drug therapy (OR 0.14, [95%CI, 0.05–0.58]; p = 0.002) were significantly related to the lower risk of ISR. Conclusion- Collateral circulation is an independent factor related with ISR after successful cerebral anterior circulation large artery stenting, and long-term standard drug therapy after stenting should be strictly carried out in such patients.

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