Objective To examine the molecular mechanisms of action of miR-92a-3p in ischemic stroke(IS).Methods Database analysis was performed to evaluate miR-92a-3p expression in patients with IS.Oxygen-glucose deprivation/reoxygenation(OGD/R)of HT22 hippocampal neurons was used as an in vitro IS model.PCR was performed to analyze miR-92a-3p expression in HT22 cells fol-lowing 2,4,6,and 8 h of OGD/R.Western blotting was used to analyze the protein expression levels of silent information regulator 1(SIRT1),an miR-92a-3p target gene,and the apoptosis-related protein caspase-3 in HT22 cells after 4 h of OGD/R.Middle cerebral artery occlusion(MCAO)was used as an animal model of IS.Western blotting and PCR were used to analyze the mRNA and protein expression levels of SIRT1 and caspase-3 in the brain tissues of mice following MCAO.Results Database analysis showed increased miR-92a-3p expression in fetal rat cortical neurons after 12 h of OGD and in the brain tissues of mice 3 days post-MCAO.Following 2,4,6,and 8 h of OGD/R in HT22 cells,the expression of miR-92a-3p increased,accompanied by decreased expression of SIRT1 and increased expres-sion of caspase-3.In the brain tissues of mice model of IS,SIRT1 expression decreased and caspase-3 expression increased.Conclusion miR-92a-3p is involved in IS by promoting neuronal apoptosis via SIRT1 inhibition.

Objective:To investigate the effect of riboflavin on cerebral infarction volume and the possible mecha-nism of apoptotic factors with cerebral ischemic injury in mice.Methods:Eighteen C57BL/6J male mice were divided into the sham group,middle cerebral artery occlusion(MCAO)group and riboflavin intervention group(MCAO+RF)randomly.TTC staining was used to observe the infarction of the cerebral tissues;Quantitative real-time PCR(RT-qPCR)was used to detect the mRNA expression of tumor protein p53(p53),cytochrome C(CytC),B-cell lymphoma-2(Bcl-2),Bcl-2-associated X(Bax),cysteinyl aspartate specific proteinase-3(caspase-3),poly ADP-ribose poly-merase(PARP),cysteinyl aspartate specific proteinase-6(caspase-6)and apoptosis inducing factor(AIF)in different groups,to study the possible mechanism of riboflavin inhibiting neuronal apoptosis.The proteins expression of acetyl-p53(AC-p53),caspase-3 and PARP were analyzed by Western blot.Results:Compared with the MCAO group,the cerebral infarct volume of the MCAO+RF group was obviously reduced(P＜0.01);The relative expression of p53,CytC,caspase-3,PARP,caspase-6 and AIF were significantly lower in the MCAO+RF group(P＜0.05).Addition-ally,significant differences were observed in the proteins expression of AC-p53,caspase-3 and PARP between the MCAO group and MCAO+RF group.Conclusion:Riboflavin has a protective effect against cerebral ischemic injury,which is possibly realized by inhibiting neuronal apoptosis through multiple pathways.

Objective:To investigate the effect of riboflavin on cerebral infarction volume and the possible mecha-nism of apoptotic factors with cerebral ischemic injury in mice.Methods:Eighteen C57BL/6J male mice were divided into the sham group,middle cerebral artery occlusion(MCAO)group and riboflavin intervention group(MCAO+RF)randomly.TTC staining was used to observe the infarction of the cerebral tissues;Quantitative real-time PCR(RT-qPCR)was used to detect the mRNA expression of tumor protein p53(p53),cytochrome C(CytC),B-cell lymphoma-2(Bcl-2),Bcl-2-associated X(Bax),cysteinyl aspartate specific proteinase-3(caspase-3),poly ADP-ribose poly-merase(PARP),cysteinyl aspartate specific proteinase-6(caspase-6)and apoptosis inducing factor(AIF)in different groups,to study the possible mechanism of riboflavin inhibiting neuronal apoptosis.The proteins expression of acetyl-p53(AC-p53),caspase-3 and PARP were analyzed by Western blot.Results:Compared with the MCAO group,the cerebral infarct volume of the MCAO+RF group was obviously reduced(P＜0.01);The relative expression of p53,CytC,caspase-3,PARP,caspase-6 and AIF were significantly lower in the MCAO+RF group(P＜0.05).Addition-ally,significant differences were observed in the proteins expression of AC-p53,caspase-3 and PARP between the MCAO group and MCAO+RF group.Conclusion:Riboflavin has a protective effect against cerebral ischemic injury,which is possibly realized by inhibiting neuronal apoptosis through multiple pathways.

Objective To examine the molecular mechanisms of action of miR-92a-3p in ischemic stroke(IS).Methods Database analysis was performed to evaluate miR-92a-3p expression in patients with IS.Oxygen-glucose deprivation/reoxygenation(OGD/R)of HT22 hippocampal neurons was used as an in vitro IS model.PCR was performed to analyze miR-92a-3p expression in HT22 cells fol-lowing 2,4,6,and 8 h of OGD/R.Western blotting was used to analyze the protein expression levels of silent information regulator 1(SIRT1),an miR-92a-3p target gene,and the apoptosis-related protein caspase-3 in HT22 cells after 4 h of OGD/R.Middle cerebral artery occlusion(MCAO)was used as an animal model of IS.Western blotting and PCR were used to analyze the mRNA and protein expression levels of SIRT1 and caspase-3 in the brain tissues of mice following MCAO.Results Database analysis showed increased miR-92a-3p expression in fetal rat cortical neurons after 12 h of OGD and in the brain tissues of mice 3 days post-MCAO.Following 2,4,6,and 8 h of OGD/R in HT22 cells,the expression of miR-92a-3p increased,accompanied by decreased expression of SIRT1 and increased expres-sion of caspase-3.In the brain tissues of mice model of IS,SIRT1 expression decreased and caspase-3 expression increased.Conclusion miR-92a-3p is involved in IS by promoting neuronal apoptosis via SIRT1 inhibition.