Protective effects of sulforaphen on neuronal apoptosis after focal cerebral ischemia reperfusion injury in rats

Objective To investigate the protective effects of sulforaphen (SFN) on focal cerebral ischemia/reperfusion injuy (IRI) in rats in order to explore the mechanisms.Methods Twenty-four male SD rats were randomly (random number) divided into Sham-operated group (A group,n =8),IRI group (B group,n =12),sulforaphen group (C group,n =8).SD rats were made to be transient focal cerebral IRI models.SFN 5 mg/kg was injected intraperitoneally to rats 15 minutes after IRI in C group,and rats of group A and group B received equal volume PBS instead.Infarct volume was measured by TTC staining and morphologic changes were observed with HE staining.Neuronal cell apoptosis index was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) assay.Rats were sacrificed at 24 h after IRI.The protein levels of NF-κB p65 and iNOS were detected by using western bloting and the mRNA expressions of NF-κB p65 and iNOS were detected by using RT-PCR.Results Compared with the group B,infarct volume was significantly smaller in group C,the number of neuronal cell apoptosis in brain tissue were decreased significantly in group C [(96.34 ±3.72) vs.(124.65 ±3.85),P ＜ 0.01],the levels of NF-κB and iNOS in brain tissue of rats were decreased in the SFN group (P ＜ 0.01).SFN reduced neuronal cell apoptosis,injury,and infarct volume [(0.26 ± 0.018) vs.(0.43 ±0.031),P ＜0.01].The mRNA expression and protein level of NF-κBp65 were decreased in the group C.And the mRNA expression and protein level of induced nitric oxide synthase (iNOS) in IRI affected brain tissue were decreased in the group C [(0.67 ± 0.042) vs.(0.56 ± 0.032),P ＜ 0.01].Conclusions SFN might decrease the neuronal cell apoptosis caused by ischemia/repeffusion injury,and this protective effect is mediated by decreasing the level of NF-κB and iNOS. Key words: Sulforaphen ;  Ischemia/reperfusion ;  Injury ;  Neuronal;  Apoptosis ;  TUNEL;  NF-κB ; iNOS