RESUMO
Objective To investigate the effects of penehyclidine hydrochloride (PHCD)on cerebral ischemia-reperfusion injury induced by intrauterine distress in fetal rats.Methods Eighty mature fetal rats weighing 4.52-4.81 g were randomly divided into four groups (n =20):sham opera-tion group(group S),PHCD control group (group S+ P),cerebral IR group (group IR),PHCD treatment group(group IR+P).Fetal rat intrauterine distress model was set up by clamping bilateral uterine horn vessels of pregnant rats.PHCD 2 mg/kg was injected in pregnant rat’s gluteus at 30 min before intrauterine distress model was set up in group IR+P,the same volume saline was injected in pregnant rat’s gluteus before shame operation in group S,the same volume PHCD was injected in pregnant rat’s gluteus before shame operation in group S+P.Fetal rats were decapitated at 12 h after the reperfusion,the peripheral blood of fetal rats was detected by blood gas analysis (including PH, PaO 2 ,PaCO 2 ,Lac);the infarct volume and the infarct volume fraction were detected by TTC stai-ning;pathological changes in lung tissue were observed by HE staining;the TNF-α,IL-6 content in the brain were detected by ELISA;the expression of NF-κB mRNA was detected by quantitative Real-time PCR,the expression of NF-κB p65 protein was detected by Western-blotting.Results The blood PH,PaO 2 in group IR and IR+P were lower than group S and S+P,the blood PH,PaO 2 in group IR+P was higher than group IR.Compared with group S and group S+P,the blood PaCO 2 , Lac,the infarct volume and the infarct volume fraction,the concentration of TNF-αand IL-6,the ex-pression of NF-κB mRNA and protein were significantly increased in group IR and IR+P (P <0.05), and those in group IR+P were lower than group IR (P <0.05 ).The pathological changes in brain tissue were significantly attenuated in group IR + P (P < 0.05 ).Conclusion Pretreatment with PHCDcouldattenuatecerebralischemia-reperfusioninjuryoffetalratsinducedbyintrauterinedistress. ThemechanismscouldrelatetotheinhibitionofNF-κBsignalingpathwayinbraintissues.