Effects Of Maternal Limb Ischemic Preconditioning On Mitochondrion Construction And Function Of The Fetal Hippocampal Neurons Induced By Intrauterine Distress-reoxygenation In Rats

Object: To investigate the influences of maternal limb ischemic preconditioning onmitochondrion constructions and functions of the hippocampal neurons induced byreoxygenation in the intrauterine distress fetal rats.Methods: The pregnant Sprague Dawley rats were anesthetized and underwentlaparotomy on embryonic Day20. Intrauterine ischemia was induced by clamping thearteriovenous of the uterine and ovarian with aneurysm clamps for15min, followedby reperfusion through removal of the clamps. At the same time, limb ischemicpreconditioning in the pregnant rats was generated by occlusion of the right hindfemoral artery for5min followed by reperfusion for the same period. The cycle wasrepeated for three times.24pregnant rats were randomly assigned into4groups: sham(S) group, control (LIP) group, fetal distress (FD) group and fetal distress that receiveLIP (LIP+FD) group. The fetal rats were obtained through the Cesarean Section onembryonic Day21, and the brain tissue was selected. Six live fetal rats were requiredfor each group. The ultrastructure of mitochondrion in the CA1area of thehippocampus was observed with transmission electron microscope. The mitochondrialmembrane potential and reactive oxygen species (ROS) were measured by the flowcytometer. The content of ATP in the hippocampus tissue was measured; The activityof Mn-SOD and the content of MDA were measured with colorimetric method.Result (1) Compared with the sham group, the normal morphology of mitochondrionin the CA1area of the hippocampus was observed in the LIP group. Themitochondrial membrane potential, the content of ROS, ATP and MDA and the activity of Mn-SOD were unchanged.（P>0.05）(2) Compared with the sham group,the number of mitochondrion in the CA1area of the hippocampus was decreased inthe FD group. The mitochondrion was swollen severely. A part of mitochondria ridgewas fractured or disappeared and even vacuolization. The mitochondrial membranepotential was decreased（P<0.05）, as well as the content of ATP（P<0.05）and theactivity of Mn-SOD（P<0.05）. However, the content of ROS and MDA was increased（P<0.05）.(3) Compared with the sham group, the mitochondrion in the CA1area ofthe hippocampus was swollen slightly in the LIP plus FD group. The mitochondriaridge was fractured partially. The membrane of mitochondrion was intact. Themitochondrial membrane potential（P<0.05） and the content of ATP were decreased（P<0.05）, as well as the activity of Mn-SOD（P<0.05）. The content of ROS andMDA was increased（P<0.05）.(4) Compared with the FD group, the ultrastructure ofmitochondrion in the CA1area of the hippocampus was intact; the swelling ofmitochondrion was released; furthermore, the reduced mitochondrial membranepotential and the ATP content were inhibited（P<0.05）. The activity of Mn-SOD wasincreased（P<0.05）, but the content of MDA was decreased（P<0.05） in the LIP plusFD group.Conclusion The limb ischemia preconditioning inhibited the damage on theultrastructure of mitochondrion induced by reoxygenation in the intrauterine distressfetal rats. The limb ischemia preconditioning could enhance the ability ofmitochondrion to remove oxygen free radicals and improve the function ofmitochondrion through reducing the decreased mitochondrial membrane potential,increasing the content of ATP and reducing the generation of ROS.