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Objective To investigate the effect of different maturation methods on mitochondrial functions of oocytes and the possible mechanism. To explore novel ideas for developing assisted reproductive technology (ART). Methods Female mice were used as models and randomly allocated into three groups, COH, IVM and NC control. Oocytes maturated with different methods which were all simulated with those treatments in human IVF cycle. Immunofluorescence were used to measure the mitochondrial membrane potentials and analyze the cy-toskeleton. Results The mitochondrial membrane potential in the COH group was significantly lower than that in NC group and IVM group (P < 0.05). The proportion of normal cytoskeleton including spindle structure and chromosome configuration in the COH group and IVM group were significantly lower than that in the NC group (PCOH < 0.01, PIVM < 0.05). Conclusions Both COH and IVM can affect mitochondrial functions.
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Objective: To investigate the role of aldehyde dehydrogenase-2 (ALDH-2) for regulating human endothelial progenitor cells (EPCs) oxidative stress reaction and its mechanism. Methods: Human EPCs were isolated from peripheral blood of healthy adults and the cells were cultured in 4 groups:①Blank control group,②Alda-1 group, the cells were treated by 1μmol/L Alda-1, a speciifc activator of ALDH-2,③tBHP (10μg/ml) group and④Alda-1 pretreatment+tBHP group. EPCs reactive oxygen species (ROS) levels were evaluated by DCFH-DA staining, mitochondrial membrane potentials were detected by JC-1 method, migration capacity was measured by transwell chamber method and the activation of p38 signal pathway was examined by Western blot analysis. Results: Compared with Blank control group, ROS levels in tBHP group and Alda-1 pretreatment+tBHP group were (441.7 ± 24.8) % and (237.4 ± 12.0) %, allP<0.05. In Blank control group, tBHP group and Alda-1 pretreatment+tBHP group, the proportion of EPCs lost their mitochondrial membrane potentials were (5.7 ± 2.1) %, (81.7 ± 3.7) % and (37.4 ± 3.2) % respectively, allP<0.05; the number of EPCs migration were (108 ± 9)/HP, (22 ± 4)/HP and (67 ± 7)/HP respectively, allP<0.05. Compared with Blank control group, the activation of p38 signal pathway increased to (259.1 ± 7.7) % in tBHP group, while it was reduced to (186.4 ± 8.0) % in Alda-1 pretreatment+tBHP group. Conclusion: ALDH-2 could reduce ROS level in human EPCs, it may decrease mitochondrial membrane damage, protect migration which might be related to p38 signal pathway.
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@#Objective To investigate the effects of morroniside on hydrogen peroxide (H2O2)-induced apoptosis in SH-SY5Y neuroblastoma cells. Methods SH-SY5Y cells were pre-incubated with morroniside (1, 10, and 100 μmol/L) for 24 h prior to exposure to H2O2 (300～500 μmol/L) for 18 h. The content of malondialdehyde (MDA)，mitochondrial membrane potentials (MMP) and apoptosis ratio were determined. Results Pretreatment the cells with morroniside (1, 10 and 100 μmol/L) lowered the H2O2-induced MDA concentration and MMP, and inhibited the apoptosis. Conclusion Morroniside may protect the neurocyte from H2O2-induced apoptosis by lowered MDA and inhibits MMP.
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AIM:To observe the effect of preconditioning with pioglitazone on ischemia reperfusion/hypoxia reoxygenation-induced mitochondrial ultramicro-structure and membrane potential in rats. METHODS: Sprague-Dawley rats were randomly divided into four groups: sham-operated (SO) group, ischemia reperfusion (IR) group, pioglitazone preconditioning group (Pio-P) and 5-HD+pioglitazone (5-HD+Pio) group. Apart from the SO group, IR, Pio-P and 5-HD+Pio groups were subjected to 30 min ischemia and 4 h reperfusion. The heart was quickly removed for observing the structure of mitochondria and measurement of the apoptosis index (AI) by TUNEL. Primary cultured cardiomyocytes of Sprague-Dawley rats were divided into control, hypoxic reoxygenation (HR) and different concentrations of Pio-P group. JC-1 staining flowcytometry was adopted to examine mitochondrial membrane potential (?m). RESULTS: The injury of mitochondrial structure in IR group was severer than that in Pio-P group, while the difference between 5-HD+Pio group and IR group was not evident. Flameng score in Pio-P group(1.62?0.60) was significantly lower than that in IR group (2.75?1.09), P0.05). CONCLUSION: Pioglitazone protects the heart from ischemia reperfusion/ hypoxia reoxygenation injury evidenced by improving mitochondrial ultrastructure and lessening the loss of mitochondrial membrane potential, and decreasing apoptosis. The cardioprotective effects can be inhibited by the blocker of mitochondrial ATP-sensitive potassium channels.