旨在探究线粒体靶向抗氧化剂Mito-TEMPO在鸡精液冷冻保存中的应用效果,为鸡精液解冻后的精子品质提高提供依据。在精液冷冻稀释液中添加不同浓度的Mito-TEMPO(0、20、40、60和80μmol/m L),检测解冻后鸡精子的质量指标、抗氧化性能和线...旨在探究线粒体靶向抗氧化剂Mito-TEMPO在鸡精液冷冻保存中的应用效果,为鸡精液解冻后的精子品质提高提供依据。在精液冷冻稀释液中添加不同浓度的Mito-TEMPO(0、20、40、60和80μmol/m L),检测解冻后鸡精子的质量指标、抗氧化性能和线粒体酶活性。结果:与对照组(0μmol/m L Mito-TEMPO)相比,添加40μmol/m L Mito-TEMPO时,解冻后鸡精子的活性、线粒体活性以及顶体、质膜和DNA完整率均显著提高(P<0.05);线粒体超氧化物歧化酶(SOD)、总抗氧化能力(T-AOC)和过氧化氢酶(CAT)活性显著提高(P<0.05);琥珀酸脱氢酶(SDH)、L-乳酸脱氢酶(L-LDH)和谷草转氨酶(GOT)活性及丙二醛(MDA)含量显著降低(P<0.05)。结论:在鸡精液冷冻稀释液中添加40μmol/m L的Mito-TEMPO可显著改善解冻后精子的活率和活力,有效保护精子的质膜、顶体和DNA的完整性,提高精子的抗氧化能力和线粒体活性,并减少线粒体相关酶的活性,显著改善鸡精子解冻后的质量。展开更多
OBJECTIVE Mitochondrial dys⁃function contributes to the pathogenesis of neuro⁃degenerative diseases such as Parkinson dis⁃ease(PD).Therapeutic strategies targeting mito⁃chondrial dysfunction hold considerable promise ...OBJECTIVE Mitochondrial dys⁃function contributes to the pathogenesis of neuro⁃degenerative diseases such as Parkinson dis⁃ease(PD).Therapeutic strategies targeting mito⁃chondrial dysfunction hold considerable promise for the treatment of PD.Urolithin A(UA)is a gut metabolite produced from ellagic acid-containing foods such as pomegranates,berries,and wal⁃nuts.Recent reports have highlighted the protec⁃tive role of UA in several neurological disorders including Alzheimer disease and ischemic stroke.However,the potential role of UA in PD has not been characterized.In this study,the role of UA in 6-OHDA-induced neurotoxicity in cell cultures and mouse model of PD was investi⁃gated.METHODS In vitro,PC12 cells were exposed to 6-OHDA in the presence or absence of UA.For in vivo study,C57BL/6 mice were ste⁃reotactic injected with 6-OHDA to induce experi⁃mental PD model.UA(10 mg·kg-1)was intraperi⁃toneal injected for 7 d before surgery.RESULTS UA protected against 6-OHDA cytotoxicity and apoptosis in PC12 cells.Prior administration of UA to 6-OHDA lesioned mice ameliorated both motor deficits and nigral-straital dopaminergic neurotoxicity.Moreover,UA attenuated 6-OHDA-induced mitochondrial dysfunction in PC12 cells accompanied by enhanced mitochondrial biogen⁃esis.Mechanically,the neuroprotective effects of UA were mediated by SIRT1-PGC-1αsignaling-mediated mitochondrial biogenesis.CONCLU⁃SION These data provide new insights into the novel role of UA in promoting mitochondria bio⁃genesis and suggest that UA may have potential therapeutic applications for PD.展开更多
文摘旨在探究线粒体靶向抗氧化剂Mito-TEMPO在鸡精液冷冻保存中的应用效果,为鸡精液解冻后的精子品质提高提供依据。在精液冷冻稀释液中添加不同浓度的Mito-TEMPO(0、20、40、60和80μmol/m L),检测解冻后鸡精子的质量指标、抗氧化性能和线粒体酶活性。结果:与对照组(0μmol/m L Mito-TEMPO)相比,添加40μmol/m L Mito-TEMPO时,解冻后鸡精子的活性、线粒体活性以及顶体、质膜和DNA完整率均显著提高(P<0.05);线粒体超氧化物歧化酶(SOD)、总抗氧化能力(T-AOC)和过氧化氢酶(CAT)活性显著提高(P<0.05);琥珀酸脱氢酶(SDH)、L-乳酸脱氢酶(L-LDH)和谷草转氨酶(GOT)活性及丙二醛(MDA)含量显著降低(P<0.05)。结论:在鸡精液冷冻稀释液中添加40μmol/m L的Mito-TEMPO可显著改善解冻后精子的活率和活力,有效保护精子的质膜、顶体和DNA的完整性,提高精子的抗氧化能力和线粒体活性,并减少线粒体相关酶的活性,显著改善鸡精子解冻后的质量。
文摘OBJECTIVE Mitochondrial dys⁃function contributes to the pathogenesis of neuro⁃degenerative diseases such as Parkinson dis⁃ease(PD).Therapeutic strategies targeting mito⁃chondrial dysfunction hold considerable promise for the treatment of PD.Urolithin A(UA)is a gut metabolite produced from ellagic acid-containing foods such as pomegranates,berries,and wal⁃nuts.Recent reports have highlighted the protec⁃tive role of UA in several neurological disorders including Alzheimer disease and ischemic stroke.However,the potential role of UA in PD has not been characterized.In this study,the role of UA in 6-OHDA-induced neurotoxicity in cell cultures and mouse model of PD was investi⁃gated.METHODS In vitro,PC12 cells were exposed to 6-OHDA in the presence or absence of UA.For in vivo study,C57BL/6 mice were ste⁃reotactic injected with 6-OHDA to induce experi⁃mental PD model.UA(10 mg·kg-1)was intraperi⁃toneal injected for 7 d before surgery.RESULTS UA protected against 6-OHDA cytotoxicity and apoptosis in PC12 cells.Prior administration of UA to 6-OHDA lesioned mice ameliorated both motor deficits and nigral-straital dopaminergic neurotoxicity.Moreover,UA attenuated 6-OHDA-induced mitochondrial dysfunction in PC12 cells accompanied by enhanced mitochondrial biogen⁃esis.Mechanically,the neuroprotective effects of UA were mediated by SIRT1-PGC-1αsignaling-mediated mitochondrial biogenesis.CONCLU⁃SION These data provide new insights into the novel role of UA in promoting mitochondria bio⁃genesis and suggest that UA may have potential therapeutic applications for PD.
