title: Neuroprotection against oxidative injury by a nucleic acid-based health product (Squina DNA) through enhancing mitochondrial antioxidant status and functional capacity.
abstract: High levels of reactive oxygen species inflict oxidative damage on various cellular components that eventually culminate in a variety of diseases. This study investigated the cytoprotective effects of a nucleic acid-based health product (Squina [Hong Kong, China] DNA) against oxidative stress, particularly in neuronal cells. Adult female Sprague-Dawley rats were treated with Squina DNA, and changes in mitochondrial antioxidant status and functional capacity were assessed by the activities of antioxidant enzymes and ATP generation capacity in brain, heart ventricular, kidney, skeletal muscle, and liver tissues of control and Squina DNA-treated rats. The effects of Squina DNA pretreatment on brain/neuronal cell injury were investigated in a rat model of cerebral ischemia/reperfusion (I/R) injury and a neuroblastoma SH-SY5Y cell model of β-amyloid (Aβ) protein fragment 25-35-induced toxicity. Long-term Squina DNA treatment caused dose-dependent increases in mitochondrial antioxidant status and functional capacity in rat brain, heart ventricular, kidney, skeletal muscle, and liver tissues. Squina DNA pretreatment significantly prevented I/R injury in brain tissue. The cerebroprotection was associated with a reversal of I/R-induced impairment in mitochondrial antioxidant status and disruption in membrane integrity. Squina DNA ethanol extract also significantly inhibited the Aβ-induced apoptosis in SH-SY5Y neuronal cells, as evidenced by less caspase 3 and caspase 9 activation as well as mitochondrial cytochrome c release in Aβ-challenged cells. Squina DNA may enhance the resistance of tissues and cells to oxidative stress, particularly in pathological conditions such as stroke and aging-related neurodegenerative diseases.
authors.affiliation: Division of Life Science, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong SAR, China.
authors.forename: Phillip Y
authors.initials: PY
authors.lastname: Lam
authors.forename: Na
authors.initials: N
authors.lastname: Chen
authors.forename: Po Yee
authors.initials: PY
authors.lastname: Chiu
authors.forename: Hoi Yan
authors.initials: HY
authors.lastname: Leung
authors.forename: Kam Ming
authors.initials: KM
authors.lastname: Ko
mesh_terms: D016229:Amyloid beta-Peptides; D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D001688:Biological Products / Q000494:pharmacology / Q000627:therapeutic use; D001921:Brain / Q000187:drug effects*; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism; D020169:Caspases / Q000378:metabolism; D045744:Cell Line, Tumor; D045304:Cytochromes c / Q000378:metabolism; D004247:DNA / Q000494:pharmacology / Q000627:therapeutic use*; D004305:Dose-Response Relationship, Drug; D005260:Female; D006352:Heart Ventricles / Q000187:drug effects; D007668:Kidney / Q000187:drug effects; D008099:Liver / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D051336:Mitochondrial Membranes / Q000187:drug effects; D018482:Muscle, Skeletal / Q000187:drug effects; D019636:Neurodegenerative Diseases / Q000188:drug therapy; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D012474:Salmon; D020521:Stroke / Q000188:drug therapy
chemical_list: D016229:Amyloid beta-Peptides; D000975:Antioxidants; D001688:Biological Products; D018696:Neuroprotective Agents; D045304:Cytochromes c; D004247:DNA; D020169:Caspases