cytochrome-c-t and Cerebrovascular-Disorders

Cerebrovascular disease (CVD) is one of the leading causes of mortality worldwide. The role of cytochrome c oxidase subunit 6B1 (COX6B1) in the central nervous system remains unclear. The present study aimed to analyze the role of COX6B1 in rat hippocampal neurons extracted from fetal rats. The subcellular localization of the neuron‑specific marker microtubule‑associated protein 2 was detected by immunofluorescence assay. Cell viability was assessed using a cell counting kit, and the levels of apoptosis and cytosolic Ca2+ were analyzed by flow cytometry. The expression levels of the molecular factors downstream to COX6B1 were determined using reverse transcription‑quantitative polymerase chain reaction and western blotting. Reoxygenation following oxygen‑glucose deprivation (OGD) decreased cell viability and the expression levels of COX6B1 in a time‑dependent manner, and 60 min of reoxygenation was identified as the optimal time period for establishing an ischemia/reperfusion (I/R) model. Overexpression of COX6B1 was demonstrated to reverse the viability of hippocampal neurons following I/R treatment. Specifically, COX6B1 overexpression decreased the cytosolic concentration of Ca2+ and suppressed neuronal apoptosis, which were increased following I/R treatment. Furthermore, overexpression of COX6B1 increased the protein expression levels of apoptosis regulator BCL‑2 and mitochondrial cytochrome c (cyt c), and decreased the protein expression levels of apoptosis regulator BCL2‑associated X and cytosolic cyt c in I/R model cells. Collectively, the present study results suggested that COX6B1 overexpression may reverse I/R‑induced neuronal damage by increasing the viability of neurons, by decreasing the cytosolic levels of Ca2+ and by suppressing apoptosis. These results may facilitate the development of novel strategies for the prevention and treatment of CVD.

Topics: Animals; Apoptosis; bcl-X Protein; Cell Survival; Cerebrovascular Disorders; Cytochromes c; Electron Transport Complex IV; Female; Glucose; Mitochondria; Neurons; Oxygen; Protective Agents; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Temporal Lobe

This study investigated the effects of baicalein, a natural compound isolated from the root of scutellaria, on cognitive and motor ability impaired by chronic cerebral hypoperfusion in rats, as well as its effects on brain mitochondria. Rats subjected to permanent bilateral common carotid artery occlusion experienced cognitive deficits, oxidative stress and mitochondria dysfunction, which was associated with the elevation of reactive oxygen species level, the decrease of oxidative phosphorylation parameters, the loss of mitochondrial membrane potential, the reduce in Bcl-2/Bax ratio, and the release of cytochrome c. Baicalein alleviated cognitive and motor impairments and decreased mitochondria reactive oxygen species production, in accordance with its improvements on membrane potential level, oxidative phosphorylation process, mitochondrial swelling degree, Bcl-2/Bax ratio and cytochrome c release. These data indicated that baicalein might have therapeutic potential for the treatment of dementia caused by chronic cerebral hypoperfusion, contributed to its protections on brain mitochondrial homeostasis and function.

Topics: Animals; bcl-2-Associated X Protein; Blotting, Western; Brain; Carotid Arteries; Cerebrovascular Disorders; Cognition; Cytochromes c; Flavanones; Male; Membrane Potential, Mitochondrial; Mitochondria; Mitochondrial Swelling; Motor Activity; Oxidative Phosphorylation; Oxidative Stress; Proto-Oncogene Proteins c-bcl-2; Rats; Rats, Wistar; Reactive Oxygen Species

Topics: Cerebrovascular Circulation; Cerebrovascular Disorders; Cytochromes; Cytochromes c; Drug Therapy; Geriatrics

Topics: Cerebrovascular Disorders; Cytochromes; Cytochromes c; Heart Diseases; Humans; Pharmacology

Topics: Cerebrovascular Disorders; Cytochromes; Cytochromes c; Humans

Topics: Cerebral Hemorrhage; Cerebrovascular Disorders; Cytochromes; Cytochromes c