ubiquinone and Cerebral-Infarction

The study examined the effect of endogenous lipid-soluble antioxidant coenzyme Q10 on the expression of UbiA gene of prenyltransferase domain-containing protein 1 (UbiAd1) involved in synthesis of vitamin K2 (and probably of coenzyme Q10) on a rat model of ischemic stroke provoked by ligation of the middle cerebral artery in the left hemisphere. Ischemia enhanced expression of mRNA of UbiAd1 gene in both cerebral hemispheres, but the effect was significant only in the contralateral one. The study revealed no effect of intraperitoneal injection of coenzyme Q10 (30 mg/kg) on ischemia-produced elevation of mRNA of UbiAd1 gene. Further studies are needed to assess possible neuroprotective effects of antioxidant coenzyme Q10.

Topics: Animals; Brain Ischemia; Cerebral Infarction; Dimethylallyltranstransferase; Male; Neuroprotective Agents; Rats; Ubiquinone

Coenzyme Q10 (CoQ10) crosses the blood-brain barrier when administered intravenously and accumulates in the brain. In this study, we investigated whether CoQ10 protects against ischemia-reperfusion injury by measuring neurological function and brain infarct volumes in a rat model of transient focal cerebral ischemia. In male Wistar rats, we performed transient middle cerebral artery occlusion (tMCAO) for 60 minutes, followed by reperfusion for 24 hours or 7 days. Forty-five minutes after the onset of occlusion (or 15 minutes before reperfusion), rats received a single intravenous injection of solubilized CoQ10 (30 mg·mL(-1)·kg(-1)) or saline (2 mL/kg). Sensory and motor function scores and body weights were obtained before the rats were killed by decapitation, and brain infarct volumes were calculated using tetrazolium chloride staining. CoQ10 brain levels were measured by high-performance liquid chromatography with electrochemical detection. CoQ10 significantly improved neurological behavior and reduced weight loss up to 7 days after tMCAO (P < 0.05). Furthermore, CoQ10 reduced cerebral infarct volumes by 67% at 24 hours after tMCAO and 35% at 7 days (P < 0.05). Cerebral ischemia resulted in a significant reduction in endogenous CoQ10 in both hemispheres (P < 0.05). However, intravenous injection of solubilized CoQ10 resulted in its increase in both hemispheres at 24 hours and in the contralateral hemisphere at 7 days (P < 0.05). Our results demonstrate that CoQ10 is a robust neuroprotective agent against ischemia-reperfusion brain injury in rats, improving both functional and morphological indices of brain damage.

Topics: Animals; Brain Ischemia; Cerebral Infarction; Injections, Intravenous; Male; Nervous System Diseases; Neuroprotective Agents; Rats; Rats, Wistar; Treatment Outcome; Ubiquinone

We report a patient with MELAS treated for 24 months with idebenone and riboflavin, during which no stroke-like episodes occurred. Moreover neurological symptoms clearly improved, and a recovery of brain MRI and EEG abnormalities was observed. We conclude that the combined treatment with idebenone and riboflavin may restore the metabolic impairment in MELAS, possibly improving the long-term prognosis in these patients.

Topics: Adult; Antioxidants; Aphasia, Wernicke; Benzoquinones; Cerebral Cortex; Cerebral Infarction; Drug Administration Schedule; Drug Therapy, Combination; Electron Transport; Humans; Magnetic Resonance Imaging; Male; MELAS Syndrome; Mitochondria; Photosensitizing Agents; Riboflavin; Treatment Outcome; Ubiquinone

The effect of oxiracetam (CGP 21690E, CAS 62613-82-5) on cerebrovascular impairment was investigated in rats. 1. After injection of tranylcypromine (a MAO inhibitor), spontaneously hypertensive rats (SHR) which had been previously infused with norepinephrine (NE) for 14 days displayed stroke-related behaviour including kangaroo-like posture, seizures and death. Administration of oxiracetam at doses of 400 and 800 mg/kg/d p.o. for 14 days before tranylcypromine injection inhibited the stroke-related behaviour. 2. Bilateral common carotid and vertebral artery occlusion induced electroencephalogram (EEG) flattening, the EEG recovering gradually after re-perfusion of cerebral blood flow. Oxiracetam administered after the re-perfusion at a dose of 100 mg/kg, i.v. accelerated the recovery. This facilitatory effect was not seen when either piracetam (50 and 100 mg/kg i.v.) or idebenone (50 and 100 mg/kg i.v.) were administered. 3. Occlusion of middle cerebral artery produced cerebral infarction and disturbed the circadian rhythm of spontaneous motor activity with an relative increase of activity in the light period. Treatment with oxiracetam (400 mg/kg/d p.o.) for 14 days after the occlusion showed a tendency to an improvement in the disturbed circadian rhythm but did not influence the size of brain infarction. From these results, oxiracetam is thought to have a protective effect in cerebrovascular impairment.

Topics: Animals; Behavior, Animal; Benzoquinones; Blood Pressure; Cerebral Arteries; Cerebral Infarction; Cerebrovascular Disorders; Electroencephalography; Male; Motor Activity; Norepinephrine; Piracetam; Pyrrolidines; Rats; Rats, Inbred SHR; Rats, Inbred Strains; Tranylcypromine; Ubiquinone