ABSTRACT
Parkinson's disease (PD) affects â¼1-2% of the elderly population. Development of a neuroprotective therapy that may be initiated early in the course of the disease to retard/prevent disease progression is highly desirable. This study aimed to investigate prophylactic treatment with coenzyme Q10 (CoQ10) before paraquat (PQ) exposure, a herbicide known to increase the risk for PD, to attain neuroprotection. In addition, therapeutic intervention with CoQ10 in mice already exposed to PQ (24 h) might halt ongoing neurodegeneration and behavioural deterioration. PD was induced experimentally in mice by an injection of PQ (10 mg/kg, intraperitoneal), twice a week for 3 consecutive weeks, either before or after the initiation of treatment with CoQ10 (200 mg/kg). The results of the sustained supplementation with CoQ10, prophylactically and therapeutically, were compared with L-DOPA (100 mg/kg). A battery of behavioural tests was performed, in addition to estimation of protein carbonyl in the brain. CoQ10 elicited a remarkable improvement in most of the behavioural tests and decreased protein carbonyl content in the brain, particularly when it was initiated before rather than after PQ induction of PD. Therefore, CoQ10, which protects against mitochondrial damage, may be beneficial in slowing the progression of PD, particularly when initiated as prophylactic treatment.
Subject(s)
Parkinson Disease/drug therapy , Ubiquinone/analogs & derivatives , Animals , Disease Models, Animal , Levodopa/pharmacology , Male , Mice , Mitochondria/drug effects , Neurons/drug effects , Neuroprotective Agents/pharmacology , Oxidative Stress/drug effects , Paraquat/pharmacology , Protein Carbonylation , Ubiquinone/pharmacology , Ubiquinone/therapeutic useABSTRACT
CONTEXT: Cold-pressed oils (CPO) are commercially available in the market and characterized by their health-promoting properties. OBJECTIVE: Clove oil (CLO), coriander seed oil (COO) and black cumin oil (BCO) were evaluated for their bioactive lipids. Pharmacological screening was performed to evaluate acute toxicity, anti-inflammatory and ulcerogenic effects as well as histopathological changes in tissues of albino rats fed with CPO. MATERIALS AND METHODS: Fatty acids, tocols and total phenolics were analyzed. The acute toxicity test for each CPO was estimated during 14 d. Carrageenan-induced rat paw oedema was used for assessment of anti-inflammatory activity of CPO. Animals were fasted overnight, and via oral gavage given indomethacin (10 mg/kg) or CPO (400 mg/kg) to investigate ulcerogenecity. Histopathological changes in liver, kidney, heart, spleen and stomach were screened. RESULTS: Amounts of α-, ß-, γ- and δ-tocopherols in CLO were 1495, 58, 4177 and 177 mg/kg oil, respectively. In COO, α, ß, γ and δ-tocopherols were 10.0, 18.2, 5.1 and 34.8%, respectively. In BCO, ß-tocotrienol was the main constituent. CLO, COO and BCO contained 4.6, 4.2 and 3.6 mg GAE/g, respectively. Acute toxicity test determined that 400 mg/kg of CPO to be used. In the carrageenan model of inflammation, pretreatment of rats with indomethacin (10 mg/kg) or CLO (400 mg/kg) induced a significant (p < 0.05) reduction by 31.3 and 27.4%, respectively, in rat paw oedema as compared with the carrageenan-treated group. Indomethacin induced a significant ulcerogenic effect with an ulcer index of 19. Oral treatment of CPO showed no ulcerogenic effect, wherein no histopathological changes were observed. CONCLUSIONS: CPO, particularly CLO, could minimize acute inflammation.
