چکیده:
Background: Opioid dependence significantly disrupts cognitive activities such as learning and memory, which may be the reason for a return to drug use. Morphine (MOR) can increase oxidative damage in the brain. We aim to investigate the effect of coenzyme Q10 (CoQ10) on cognitive impairment, cue-related reinstatement, and expression of BDNF in MOR-dependent rats.
Methods: In this study, 40 male Wistar rats (200-220g) were divided into 5 experimental groups (n=8) as follows: Oil group, MOR+Oil group, MOR+Q10-100 group, MOR+Q10-200 group, MOR+Q10-400 group. The rats were administered increasing doses of MOR (25 to 100mg/kg, s.c.) once daily. After 21 days of addiction, CoQ10 treatment is administered by gavage at doses of 100, 200 and 400 mg/kg once daily for one month. CoQ10 is dissolved in 1 cc of sesame oil and administered. Behavioral assessments were performed using a novel object recognition test, working memory in the Y-maze, social interaction, and conditioned place preference. Expression of BDNF was assessed in the hippocampus by immunohistochemistry.
Results: Treatment with CoQ10 at a dosage of 100, 200 and 400 mg/kg within 4 weeks resulted in a significant improvement in the NOR task (P<0.01, P<0.001), working memory in the Y-maze (P<0.01, P<0.001), social interaction (P<0.001), cue-related reinstatement in the CPP (P<0.01, P<0.001) and significantly increased expression of BDNF (P<0.001) in the hippocampus of male rats.
Conclusions: CoQ10 could improve cognitive impairment and reduce reinstatement in MOR-addicted male rats. Histologic examination confirmed the neuroprotective effects of CoQ10 in the hippocampus. CoQ10 could be a potential therapeutic agent for MOR-induced cognitive impairment and relapse.
Methods: In this study, 40 male Wistar rats (200-220g) were divided into 5 experimental groups (n=8) as follows: Oil group, MOR+Oil group, MOR+Q10-100 group, MOR+Q10-200 group, MOR+Q10-400 group. The rats were administered increasing doses of MOR (25 to 100mg/kg, s.c.) once daily. After 21 days of addiction, CoQ10 treatment is administered by gavage at doses of 100, 200 and 400 mg/kg once daily for one month. CoQ10 is dissolved in 1 cc of sesame oil and administered. Behavioral assessments were performed using a novel object recognition test, working memory in the Y-maze, social interaction, and conditioned place preference. Expression of BDNF was assessed in the hippocampus by immunohistochemistry.
Results: Treatment with CoQ10 at a dosage of 100, 200 and 400 mg/kg within 4 weeks resulted in a significant improvement in the NOR task (P<0.01, P<0.001), working memory in the Y-maze (P<0.01, P<0.001), social interaction (P<0.001), cue-related reinstatement in the CPP (P<0.01, P<0.001) and significantly increased expression of BDNF (P<0.001) in the hippocampus of male rats.
Conclusions: CoQ10 could improve cognitive impairment and reduce reinstatement in MOR-addicted male rats. Histologic examination confirmed the neuroprotective effects of CoQ10 in the hippocampus. CoQ10 could be a potential therapeutic agent for MOR-induced cognitive impairment and relapse.
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