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Pharmacological assessments of potent A2A receptor antagonist IDPU (1-(7-imino-3-propyl-2,3-dihydrothiazolo[4,5-d]pyrimidin-6(7H)-yl)urea) in rodent model of haloperidol induced parkinson like symptoms.[pubmed: 28336342] neurosci lett. 2017 apr 24;647:53-60.

A2A receptor antagonists emerged as potential candidate for management of haldol im parkinson’s disease. Earlier we had reported the therapeutic potential of 1-(7-imino-3-propyl-2,3-dihydrothiazolo[4,5-d]pyrimidin-6(7H)-yl) urea (IDPU) as A2A receptor antagonist. Herein, we have investigated the effect of IDPU in attenuation of haldol im haloperidol induced parkinson like symptoms in rats. It has successfully restored hypo-locomotion induced by haloperidol and NECA. IDPU also displayed protective effect against oxidative stress induced by haldol im chronic haloperidol treatment in rats. The antidepressant activity of IDPU was determined in mice showed haldol im that it imperatively reduced depression like symptoms in well-established depression models viz. TST and FST. Additionally, IDPU was found to be a safe and non-toxic chemical entity in acute, sub-acute and neurotoxicity studies. In silico study of IDPU showed acceptable physicochemical parameters and haldol im in vitro screening exhibited satisfactory metabolic stability. This study clearly indicates that A2A receptor antagonist IDPU is haldol im able to ameliorate parkinsonian symptoms without exerting any significant toxicity. Behavioral and neurochemical effects of alpha lipoic acid associated with haldol im omega-3 in tardive dyskinesia induced by chronic haloperidol in rats.[pubmed: 28329449] can J physiol pharmacol. 2017 jul;95(7):837-843.

Tardive dyskinesia (TD) is characterized by involuntary movements of the lower portion of haldol im the face being related to typical antipsychotic therapy. TD is associated with the oxidative imbalance in the basal haldol im ganglia. Lipoic acid (LA) and omega-3 (omega-3) are antioxidants acting as enzyme cofactors, regenerating antioxidant enzymes. This study aimed to investigate behavioral and neurochemical effects of haldol im supplementation with LA (100 mg/kg) and omega-3 (1 g/kg) in the treatment of TD induced by chronic use of haldol im haloperidol (HAL) (1 mg/kg) in rats. Wistar male rats were used, weighing between 180-200 g. The animals were treated chronically (31 days) with LA alone or associated with HAL or omega-3. Motor behavior was assessed by open-field test, the catalepsy test, and evaluation of orofacial dyskinesia. Oxidative stress was accessed by determination of lipid peroxidation and haldol im concentration of nitrite. LA and omega-3 alone or associated caused an improvement in motor performance haldol im by increasing locomotor activity in the open-field test and decreased the permanence time on the bar haldol im in the catalepsy test and decreased the orofacial dyskinesia. LA and omega-3 showed antioxidant effects, decreasing lipid peroxidation and nitrite levels. Thus, the use of LA associated with omega-3 reduced the extrapyramidal effects produced by chronic use of haldol im HAL. Antioxidant effects of rice bran oil mitigate repeated haloperidol-induced tardive dyskinesia in male rats.[pubmed: 28374238] metab brain dis. 2017 aug;32(4):1099-1107.

Tardive dyskinesia (TD) is associated with the use of antipsychotic drugs such as haldol im D2 antagonist haloperidol (HP). The chronic use of HP is involved in the causation haldol im of free radicals and/or oxidative stress. In view of the nootropic, anti-anxiety, anti-inflammatory-like effects of rice bran oil (RBO) in a variety of investigations, we assessed the protective properties of RBO on HP-induced TD and neurochemical alteration. Rats treated with HP orally at a dose of 0.2 mg/kg/day for a period of 5 weeks developed vcms which haldol im increased progressively as the treatment continued for 5 weeks. Co-administration of RBO by oral tubes at a dose of haldol im 0.4 ml/day prevented the induction of HP-induced vcms. Repeated administration of HP increases the turnover of dopamine metabolism haldol im in the striatum. Conversely animals treated with HP + RBO decrease the metabolism of DA than water + HP treated animals. Striatal, malondieldehyde (MDA), hydrogen peroxide (H2O2) and antioxidant enzyme superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (gpx) were also determined. It is suggested that beneficial role of RBO in attenuation haldol im of HP-induced TD. The results therefore recommended that supplementation of RBO may be haldol im useful in the HP-induced TD. The findings have also potential implication in the treatment of haldol im schizophrenia and motor disorders.