Beneficial effect of candesartan and lisinopril against haloperidol-induced tardive dyskinesia in rat

Thakur, K.P.; Prakash, Atish; Bisht, Rohit; Bansal, Puneet

doi:10.1177/1470320313515038

Cited by 34 publications

(35 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Co-administration of peroxisome proliferator-activated receptor-gamma (PPARγ) antagonist significantly reduced this effect indicating that candesartan's neuroprotective effect occurs through AT1-receptor blocking and PPARγ activation ( 35 ). In male Wistar rats, oral candesartan (3 and 5 mg/kg) for three weeks improved the tardive dyskinesia induced by the typical antipsychotics possibly via antioxidant and anti-inflammatory effects ( 36 ). In contrast, treatment with subcutaneous losartan (10 mg·kg −1 ·day −1 ) for 2 weeks in male Wistar rats did not cause any difference in motor coordination ( 37 ).…”

Section: Discussionmentioning

confidence: 99%

Candesartan, rather than losartan, improves motor dysfunction in thioacetamide-induced chronic liver failure in rats

Murad

Gazzaz

Ali

et al. 2017

Braz J Med Biol Res

View full text Add to dashboard Cite

Minimal hepatic encephalopathy is more common than the acute syndrome. Losartan, the first angiotensin-II receptor blocker (ARB), and candesartan, another widely-used ARB, have protected against developing fibrogenesis, but there is no clear data about their curative antifibrotic effects. The current study was designed to examine their effects in an already-established model of hepatic fibrosis and also their effects on the associated motor dysfunction. Low-grade chronic liver failure (CLF) was induced in 3-month old Sprague-Dawley male rats using thioacetamide (TAA, 50 mg·kg−1·day−1) intraperitoneally for 2 weeks. The TAA-CLF rats were randomly divided into five groups (n=8) treated orally for 14 days (mg·kg−1·day−1) as follows: TAA (distilled water), losartan (5 and 10 mg/kg), and candesartan (0.1 and 0.3 mg/kg). Rats were tested for rotarod and open-field tests. Serum and hepatic biochemical markers, and hepatic histopathological changes were evaluated by H&E and Masson's staining. The TAA-CLF rats showed significant increases of hepatic malondialdehyde, hepatic expression of tumor necrosis factor-α (TNF-α), and serum ammonia, alanine aminotransferase, γ-glutamyl transferase, TNF-α, and malondialdehyde levels as well as significant decreases of hepatic and serum glutathione levels. All treatments significantly reversed these changes. The histopathological changes were moderate in losartan-5 and candesartan-0.1 groups and mild in losartan-10 and candesartan-0.3 groups. Only candesartan significantly improved TAA-induced motor dysfunction. In conclusion, therapeutic antifibrotic effects of losartan and candesartan in thioacetamide-induced hepatic fibrosis in rats are possibly through angiotensin-II receptor blocking, antioxidant, and anti-inflammatory activities. Improved motor dysfunction by candesartan could be attributed to better brain penetration and slower “off-rate” from angiotensin-II receptors. Clinical trials are recommended.

show abstract

Section: Discussionmentioning

confidence: 99%

Candesartan, rather than losartan, improves motor dysfunction in thioacetamide-induced chronic liver failure in rats

Murad

Gazzaz

Ali

et al. 2017

Braz J Med Biol Res

View full text Add to dashboard Cite

show abstract

“…In a different study, the increase in lipid peroxidation in the striatum has been observed [106]. Increased lipid peroxidation and H 2 O 2 production paralleled by decreased activity of antioxidant enzymes (SOD, GPX, and CAT) have been found in rats with TD induced by haloperidol [107]. Another way through which haloperidol leads to oxidative stress phenomena is related to its ability to modulate cell metabolism; in fact, it has been shown that the treatment with this drug is also able to induce mitochondrial activity that in turn leads to an enhancement of ROS production in the whole blood of rats [108].…”

Section: First-generation Antipsychotics (Fgas) and Oxidative Stress: The Strange Case Of Haloperidolmentioning

confidence: 89%

Antioxidant Properties of Second-Generation Antipsychotics: Focus on Microglia

et al. 2020

View full text Add to dashboard Cite

Recent studies suggest a primary role of oxidative stress in an early phase of the pathogenesis of schizophrenia and a strong neurobiological link has been found between dopaminergic system dysfunction, microglia overactivation, and oxidative stress. Different risk factors for schizophrenia increase oxidative stress phenomena raising the risk of developing psychosis. Oxidative stress induced by first-generation antipsychotics such as haloperidol significantly contributes to the development of extrapyramidal side effects. Haloperidol also exerts neurotoxic effects by decreasing antioxidant enzyme levels then worsening pro-oxidant events. Opposite to haloperidol, second-generation antipsychotics (or atypical antipsychotics) such as risperidone, clozapine, and olanzapine exert a strong antioxidant activity in experimental models of schizophrenia by rescuing the antioxidant system, with an increase in superoxide dismutase and glutathione (GSH) serum levels. Second-generation antipsychotics also improve the antioxidant status and reduce lipid peroxidation in schizophrenic patients. Interestingly, second-generation antipsychotics, such as risperidone, paliperidone, and in particular clozapine, reduce oxidative stress induced by microglia overactivation, decreasing the production of microglia-derived free radicals, finally protecting neurons against microglia-induced oxidative stress. Further, long-term clinical studies are needed to better understand the link between oxidative stress and the clinical response to antipsychotic drugs and the therapeutic potential of antioxidants to increase the response to antipsychotics.

show abstract

“…On treating with haloperidol resulted in significantly increases in the level of TNF-α in the cortex and striatum region of the mice brain. Many cellular studies indicated that haloperidol has been associated with an increased expression of inflammatory markers such as TNF-α and NF-kB against oxidative damage induced by haloperidol that may lead to neurotoxicity 21 .However, with chronic haloperidol, there is a downregulation of phospho-Thr34-DARPP-32 because of an increase in TNFα signaling. In the CNS, the effects of TNFα are complex, with evidence for both injury-promoting and neuroprotective effects.…”

Section: Discussionmentioning

confidence: 99%

Effect of Eclipta alba and Ocimum sanctum on haloperidol induced parkinsonism

Chahal

Sharma

2018

J. Drug Delivery Ther.

View full text Add to dashboard Cite

The aim of the study is protective effect of compound Eclipta alba and Ocimum sanctum on Parkinsonism induced mice by haloperidol injection. Parkinsonism is neurodegenerative disease due to the deficiency of dopamine in brain. The pathological hallmark of Parkinson’s disease in the cell loss within substantia nigra pars compacta (SNpc) region and the disease is charactrised by bradykinesia, rigidity, postural instability, orofacial dyskinesia, muscular stiffness and tremor1. Mice were injected 1mg/kg haloperidol and then treated with test and standard substance for 15 days. The impairment in catatonia in mice were tested using catatonic activity. Biochemical analysis of brain homogenate was performed so ass to assess brain Thiobarbituric acid reactive substance (TBARS) level and reduced glutathione (GSH) and TNF-α level were measured to assess total oxidative stress. EA 300mg/kg and OS 400mg/kg show slightly change in catatonic activity in mice while EA 600mg/kg and 800mg/kg significantly change in catatonic activity. Furthermore, Eclipta alba and Ocimum sanctum prevent the haloperidol induced changes in the level of brain TBARS, GSH and TNF-α. From the results we conclude that Eclipta alba and Ocimum sanctum has protective action against impairment in catatonic activity and pathological damage due to oxidative stress induced by intraperitoneally injection of haloperidol in mice. Keywords: Eclipta alba, Ocimum Sanctum, Parkinsonism, Anti-oxidant.

show abstract

Beneficial effect of candesartan and lisinopril against haloperidol-induced tardive dyskinesia in rat

Abstract: The present study supports the therapeutic use of candesartan and lisinopril in the treatment of typical antipsychotic-induced orofacial dyskinesia and possible antioxidant and neuro-inflammatory mechanisms.

Cited by 34 publications

References 60 publications

Candesartan, rather than losartan, improves motor dysfunction in thioacetamide-induced chronic liver failure in rats

Candesartan, rather than losartan, improves motor dysfunction in thioacetamide-induced chronic liver failure in rats

Antioxidant Properties of Second-Generation Antipsychotics: Focus on Microglia

Effect of Eclipta alba and Ocimum sanctum on haloperidol induced parkinsonism

Contact Info

Product

Resources

About