Naringin Ameliorates Haloperidol-Induced Neurotoxicity and Orofacial Dyskinesia in a Rat Model of Human Tardive Dyskinesia

Wang, Mao‐Hsien; Yang, Chao‐Hsun; Tseng, Hsiang-Chien; Fang, Chia Lang; Lin, Yi‐Wen; Soung, Hung-Sheng

doi:10.1007/s12640-021-00333-1

Cited by 15 publications

(25 citation statements)

References 48 publications

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“…A widely measured endpoint upon TD induction is the severity of apoptosis in different brain areas. Caspase-3 was elevated in animals with TD ( Bishnoi and Boparai 2012 ; Soung et al, 2018 ; Wang et al, 2021a ). Furthermore, the transcription level of the proapoptotic BAX was elevated, whereas antiapoptotic BAD mRNA was decreased ( An et al, 2016 ).…”

Section: Preclinical Studies Of Tardive Dyskinesia Developmentmentioning

confidence: 99%

“…Animal experiments studied candidate pathways involved in TD development on the level of functional perturbations due to treatment with antipsychotics. Inflammation ( Bishnoi and Boparai 2012 ; Grover et al, 2013 ; Thakur et al, 2015 ; Datta et al, 2016 ; Peroza et al, 2016 ; Sonego et al, 2018 ; Soung et al, 2018 ; Wang et al, 2021a ) and oxidative stress defense ( Patil et al, 2012 ; Grover et al, 2013 ; Nade et al, 2013 ; Thakur et al, 2015 ; Wang et al, 2015 ; Datta et al, 2016 ; Schaffer et al, 2016 ; Samad and Haleem 2017 ; Dhingra et al, 2018 ; Sonego et al, 2018 ; Soung et al, 2018 ; Tsai et al, 2019 ; Wang et al, 2021a ) pathways were among the most studied ones. Accordingly, different antioxidants were tested as potential agents for the treatment of TD.…”

Section: Preclinical Studies Of Tardive Dyskinesia Developmentmentioning

confidence: 99%

“…Many studies showed decreased levels of catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH), either in their quantity or antioxidant capacity, upon treatment with haloperidol ( Grover et al, 2013 ; Thakur et al, 2015 ; Datta et al, 2016 ; Samad and Haleem 2017 ; Dhingra et al, 2018 ; Sonego et al, 2018 ; Tsai et al, 2019 ; Wang et al, 2021a ), reserpine ( Patil et al, 2012 ; Nade et al, 2013 ; Wang et al, 2015 ; Soung et al, 2018 ) or fluphenazine ( Schaffer et al, 2016 ). Studies have also shown that a plethora of cytokines are elevated upon treatment with antipsychotics, such as TNF- α ( Bishnoi and Boparai 2012 ; Grover et al, 2013 ; Thakur et al, 2015 ; Datta et al, 2016 ; Peroza et al, 2016 ; Sonego et al, 2018 ; Soung et al, 2018 ; Wang et al, 2021a ), IL-1 β ( Grover et al, 2013 ; Thakur et al, 2015 ; Datta et al, 2016 ; Peroza et al, 2016 ; Sonego et al, 2018 ; Wang et al, 2021a ), IL6 ( Datta et al, 2016 ; Peroza et al, 2016 ; Sonego et al, 2018 ; Soung et al, 2018 ; Wang et al, 2021a ), and IFN- γ ( Peroza et al, 2016 ). On the contrary, IL-10 is decreased, due to its role as an anti-inflammatory cytokine ( Peroza et al, 2016 ; Sonego et al, 2018 ).…”

Section: Preclinical Studies Of Tardive Dyskinesia Developmentmentioning

confidence: 99%

“…Consequently, some agents with antioxidative and anti-inflammatory properties were tested as potential drugs for TD, such as resveratrol ( Busanello et al, 2012 , Busanello et al, 2017 ), vitamin E ( An et al, 2016 ; Shi et al, 2016 ), lycopene ( Datta et al, 2016 ), L-theanine ( Chen et al, 2018 ; Soung et al, 2018 ; Tsai et al, 2019 ), cannabidiol ( Sonego et al, 2018 ; Kajero et al, 2020 ), and catechin ( Wang et al, 2015 ; Reinheimer et al, 2020 ). Additionally, several different plant-based compounds were tested ( Patil et al, 2012 ; Sekiguchi et al, 2012 ; An et al, 2013 ; An et al, 2016 ; Shi et al, 2016 ; Samad and Haleem 2017 ; Dhingra et al, 2018 ; Wang et al, 2021a ). A widely measured endpoint upon TD induction is the severity of apoptosis in different brain areas.…”

Section: Preclinical Studies Of Tardive Dyskinesia Developmentmentioning

confidence: 99%

“…All of the above indicate a lack of adaptation of the aminergic neurotransmission in TD development ( Lévesque et al, 2017 ; Hauser and Truong 2018 ). Not only were those components of serotonergic and dopaminergic systems dysregulated, but the concentrations of neurotransmitters themselves were decreased ( Dhingra et al, 2018 ; Soung et al, 2018 ; Wang et al, 2021a ).…”

Section: Preclinical Studies Of Tardive Dyskinesia Developmentmentioning

confidence: 99%

See 4 more Smart Citations

Genetic Factors Associated With Tardive Dyskinesia: From Pre-clinical Models to Clinical Studies

2022

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Tardive dyskinesia is a severe motor adverse event of antipsychotic medication, characterized by involuntary athetoid movements of the trunk, limbs, and/or orofacial areas. It affects two to ten patients under long-term administration of antipsychotics that do not subside for years even after the drug is stopped. Dopamine, serotonin, cannabinoid receptors, oxidative stress, plasticity factors, signaling cascades, as well as CYP isoenzymes and transporters have been associated with tardive dyskinesia (TD) occurrence in terms of genetic variability and metabolic capacity. Besides the factors related to the drug and the dose and patients’ clinical characteristics, a very crucial variable of TD development is individual susceptibility and genetic predisposition. This review summarizes the studies in experimental animal models and clinical studies focusing on the impact of genetic variations on TD occurrence. We identified eight genes emerging from preclinical findings that also reached statistical significance in at least one clinical study. The results of clinical studies are often conflicting and non-conclusive enough to support implementation in clinical practice.

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Section: Preclinical Studies Of Tardive Dyskinesia Developmentmentioning

confidence: 99%

Section: Preclinical Studies Of Tardive Dyskinesia Developmentmentioning

confidence: 99%

Section: Preclinical Studies Of Tardive Dyskinesia Developmentmentioning

confidence: 99%

Section: Preclinical Studies Of Tardive Dyskinesia Developmentmentioning

confidence: 99%

Section: Preclinical Studies Of Tardive Dyskinesia Developmentmentioning

confidence: 99%

See 3 more Smart Citations

Genetic Factors Associated With Tardive Dyskinesia: From Pre-clinical Models to Clinical Studies

2022

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Protective effect of naringin against oxaliplatin‐induced peripheral neuropathy in rats: A behavioral and molecular study

Semis

Kandemir

Çağlayan

et al. 2022

J Biochem & Molecular Tox

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Oxaliplatin (OXL) is a chemotherapeutic drug used for metastatic and other types of cancer, but it causes peripheral neuropathy as a dose‐limiting side effect. Herein, we used the rat model of OXL‐induced peripheral neuropathy to demonstrate the protective effects of naringin (NRG) in this neuropathy. In this study, rats were injected with OXL (4 mg/kg, body weight, i.p.) in 5% glucose solution 30 min after oral administration of NRG (50 and 100 mg/kg, body weight) on the 1st, 2nd, 5th, and 6th days. OXL caused sensory and motor neuropathy (as revealed by the hot plate, tail flick, rota‐rod, and cold hyperalgesia tests) in the sciatic nerve of rats. Coadministration of oral NRG alleviated OXL‐induced sensory and motor neuropathy. Levels of superoxide dismutase, catalase, glutathione peroxidase, nuclear factor erythroid 2‐related factor 2, Heme oxygenase‐1, nuclear factor‐κ B, tumor necrosis factor‐α, interleukin‐1β, Bax, Bcl‐2, caspase‐3, paraoxonase, mitogen‐activated protein kinase 14, neuronal nitric oxide synthase (nNOS), acetylcholinesterase, and arginase 2 in the sciatic nerve tissues were assessed by real‐time polymerase chain reaction. Moreover, the protein levels of caspase‐3, Bax, Bcl‐2, intercellular adhesion molecules‐1, glial fibrillary acidic protein, and nNOS were examined by Western blot analysis. NRG treatment significantly improved all the above‐mentioned parameters and reduced OXL‐induced oxidative stress, inflammation, and apoptosis in the sciatic nerve tissue. In conclusion, this study demonstrated that NRG significantly attenuated OXL‐induced peripheral neuropathy and might be considered as a new protective agent to prevent the OXL‐induced peripheral neuropathy.

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Naringin attenuates oxaliplatin‐induced nephrotoxicity and hepatotoxicity: A molecular, biochemical, and histopathological approach in a rat model

Ileriturk,

Kandemir

et al. 2023

J Biochem & Molecular Tox

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Oxaliplatin (OXL) is a significant therapy agent for the worldwide increase in cancer cases. Naringin (4′,5,7‐trihydroxy flavonon 7‐rhamnoglucoside, NRG) has a wide range of biological and pharmacological activities, including antioxidant and anti‐inflammatory potentials. This research aimed to investigate NRG activity in OXL‐induced hepatorenal toxicity. Accordingly, OXL (4 mg/kg b.w.) in 5% glucose was injected intraperitoneally on the first, second, fifth, and sixth days, and NRG (50 and 100 mg/kg b.w.) was given orally 30 min before to treatment. Biochemical, genetic, and histological methods were utilized to investigate the function tests, oxidant/antioxidant status, inflammation, apoptosis, and endoplasmic reticulum (ER) stress pathways in kidney and liver tissues. Administration of NRG demonstrated an antioxidant effect by increasing the activities of OXL‐induced reduced antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) and decreasing the elevated lipid peroxidation parameter malondialdehyde levels. Nuclear factor‐κB, tumor necrosis factor‐α, interleukin‐1β, and inducible nitric oxide synthase levels increased in OXL administered groups but reduced in NRG‐treated groups. In the OXL‐administered groups, NRG reduced the apoptosis‐inducing factors Caspase‐3 and B‐cell lymphoma 2 (Bcl‐2)‐associated X protein levels, while elevating the antiapoptotic factor Bcl‐2 levels. OXL triggered prolonged ER stress by increasing the levels of ER stress parameters activating transcription factor 6, protein kinase R‐like ER kinase, inositol‐requiring enzyme 1α, and glucose‐regulated protein 78. Therefore, with the NRG administration, this activity was reduced and the ER stress level decreased. Taken together, it was found that OXL induced toxicity by increasing the levels of urea and creatinine, alanine transaminase, aspartate aminotransferase, and alkaline phosphatase activities, inflammation, apoptosis, ER stress, and oxidants in the liver and kidney tissue, and NRG had a protective effect by reversing the deterioration in these pathways.

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Naringin Ameliorates Haloperidol-Induced Neurotoxicity and Orofacial Dyskinesia in a Rat Model of Human Tardive Dyskinesia

Cited by 15 publications

References 48 publications

Genetic Factors Associated With Tardive Dyskinesia: From Pre-clinical Models to Clinical Studies

Genetic Factors Associated With Tardive Dyskinesia: From Pre-clinical Models to Clinical Studies

Protective effect of naringin against oxaliplatin‐induced peripheral neuropathy in rats: A behavioral and molecular study

Naringin attenuates oxaliplatin‐induced nephrotoxicity and hepatotoxicity: A molecular, biochemical, and histopathological approach in a rat model

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