Berberine Ameliorate Haloperidol and 3-Nitropropionic Acid-Induced Neurotoxicity in Rats

Kadir, Abdul; Singh, Joginder; Rahi, Vikrant; Kumar, Puneet

doi:10.1007/s11064-022-03677-y

Cited by 15 publications

(15 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In both tests, the rotating shaft had a seven cm diameter and rotated at a constant speed of 25 rpm while the rats were being trained. A restricted duration of 180 s was implemented to evaluate the drop-down delay [ 20 , 21 , 22 , 26 ].…”

Section: Methodsmentioning

confidence: 99%

“…Animals treated with 3-NPA display motor behavioral problems, such as abnormal gait, inability to balance over a small beam, deficiencies in exploratory behaviors, and/or elevated levels of anxiety. This model is a useful resource for evaluating the efficacy of potential HD therapeutics because the 3-NPA injection is known to cause HD-like symptoms in animals with a phenotype comparable to the inherited human disease [ 17 , 18 , 19 , 20 , 21 , 22 ]. Previously, europinidin has been reported as showing a favorable effect against alcohol-induced liver damage [ 23 ], streptozotocin-induced memory impairment [ 24 ], and rotenone-activated Parkinson’s disease in rats [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Europinidin Mitigates 3-NPA-Induced Huntington’s Disease Symptoms in Rats: A Comprehensive Analysis of Oxidative Stress, Mitochondrial Enzyme Complex Activity, Pro-Inflammatory Markers and Neurotransmitter Alterations

Alharbi

2024

Biomedicines

View full text Add to dashboard Cite

Huntington’s disease (HD) is a neurodegenerative disease that causes progressive motor and cognitive dysfunction. There is no cure for HD, and current therapeutics can only manage the signs and symptoms as well as slowing disease progression. This investigation examines the possible therapeutic advantages of europinidin in 3-nitropropionic acid (3-NPA) injected HD in rats. Wistar rats were randomly assigned to five groups (n = 6): normal control, 3-NPA (10 mg/kg, i.p.), 3-NPA + europinidin-10 (10 mg/kg, p.o.), 3-NPA + europinidin-20 (20 mg/kg, p.o.), and europinidin alone (20 mg/kg, p.o.) for 15-day. Various behavioral and biochemical parameters including antioxidant levels, oxidative stress, pro-inflammatory markers, mitochondrial enzyme complex, and neurotransmitters were assessed. Europinidin restored biochemical, mitochondrial dysfunction, oxidative stress, neurotransmitter, and pro-inflammatory parameters disrupted by 3-NPA. Here we show that europinidin attenuates 3-NPA-induced neurodegeneration in rat models of HD. Europinidin modulates oxidative stress, enhances antioxidants, restores mitochondrial enzyme complex activity, reduces neuroinflammation, and modulates neurotransmitter levels. Our findings reveal the potential of europinidin as a novel therapeutic agent for the treatment of HD. This study also provides new insights into the molecular mechanisms of europinidin-mediated neuroprotection and may have a beneficial role in the management of neurological diseases.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Europinidin Mitigates 3-NPA-Induced Huntington’s Disease Symptoms in Rats: A Comprehensive Analysis of Oxidative Stress, Mitochondrial Enzyme Complex Activity, Pro-Inflammatory Markers and Neurotransmitter Alterations

Alharbi

2024

Biomedicines

View full text Add to dashboard Cite

show abstract

“…Animals were sacrificed via decapitation method for biochemical estimation, and the brains (excluding the cerebellum) were taken out and homogenized (10% w/v) with chilled phosphate buffer (pH 7.4) to prevent lipid peroxidation during tissue processing. Next, the homogenate was centrifuged at 10 000 g for 15 min at 4°C and supernatant was collected to assess biochemical parameters 27 …”

Section: Methodsmentioning

confidence: 99%

“…Next, the homogenate was centrifuged at 10 000 g for 15 min at 4 C and supernatant collected to assess biochemical parameters. 27 The MDA was considered the end product of lipid peroxidation and assessed in the brain homogenate using the Wills 1966 method. 28 The 0.1 mL of supernatant was first incubated with 0.5 mL of TrisHCl for 2 h and then added 1 mL (0.67% w/v) of thiobarbituric acid to the 1 mL of incubated supernatant.…”

Section: Biochemical Estimationsmentioning

confidence: 99%

Impact of noscapine on halting the progression of pentylenetetrazole induced kindling epilepsy in mice

Gupta,

Soni,

Upadhayay

et al. 2023

Clin Exp Pharma Physio

Self Cite

View full text Add to dashboard Cite

Epilepsy is caused by an excessive recurrent excitatory neuronal firing, characterized by motor, psychomotor, and sensory impairments. Current therapies fail to produce 100% outcomes because of the complexity of the disease, poor diagnosis, and upsurge to drug‐resistant epilepsy. The study repurposed the drug ‘noscapine’ mainly known for its anti‐tussive properties. For the management of epilepsy and its associated secondary complications. To confirm the effect of noscapine, adult mice were injected with pentylenetetrazole (PTZ) (35 mg/kg i.p.) on an alternate day for 29 days to induce epilepsy. Animals were pretreated with noscapine in three doses (5, 10, and 20 mg/kg i.p.) for 33 days. Various behavioural assessments like the open field test, Morris water maze, and tail suspension test were performed to observe animals' locomotor activity, spatial memory, and anxiety‐depressive behaviour. On the 34th day, animals were sacrificed, and brains were removed for biochemical estimations. Prolonged PTZ treatment reduced locomotor, learning activity, and increased anxiety‐depressive behaviour, which was further confirmed by reduced antioxidant levels such as reduced glutathione (GSH), superoxide dismutase (SOD), and catalase because of increased oxido‐nitrosative stress, that is, malondialdehyde (MDA) and nitrite in the brain. In comparison, noscapine pretreatment attenuated PTZ‐induced behavioural and biochemical changes in the animals. The results indicate that noscapine ameliorates the oxido‐nitrosative stress. However, studies indicate that oxido‐nitrosative stress is a significant concern for the GABAergic neurons and promotes the disease progression. Further studies are required to explore the molecular mechanism of noscapine, which might be a practical approach as a newer antiepileptic agent.

show abstract

“…HD is also a neurological disorder marked by motor dysfunction, which contributes to striatal neuronal death and psychiatric symptoms (Kadir et al, 2022). According to a study, the Huntington's group had higher glutamate and dopamine levels in their tissues, as well as impaired neurobehavioral parameters, whereas moringa treatment preserved the normal parameters (Ogundipe, 2019).…”

Section: Oleifera In Huntington's Disease (Hd)mentioning

confidence: 99%

Neuroprotective potential of Moringa oleifera mediated by NF‐kB/Nrf2/HO‐1 signaling pathway: A review

Mundkar

Bijalwan

Soni

et al. 2022

Journal of Food Biochemistry

View full text Add to dashboard Cite

Moringa oleifera is a traditional Indian herb belonging to the Moringaceae family, it is commonly known as the horse‐radish tree, drumstick, or sahajna. In developing countries, Moringa is used as feed for both humans and animals due to its well‐known antioxidant, anti‐inflammatory, and anti‐apoptotic properties owing to its several phytoconstituents including β‐carotene, quercetin, kaempferol, ascorbic acid, flavonoids, phenolic acid, rhamnose, glycosylates, glucomoringin, and isothiocyanates. These constituents help to maintain the brain antioxidant enzyme levels, mitochondrial functions, and neurogenesis, showing neuroprotective effects in several neurodegenerative disorders including Parkinson's Disease, Alzheimer's Disease, Huntington's Disease, and Amyotrophic lateral sclerosis. This review discusses various phytoconstituent of moringa and their therapeutic potential in various neurological disorders. Additionally, we also concise the safety and toxicity profile, of different molecular pathways involved in the neuroprotective effect of M. oleifera including M. oleifera nanoparticles for better therapeutic value. Practical applications Several clinical and preclinical studies on Moringa oleifera have been conducted, and the outcomes indicate moringa could be used in the treatment of brain disorders. As a result, we conclude that moringa and its nanoformulations could be employed to treat neurological problems. In the future, M. oleifera phytoconstituents could be evaluated against specific signaling pathways, which could aid researchers in discovering their mechanism of action. Furthermore, the use of moringa as a nutraceutical owing to its myriad pharmacological potential will go a long way in boosting the economy of countries that grow moringa on a large scale.

show abstract

Berberine Ameliorate Haloperidol and 3-Nitropropionic Acid-Induced Neurotoxicity in Rats

Cited by 15 publications

References 53 publications

Europinidin Mitigates 3-NPA-Induced Huntington’s Disease Symptoms in Rats: A Comprehensive Analysis of Oxidative Stress, Mitochondrial Enzyme Complex Activity, Pro-Inflammatory Markers and Neurotransmitter Alterations

Europinidin Mitigates 3-NPA-Induced Huntington’s Disease Symptoms in Rats: A Comprehensive Analysis of Oxidative Stress, Mitochondrial Enzyme Complex Activity, Pro-Inflammatory Markers and Neurotransmitter Alterations

Impact of noscapine on halting the progression of pentylenetetrazole induced kindling epilepsy in mice

Neuroprotective potential of Moringa oleifera mediated by NF‐kB/Nrf2/HO‐1 signaling pathway: A review

Contact Info

Product

Resources

About