Neuromodulatory Propensity of Bacopa monnieri Leaf Extract Against 3-Nitropropionic Acid-Induced Oxidative Stress: In Vitro and In Vivo Evidences

Oxidative stress has gained attention as one of the fundamental mechanisms responsible for the development of hypertension. The present study investigated in vitro and in vivo antioxidant effects of 70% ethanol-water (v/v) leaf and root extracts of T. officinale (TOL and TOR, respectively). Total phenolic and flavonoid content of plant extracts were assessed using Folin Ciocalteau and aluminium chloride colorimetric methods; while, 2,2-diphenyl-1-picrlhydrazyl (DPPH), 2,2-azinobis (3-ethylbenzothiazoline-6-sulfonic acid (ABTS) and ferric reducing antioxidant power (FRAP) protocols were used to determine the free radical scavenging and total antioxidant capacities (TAC), respectively. The in vivo total antioxidant capacity and malondialdehyde acid (MDA) levels for lipid peroxidation tests were performed on organ homogenate samples from Nω-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats treated with leaf extract, TOL (500 mg/kg/day) and TOR (500 mg/kg/day) for 21 days. Results showed that compared to TOR, TOL possessed significantly higher (p < 0.01) polyphenol (4.35 ± 0.15 compared to 1.14 ± 0.01) and flavonoid (23.17 ± 0.14 compared to 3 ± 0.05) content; free radical scavenging activity (EC50 0.37 compared to 1.34 mg/mL) and total antioxidant capacities (82.56% compared to 61.54% ABTS, and 156 ± 5.28 compared to 40 ± 0.31 FRAP) and both extracts showed no toxicity (LD50 > 5000 mg/kg). TOL and TOR significantly (p < 0.01) elevated TAC and reduced MDA levels in targets organs. In conclusion, T. officinale leaf extract possesses significant anti-oxidant effects which conferred significant in vivo antioxidant protection against free radical-mediated oxidative stress in L-NAME-induced hypertensive rats.

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Orphenadrine prevents 3-nitropropionic acid-induced neurotoxicity in vitro and in vivo

British Journal of Pharmacology ◽

10.1038/sj.bjp.0703869 ◽

2001 ◽

Vol 132 (3) ◽

pp. 693-702 ◽

Cited By ~ 29

Author(s):

David Pubill ◽

Ester Verdaguer ◽

Anna Ma Canudas ◽

Francesc Xavier Sureda ◽

Elena Escubedo ◽

...

Keyword(s):

Nitropropionic Acid ◽

3 Nitropropionic Acid

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Potential role of TrkB agonist in neuronal survival by promoting CREB/BDNF and PI3K/Akt signaling in vitro and in vivo model of 3-nitropropionic acid (3-NP)-induced neuronal death

APOPTOSIS ◽

10.1007/s10495-020-01645-x ◽

2020 ◽

Author(s):

Sahabuddin Ahmed ◽

Mohit Kwatra ◽

Basveshwar Gawali ◽

Samir Ranjan Panda ◽

V. G. M. Naidu

Keyword(s):

Neuronal Death ◽

Potential Role ◽

Neuronal Survival ◽

Akt Signaling ◽

In Vivo Model ◽

Nitropropionic Acid ◽

3 Nitropropionic Acid

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Bacopa monnierias an Antioxidant Therapy to Reduce Oxidative Stress in the Aging Brain

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2015/615384 ◽

2015 ◽

Vol 2015 ◽

pp. 1-9 ◽

Cited By ~ 24

Author(s):

Tamara Simpson ◽

Matthew Pase ◽

Con Stough

Keyword(s):

Oxidative Stress ◽

Cognitive Function ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Bacopa Monnieri ◽

Aging Brain ◽

Resonance Spectroscopy ◽

Age Related

The detrimental effect of neuronal cell death due to oxidative stress and mitochondrial dysfunction has been implicated in age-related cognitive decline and neurodegenerative disorders such as Alzheimer’s disease. The Indian herbBacopa monnieriis a dietary antioxidant, with animal andin vitrostudies indicating several modes of action that may protect the brain against oxidative damage. In parallel, several studies using the CDRI08 extract have shown that extracts ofBacopa monnieriimprove cognitive function in humans. The biological mechanisms of this cognitive enhancement are unknown. In this review we discuss the animal studies andin vivoevidence forBacopa monnierias a potential therapeutic antioxidant to reduce oxidative stress and improve cognitive function. We suggest that future studies incorporate neuroimaging particularly magnetic resonance spectroscopy into their randomized controlled trials to better understand whether changes in antioxidant statusin vivocause improvements in cognitive function.

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Protective Effects of Aqueous Extract ofLuehea divaricataagainst Behavioral and Oxidative Changes Induced by 3-Nitropropionic Acid in Rats

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2015/723431 ◽

2015 ◽

Vol 2015 ◽

pp. 1-11 ◽

Cited By ~ 9

Author(s):

Aline Alves Courtes ◽

Letícia Priscila Arantes ◽

Rômulo Pillon Barcelos ◽

Ingrid Kich da Silva ◽

Aline Augusti Boligon ◽

...

Keyword(s):

Locomotor Activity ◽

Aqueous Extract ◽

Antioxidant Properties ◽

Male Rats ◽

Protective Effects ◽

Neuroprotective Effects ◽

Nitropropionic Acid ◽

3 Nitropropionic Acid

Huntington’s disease (HD) is an autosomal dominant neurodegenerative disease. Accordingly, 3-nitropropionic acid (3-NP) has been found to effectively produce HD-like symptoms.Luehea divaricata(L. divaricata), popularly known in Brazil as “açoita-cavalo,” may act as a neuroprotective agentin vitroandin vivo. We evaluated the hypothesis that the aqueous extract ofL. divaricatacould prevent behavioral and oxidative alterations induced by 3-NP in rats. 25 adult Wistar male rats were divided into 5 groups: (1) control, (2)L. divaricata(1000 mg/kg), (3) 3-NP, (4)L. divaricata(500 mg/kg) + 3-NP, and (5)L. divaricata(1000 mg/kg) + 3-NP. Groups 2, 4, and 5 receivedL. divaricatavia intragastric gavage daily for 10 days. Animals in groups 3, 4, and 5 received 20 mg/kg 3-NP daily from days 8–10. At day 10, parameters of locomotor activity and biochemical evaluations were performed. Indeed, rats treated with 3-NP showed decreased locomotor activity compared to controls. Additionally, 3-NP increased levels of reactive oxygen species and lipid peroxidation and decreased ratio of GSH/GSSG and acetylcholinesterase activity in cortex and/or striatum. Our results suggest that rats pretreated withL. divaricataprior to 3-NP treatment showed neuroprotective effects when compared to 3-NP treated controls, which may be due to its antioxidant properties.

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Neuroprotective efficacy of a combination of fish oil and ferulic acid against 3-nitropropionic acid-induced oxidative stress and neurotoxicity in rats: behavioural and biochemical evidence

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2013-0262 ◽

2014 ◽

Vol 39 (4) ◽

pp. 487-496 ◽

Cited By ~ 9

Author(s):

Denny Joseph K.M. ◽

Muralidhara

Keyword(s):

Oxidative Stress ◽

Fish Oil ◽

Ferulic Acid ◽

Cytosolic Calcium ◽

Brain Regions ◽

Male Rats ◽

Activity Levels ◽

Nitropropionic Acid ◽

3 Nitropropionic Acid

The beneficial effects of fish oil (FO) supplements on the central nervous system have been adequately demonstrated. However, FO supplementation at higher doses for longer duration is likely to cause oxidative stress in vivo. To overcome this, attempts have been made to enrich FO with known antioxidants/phytochemicals. In the present study, we examined the hypothesis that a combination of FO with ferulic acid (FA), a naturally occurring phenolic compound, is likely to provide higher degree of neuroprotection. This was examined by employing 3-nitropropionic acid (NPA), a well-known neurotoxin used to mimic behavioural and neurochemical features of Huntington’s disease. Growing male rats administered with NPA (25 mg/kg of body weight (bw) for 4 days) were provided with either FO (2 mL/kg bw), FA (50 mg/kg bw) or FO+FA for 2 weeks. Interestingly, FO+FA not only offered significant protection against NPA-induced behavioural impairments, but also markedly attenuated oxidative stress in brain regions (striatum/cerebellum) as evidenced by the reduction in reactive species, malondialdehyde, hydroperoxides and nitric oxide (NO) levels. Further, FO+FA combination restored the activities of various antioxidant enzymes and the levels of cytosolic calcium. In striatum, activity levels of acetylcholinesterase enzyme and dopamine levels were markedly restored among FO+FA rats. Interestingly, NPA-induced mitochondrial dysfunctions were also attenuated among FO+FA rats. Collectively, our findings suggest the advantage of co-treatment of FO with known antioxidants to achieve a higher therapeutic benefit in the treatment of oxidative stress-mediated neurodegenerative conditions.

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