Naringin in a combined therapy with phenytoin on pentylenetetrazole-induced kindling in rats

Kola, Phani Kumar; Akula, Annapurna; Rao, Lakshmi Sudeepthi Nissankara; Danduga, Ravi Chandra Sekhara Reddy; Mohammad, Abutalaha; Ineedi, Srikanth

doi:10.1016/j.yebeh.2018.10.006

Cited by 22 publications

(11 citation statements)

References 43 publications

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“…The chrysin NPs administration reduces the number of neuronal eosinophilic and pyknotic neurons, which further reduce neuronal damage, as apparent. [ 32,33 ]…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective role of chrysin‐loaded poly(lactic‐co‐glycolic acid) nanoparticle against kindling‐induced epilepsy through Nrf2/ARE/HO‐1 pathway

Zhang¹,

Zhao

Afzal

et al. 2020

J Biochem & Molecular Tox

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Chrysin is the major bioactive compound of blue passionflower, an important medicinal plant used in traditional herbal formulations since ancient times. In the present study, we report that chrysin nanoparticles (chrysin NPs) protect Wistar rats against kindling‐induced epilepsy. Nanoparticles of sizes less than 150 nm with a spherical shape were prepared using poly(d,l‐lactic‐co‐glycolic acid) and polyvinyl alcohol, respectively, as polymer and stabilizer. Rats were injected with subconvulsive doses of pentylenetetrazole (PTZ) (35 mg/kg, intraperitoneal) every second day, with 22 injections in total, and on the same days, they received protective doses of the chrysin NPs (5 and 10 µg/mL, PO), respectively, 45 min before each PTZ injection. After the last PTZ injection, an average of thirteen seizure scores was recorded. Animals were killed by decapitation 24 h after a seizure. The cortex and hippocampus were removed and stored in liquid nitrogen for determining oxidative stress terminal deoxynucleotidyl transferase dUTP nick‐end labeling assay, histopathology, and reverse transcription‐polymerase chain reaction for messenger RNA expression. The result showed chrysin NPs treatment has counteracted oxidative stress, reduced neuronal apoptosis, and upregulated nuclear factor erythroid 2‐related factor 2 (Nrf2), heme oxygenase‐1 (HO‐1), and NAD(P)H quinone oxidoreductase 1. In conclusion, our findings demonstrate that the neuroprotective effect of chrysin NPs against kindling‐induced epilepsy might be escorted by the alleviation of oxidative stress through the Nrf2/antioxidant response element/HO‐1 pathway signal pathway.

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“…The chrysin NPs administration reduces the number of neuronal eosinophilic and pyknotic neurons, which further reduce neuronal damage, as apparent. [ 32,33 ]…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective role of chrysin‐loaded poly(lactic‐co‐glycolic acid) nanoparticle against kindling‐induced epilepsy through Nrf2/ARE/HO‐1 pathway

Zhang¹,

Zhao

Afzal

et al. 2020

J Biochem & Molecular Tox

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“…Unfortunately, phenytoin efficacy on epileptic seizure is apparently reduced with its chronic use so it was categorized as a highly resistant AED. In addition, it has a worsening effect on neurological derangements of epilepsy, especially memory loss and cognitive dysfunction 10,11 . Therefore, it is important to find new AEDs with expanded safety profiles and positive effect on cognition.…”

Section: Introductionmentioning

confidence: 99%

Pentoxifylline prevents epileptic seizure via modulating HMGB1/RAGE/TLR4 signalling pathway and improves memory in pentylenetetrazol kindling rats

Badawi

Shokr

Zaki

et al. 2021

Clin Exp Pharma Physio

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Epilepsy is a chronic widely prevalent neurologic disorder, affecting brain functions with a broad spectrum of deleterious consequences. High mobility group box1 (HMGB1) is a nuclear non‐histone protein that targets vital cell receptor of toll‐like receptor 4 (TLR4) and advanced glycation end products (RAGE). HMGB1 mediated TLR4/RAGE cascade has been scored as a key culprit in neuroinflammatory signalling that critically evokes development of impaired cognition and epilepsy. The current study aimed to investigate the neuroprotective effect of pentoxifylline (PTX) on pentylenetetrazol (PTZ)‐kindling rats by its anti‐inflammatory/antioxidant capacity and its impact on memory and cognition were investigated, too. PTZ was intraperitoneally injected 35 mg/kg, every 48 h, for 14 doses, to evoke kindling model. Phenytoin (30 mg/kg, i.p.) and PTX (60 mg/kg, i.p.) or their combination were given once daily for 27 days. PTX treatment showed a statistically significant effect on behavioural, histopathological and neurochemical analysis. PTX protected the PTZ kindling rats from epileptic seizures and improved memory and cognitive impairment through the Morris water maze (MWM) test. Furthermore, PTX reversed PTZ hippocampal neuronal loss by decreasing protein expression of amyloid‐β peptide (Aβ), Tau and β site‐amyloid precursor protein cleavage enzyme 1 (BACE1), associated with a marked reduction in expression of inflammatory mediators such as HMGB1, TL4, and RAGE proteins. Furthermore, PTX inhibited hippocampal apoptotic caspase 1 protein, total reactive oxygen species (TROS) along with upregulated erythroid 2‐related factor 2 (Nrf2) content. In conclusion, PTX or its combination with phenytoin represent a promising drug to inhibit the epilepsy progression via targeting the HMGB1/TLR4/RAGE signalling pathway.

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“…This combination can improve the neurochemical balance by elevating the levels of GABA and dopamine, decrease the levels of Glu and MDA, and increase the levels of antioxidants GSH, SOD, CAT, and total thiol. Therefore, the co-administration of naringin with phenytoin offers a potential treatment option for epilepsy (Phani et al, 2018).…”

Section: Naringin and Phenytoinmentioning

confidence: 99%

Natural Medicines for the Treatment of Epilepsy: Bioactive Components, Pharmacology and Mechanism

et al. 2021

Front. Pharmacol.

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Epilepsy is a chronic disease that can cause temporary brain dysfunction as a result of sudden abnormal discharge of the brain neurons. The seizure mechanism of epilepsy is closely related to the neurotransmitter imbalance, synaptic recombination, and glial cell proliferation. In addition, epileptic seizures can lead to mitochondrial damage, oxidative stress, and the disorder of sugar degradation. Although the mechanism of epilepsy research has reached up to the genetic level, the presently available treatment and recovery records of epilepsy does not seem promising. Recently, natural medicines have attracted more researches owing to their low toxicity and side-effects as well as the excellent efficacy, especially in chronic diseases. In this study, the antiepileptic mechanism of the bioactive components of natural drugs was reviewed so as to provide a reference for the development of potential antiepileptic drugs. Based on the different treatment mechanisms of natural drugs considered in this review, it is possible to select drugs clinically. Improving the accuracy of medication and the cure rate is expected to compensate for the shortage of the conventional epilepsy treatment drugs.

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Naringin in a combined therapy with phenytoin on pentylenetetrazole-induced kindling in rats

Cited by 22 publications

References 43 publications

Neuroprotective role of chrysin‐loaded poly(lactic‐co‐glycolic acid) nanoparticle against kindling‐induced epilepsy through Nrf2/ARE/HO‐1 pathway

Neuroprotective role of chrysin‐loaded poly(lactic‐co‐glycolic acid) nanoparticle against kindling‐induced epilepsy through Nrf2/ARE/HO‐1 pathway

Pentoxifylline prevents epileptic seizure via modulating HMGB1/RAGE/TLR4 signalling pathway and improves memory in pentylenetetrazol kindling rats

Natural Medicines for the Treatment of Epilepsy: Bioactive Components, Pharmacology and Mechanism

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