Pharmacology - Research Publications

Permanent URI for this collectionhttps://kr.cup.edu.in/handle/32116/111

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Author: search.filters.author.Arthur, RichmondSubject: search.filters.subject.Oxidative stress

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    Trans-cinnamaldehyde mitigates rotenone-induced neurotoxicity via inhibiting oxidative stress in rats
    (Elsevier B.V., 2022-12-21T00:00:00) Kumar, Sandeep; Kumar, Sachin; Arthur, Richmond; Kumar, Puneet
    Background: The second most prevalent age-related brain condition, Parkinson's disease (PD) is characterised by the loss of neurons in the substantia nigra pars compacta (SNpc). It is associated with symptoms like bradykinesia, stiffness, tremor, and impaired postural responses. Motor dysfunction, and neurochemical imbalance, are involved in the pathophysiology of PD. It has been hypothesised that trans cinnamaldehyde (TCA) a component of Traditional Chinese Medicine (TCM) can ameliorate Parkinson-like symptoms by altering the levels of different biochemical markers and reverse motor impairments. This research sought to determine the neuroprotective effect of TCA against the neurotoxicity caused by rotenone. Basic Procedure: Rotenone (1.5 mg/kg/day; s.c. for 35 days) was given to rats to induce Parkinson-like symptoms. TCA (5, 10, and 20 mg/kg) and concomitant treatment of TCA (5 mg/kg) with L-NAME (10 mg/kg) were given one hour prior to rotenone administration. Every week until the 35th day, behavioral parameters (muscle coordination, spontaneous motor movement and gait abnormalities) were assessed using rotarod, actophotometer, and narrow beam apparatus respectfully. Rats were decapitated on the 35th day, the striatum and cortex were isolated for biochemical tests. Main findings: Rotenone treatment reduced body weight, altered motor coordination and reduced the oxidative defense system. Treatment with TCA significantly improved the alterations in antioxidant levels as well as behavioral parameters. Furthermore, L-NAME (nitric oxide synthase inhibitor) in combination with TCA had a more significant effect as compared to TCA alone, signifying a possible drug interaction. Principal conclusion: TCA could be employed as an adjuvant in PD management. � 2022 The Authors
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    Ferulic acid ameliorates neurodegeneration via the Nrf2/ARE signalling pathway: A Review
    (Elsevier B.V., 2022-10-30T00:00:00) Singh, Surbhi; Arthur, Richmond; Upadhayay, Shubham; Kumar, Puneet
    Background: Ferulic acid is a polyphenolic phytoconstituent synthesized from the metabolism of amino acids phenylalanine and tyrosine found in fruits and vegetables. Neurodegenerative disorders have been a thorn in the flesh of neuroscientists owing in part to the increase in the aged population. Several drugs used in the management of these disorders are either ineffective or come with unbearable side effects. We present a review of ferulic acid focusing on leveraging its antioxidant property in an attempt to explain its role in neurodegenerative disorders. Basic procedure: data were obtained by perusing scientific databases including Web of Science and PubMed. It was realised that 18,000 articles were associated with ferulic acid from 1960-to 2022. We narrowed it down using the keywords neuroprotection, and antioxidant of which we had 239 articles. Main findings: results indicated that ferulic acid has wide neuropharmacological applications due to its antioxidant, anti-inflammatory, neuroprotective and antiapoptotic effects among others. The neuroprotective effect of ferulic acid has been studied in many diseases like Alzheimer's, Epilepsy, and Parkinson's disease. Principal conclusion: the neuroprotective potential of FA may be due to its ability to absorb active forms of oxygen and nitrogen and use redox-bearing compounds to regulate genetic expression including, encoding for antioxidant enzymes, the anti-apoptotic protein family Bcl-2, and pro-survival neurotrophic factors like BDNF. Its higher bioavailability and lipophilic nature make it a better drug candidate than other polyphenols for neurological disorders. � 2022 The Author(s)