Nur Khalisah Kaswan

Universiti Putra Malaysia

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Noor Aishah Mohammed Izham

Management and Science University

Enoch Kumar Perimal

Curtin University

Mohd Roslan Sulaiman

Leiden University Medical Center

Tengku Azam Shah Tengku Mohamad

Universiti Putra Malaysia

Hemabarathy Bharatham

National University of Malaysia

Nurul Syazwani Mohd Suhaimi

Universiti Putra Malaysia

Sharmili Vidyadaran

Universiti Putra Malaysia

Jasmine Siew Min Chia

Management and Science University

Kavitha Sukirthalingam

Universiti Putra Malaysia

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Universiti Putra Malaysia

National University of Malaysia

Institute of Biomedical Science

Management and Science University

University of Malaya

Curtin University

University of Adelaide

Australian Research Council

University of Kuala Lumpur

Universiti Teknologi MARA

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Cardamonin Modulates Neuropathic Pain through the Possible Involvement of Serotonergic 5-HT1A Receptor Pathway in CCI-Induced Neuropathic Pain Mice Model

Molecules (2021)

Nur Khalisah Kaswan Noor Aishah Mohammed Izham Tengku Azam Shah Tengku Mohamad Mohd Roslan Sulaiman Enoch Kumar Perimal

Cardamonin, a naturally occurring chalcone isolated from Alpinia species has shown to possess strong anti-inflammatory and anti-nociceptive activities. Previous studies have demonstrated that cardamonin exerts antihyperalgesic and antiallodynic properties in chronic constriction injury (CCI)-induced neuropathic pain animal model. However, the mechanisms underlying cardamonin’s effect have yet to be fully understood. The present study aims to investigate the involvement of the serotonergic system in cardamonin induced antihyperalgesic and antiallodynic effects in CCI-induced neuropathic pain mice model. The neuropathic pain symptoms in the CCI mice model were assessed using Hargreaves Plantar test and von-Frey filament test on day 14 post-surgery. Central depletion of serotonin along the descending serotonergic pathway was done using ρ-chlorophenylalanine (PCPA, 100 mg/kg, i.p.), an inhibitor of serotonin synthesis for four consecutive days before cardamonin treatment, and was found to reverse the antihyperalgesic and antiallodynic effect produced by cardamonin. Pretreatment of the mice with several 5-HT receptor subtypes antagonists: methiothepin (5-HT1/6/77 receptor antagonist, 0.1 mg/kg), WAY 100635 (5-HT1A receptor antagonist, 1 mg/kg), isamoltane (5-HT1B receptor antagonist, 2.5 mg/kg), ketanserin (5-HT2A receptor antagonist, 0.3 mg/kg), and ondansetron (5-HT3 receptor antagonist, 0.5 mg/kg) were shown to abolish the effect of cardamonin induced antihyperalgesic and antiallodynic effects. Further evaluation of the 5-HT1A receptor subtype protein expressions reveals that cardamonin significantly upregulated its expression in the brainstem and spinal cord. Our results suggest that the serotonergic pathway is essential for cardamonin to exert its antineuropathic effect in CCI mice through the involvement of the 5-HT1A receptor subtype in the central nervous system.

Ketanserin

10.3390/molecules26123677

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Exploring the possibilities of using in vitro model for neuropathic pain studies

Neuroscience Research Notes (2022)

Noor Aishah Mohammed Izham Jasmine Siew Min Chia Nur Khalisah Kaswan Kavitha Sukirthalingam Sharmili Vidyadaran

Establishing experimental models to study neuropathic pain has been challenging due to the complex mechanism underlying the condition. Although in vivo models have been useful in the observation of behavioural pain responses, it should be acknowledged that species-to-species variance can lead to differences in terms of molecular mechanism and genetic expression. The study of molecular and signal transduction of neuropathic pain using in vivo models faces limitations due to ethical considerations involving pain induction in animals and the intricacy of molecular interactions in the pathophysiology of the condition. Hence, developing relevant in vitro models to study neuropathic pain is important, as it considers the physiological microenvironment and reduces the use of experimental animals. Several considerations should be taken into account in developing an in vitro model of neuropathic pain, including the use of either primary culture of cell lines with considerations to their origins; human or animal, the method of neuropathic pain-like induction and the relevant assays to assess pain. This review recapitulates previous research employing in vitro models in investigating the molecular mechanism of neuropathic pain, intending to provide an alternative to the growing concerns on in vivo neuropathic pain models.

10.31117/neuroscirn.v5i3.144

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Cardamonin inhibits nitric oxide production modulated through NMDA receptor in LPS-Induced SH-SY5Y cell in vitro model

Life Sciences Medicine and Biomedicine (2020)

Nur Khalisah Kaswan Nurul Syazwani Mohd Suhaimi Noor Aishah Mohammed Izham Tengku Azam Shah Tengku Mohamad Mohd Roslan Sulaiman

Background: Cardamonin is a naturally occurring chalcone from the Alpinia species. It is known to possess antioxidant and anti-inflammatory properties. Our previous studies have shown that cardamonin has antihyperalgesic and antiallodynic effects on CCI-induced neuropathic pain in mice. Although the evidence of the association between cardamonin and neuropathic pain has been reported in animal studies, specific targets using in vitro models are still lacking. Objectives/Methods: This study aims to investigate the effect of cardamonin on nitric oxide production using the LPS-induced neuropathic pain-like SH-SY5Y in vitro model through NMDA receptor expression. Results: Cardamonin administration in differentiated SH-SY5Y cells significantly reduced nitric oxide production assessed using Griess reagent. Western blot analysis demonstrated a significant reduction in GluN2B receptor expression in the cardamonin treated SH-SY5Y cells compared to the vehicle treated group. Conclusions: These data suggest that cardamonin reduces nitric oxide production modulated through NMDA GluN2B receptor subunit. Our results provides preliminary data to support the in vivo studies using cardamonin and may contribute to further understanding the mechanisms of action of cardamonin.

SH-SY5Y

10.28916/lsmb.4.9.2020.58

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Citations (3)