Browsing by Author "Kannika Permpoonputtana"

Filter results by typing the first few letters
Now showing 1 - 10 of 10
  • No Thumbnail Available
    PublicationMetadata only
    The anti-inflammatory effect of melatonin in SH-SY5Y neuroblastoma cells exposed to sublethal dose of hydrogen peroxide
    (2017-06-01) Chutikorn Nopparat; Varunya Chantadul; Kannika Permpoonputtana; Piyarat Govitrapong; Mahidol University; Chulabhorn Royal Academy
    © 2017 Elsevier B.V. Brain inflammaging is considered as one of the underlying factors of neurodegenerative diseases. The present study aimed to investigate the effects of melatonin, an endogenous indoleamine mainly synthesized by the pineal gland, on hydrogen peroxide (H2O2)-induced inflammaging state in SH-SY5Y cells. Our data showed that p21Cip1 and p16INK4a, cell cycle arrest markers, and the number of senescence-associated β-galactosidase (SA-βgal) staining increased significantly in H2O2-treated cells. Melatonin treatment could reverse this effect. Flow cytometry analysis showed a significantly higher percentage in the G0/G1 phase and a lower proportion in the S phase of H2O2 treated cells. Cells pretreated with H2O2 showed a dramatic decrease in the formation of Ki67 immunoactivity while the treatment with melatonin increased Ki67-positive cell. Both mRNA and protein expression levels of the pro-inflammatory cytokines, interleukin-1β (IL-1β), IL-6 and, tumor necrosis factor-α (TNF-α) which were increased after induction with H2O2, could be attenuated by melatonin. In addition, melatonin decreased the phospho-nuclear factor kappa B (pNF-κB) expression and prevented its nuclear translocation, as well as abrogated the reduction of nuclear factor erythroid 2-related factor 2 (Nrf2) in SH-SY5Y cells exposed to H2O2. The present data suggested the importance of melatonin on ameliorating inflammation in SH-SY5Y cells.
  • No Thumbnail Available
    PublicationMetadata only
    The anti-inflammatory effect of melatonin on methamphetamine-induced proinflammatory mediators in human neuroblastoma dopamine SH-SY5Y cell lines
    (2013-01-01) Kannika Permpoonputtana; Piyarat Govitrapong; Mahidol University
    Methamphetamine (METH) is a highly addictive drug that is commonly abused worldwide. This psychostimulant drug causes the disturbances in the dopaminergic and serotonergic neurons of several brain areas. Exposure to METH has been shown to induce oxidative stress, reactive oxygen species, reactive nitrogen species, and neuroinflammation. However, the mechanism underlying METH-induced inflammation in neurons is still unclear. In this study, we investigated whether METH caused inflammatory effects in human dopaminergic neuroblastoma SH-SY5Y cells and whether this effect involved the nuclear factor-κB (NF-κB) transcription factor pathway. The present results showed that METH significantly increased inducible nitric oxide synthase (iNOS) expression in a concentration-dependent manner and significantly increased the levels of tumor necrosis factor (TNF)-α mRNA and phosphorylated NF-κB, which is translocated into the nucleus. Moreover, our results also show that METH downregulated another transcription factor, the nuclear factor erythroid 2-related factor (Nrf2), a transcription factor implicated in the expression of several antioxidant/detoxificant enzymes. Furthermore, we also examined the anti-inflammatory effect of melatonin against these METH-induced neuroinflammatory functions. The results show that melatonin significantly decreases the iNOS protein expression and TNF-α mRNA levels caused by METH. The activation and the level of pNF-κB were decreased while Nrf2 expression was increased when cells were pre-incubated with 100 nM of melatonin. In order to show the relationship between cell death and the increase of iNOS, 100 μM of l-NAME, an iNOS inhibitor pretreatment significantly prevented cell death caused by METH. These results demonstrate, for the first time, that METH directly induces inflammation in neurons via an NF-κB-dependent pathway and that the anti-neuroinflammatory effects of melatonin result from the inhibition of activated NF-κB in parallel with potentiated antioxidant/detoxificant defense by activated Nrf2 pathway. © 2012 Springer Science+Business Media, LLC.
  • No Thumbnail Available
    PublicationMetadata only
    Calcitonin gene-related peptide mediates an inflammatory response in Schwann cells via cAMP-dependent ERK signaling cascade
    (2016-01-01) Kannika Permpoonputtana; James E. Porter; Piyarat Govitrapong; Mahidol University; University of North Dakota
    © 2015 Elsevier Inc. Aims Calcitonin gene-related peptides (CGRP), an endogenous neuropeptide, play an important role in the development of neuroinflammation by acting upon its receptor. The CGRP receptor immunoreactivity was identified on Schwann cells. However the effects of CGRP on Schwann cells are unknown and the exact signaling mechanisms associated with CGRP receptor activation related to Schwann cells inflammatory responses are not well understood. We investigated the effect of CGRP on CGRP receptor activation mediates a proinflammatory signaling response in Schwann cells. Main methods CGRP-induced ERK-MAPK phosphorylation and proinflammatory cytokines, interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor (TNF-α) expressions were measured by immune blotting. We also used specific antagonist and inhibitors to confirm the exactly signaling pathway including CGRP (8-37), SQ 22536 and H-89. Key findings Treatment with CGRP demonstrated a significant generation of IL-1β and IL-6 but not in the level of TNF-α. In addition, there was a temporal increase in the activated form of ERK caused by CGRP that was prevented after pretreatment with CGRP (8-37), SQ 22536 and H-89. Furthermore, use of the CGRP (8-37), ERK inhibitor PD 98059, SQ 22536 or H-89 abolished the CGRP mediated increase in IL-1β. Significance This investigation provides evidence for a novel CGRP activation on Schwann cells that mediates inflammatory response by increasing of IL-1β and IL-6 expression. CGRP activates the cAMP-PKA-ERK signaling cascade leading to IL-1β production. These results support the notion that CGRP may play a direct role to initiate inflammatory processes in the peripheral nervous system.
  • Thumbnail Image
    ItemOpen Access
    The effect of equine-assisted therapy on visual-motor integration in adolescent autism spectrum disorders
    (2015-03) Paranan Chorachit; Panadda Thanasetkorn; Nootchanart Ruksi; Kannika Permpoonputtana; Vasunun Chumchua; Mahidol University. National Institute for Child and Family Development; Mahidol University. Faculty of Physical Thearpy
    The goal of the present study was to examine the effect of equine-assisted therapy (EAT) on visual-motor integration (VMI) in adolescent autism spectrum disorders (ASD). EAT was applied to eleven-year-old boy with ASD. The boy was attending in Cognitive Neuroscience Research unit of Human Development Academic Research, Mahidol University. The EAT sessions took place for twice a week in a period of four weeks. The boy’s assessments were conducted in the baseline, middle, and end of four weeks’ treatment and in a follow-up session one month after. Data at fourth week demonstrated positive changes, with improvements continuing one month after the session’s completion, as measured by Test of Visual-Motor Integration (Beery VMI). The improvement reported was in visual perception, motor coordination and visual-motor coordination. Interestingly, The EAT is not only be an efficient therapeutic method of improving visual-motor integration, but also promote a positive effect on perceived communication, planning, memory, and reducing self-stimulatory behaviours, all of which may lead to elevate attention in classroom in children with ASD. Therefore, the beneficial of EAT showed the positive effect promising trend and suggest that to be considered as an alternative implement therapeutic for ASD.
  • No Thumbnail Available
    PublicationMetadata only
    Effect of melatonin on d-amphetamine-induced neuroglial alterations in postnatal rat hippocampus and prefrontal cortex
    (2012-08-22) Kannika Permpoonputtana; Sujira Mukda; Piyarat Govitrapong; Mahidol University
    Amphetamine is a psychostimulant drug that produces long-lasting neurotoxic effects on the central nervous system. Recent studies suggested that glia might contribute to amphetamine-induced neuropathy. Excessive activation of astrocytes can be deleterious to the neuron. Amphetamine-induced lesions during development have the potential to produce numerous permanent abnormalities in neural circuitry and function, including memory deficit. In the present study, postnatal rats were injected with either saline or d-amphetamine for 7 consecutive days, starting on postnatal day 4 (P4). Our results found that d-amphetamine caused a marked increase in glia fibrillary acidic protein (GFAP), an astroglia marker, expression that implicated astrogliosis in both hippocampus and prefrontal cortex. The effect of d-amphetamine on hippocampal and prefrontal cortex neurons was also investigated, and we detected a downregulation of βIII-tubulin, a marker of premature neuron expression. Furthermore, we found that pretreatment with melatonin, a major hormone secreted from the pineal gland, prevented glial cell activation and βIII-tubulin reduction, caused by d-amphetamine in both hippocampus and prefrontal cortex. The present study suggests that melatonin can attenuate the detrimental effect of d-amphetamine on glial and neuronal cells. © 2012 Elsevier Ireland Ltd.
  • No Thumbnail Available
    PublicationMetadata only
    Long-term administration of melatonin attenuates neuroinflammation in the aged mouse brain
    (2018-07-02) Kannika Permpoonputtana; Patlada Tangweerasing; Sujira Mukda; Parichart Boontem; Chutikorn Nopparat; Piyarat Govitrapong; Mahidol University; Chulabhorn Royal Academy
    © 2018, Leibniz Research Centre for Working Environment and Human Factors. All rights reserved. Aging is often accompanied by a decline in cognitive function in conjunction with a variety of neurobiological changes, including neuroinflammation. Melatonin is a key endogenous indoleamine secreted by the pineal gland that plays a crucial role in the regulation of circadian rhythms, is a potent free radical scavenger, has anti-inflammatory activity and serves numerous other functions. However, the role of melatonin in sterile inflammation in the brain has not been fully investigated. In the present study, we investigated the neuroinflammation status in aged mouse brains. The results showed that the protein levels of integrin αM (CD11b), glial fibrillary acidic protein (GFAP), the major pro-inflammatory cytokines (interleukin-1 beta [IL-1β], interleukin-6 [IL-6], and tumor necrosis factor alpha [TNF-α]) and phosphor-nuclear factor kappa B (pNFκB) were significantly increased, while Nmethyl- D-aspartate (NMDA) receptor subunits NR2A and NR2B, Ca2+/calmodulin-dependent protein kinase II (CaMKII), and brain-derived neurotrophic factor (BDNF) were down-regulated in the hippocampus and prefrontal cortex (PFC) of 22-months-old (aged) mice compared with 2-months-old (young adult) mice. Melatonin was administered in the drinking water to a cohort of the aged mice at a dose of 10 mg/kg/day, beginning at an age of 16 months for 6 months. Our results revealed that melatonin significantly attenuated the alterations in these protein levels. The present study suggests an advantageous role for melatonin in anti-inflammation, and this may lead to the prevention of memory impairment in aging.
  • No Thumbnail Available
    PublicationMetadata only
    Noradregenic depression of neuronal excitability in the entorhinal cortex activation of TREK-2 K+ channels
    (2009-04-17) Zhaoyang Xiao; Pan Yue Deng; Lalida Rojanathammanee; Chuanxiu Yang; Laurel Grisanti; Kannika Permpoonputtana; David Weinshenker; Van A. Doze; James E. Porter; Saobo Lei; University of North Dakota; The Institute of Science and Technology for Research and Development, Mahidol University; Mahidol University; Emory University
    The entorhinal cortex is closely associated with the consolidation and recall of memories, Alzheimer disease, schizophrenia, and temporal lobe epilepsy. Norepinephrine is a neurotransmitter that plays a significant role in these physiological functions and neurological diseases. Whereas the entorhinal cortex receives profuse noradrenergic innervations from the locus coeruleus of the pons and expresses high densities of adrenergic receptors, the function of norepinephrine in the entorhinal cortex is still elusive. Accordingly, we examined the effects of norepinephrine on neuronal excitability in the entorhinal cortex and explored the underlying cellular and molecular mechanisms. Application of norepinephrine-generated hyperpolarization and decreased the excitability of the neurons in the superficial layers with no effects on neuronal excitability in the deep layers of the entorhinal cortex. Norepinephrine-induced hyperpolarization was mediated by α 2A adrenergic receptors and required the functions of Gαi proteins, adenylyl cyclase, and protein kinase A. Norepinephrine-mediated depression on neuronal excitability was mediated by activation of TREK-2, a type of two-pore domain K+ channel, and mutation of the protein kinase A phosphorylation site on TREK-2 channels annulled the effects of norepinephrine. Our results indicate a novel action mode in which norepinephrine depresses neuronal excitability in the entorhinal cortex by disinhibiting protein kinase A-mediated tonic inhibition of TREK-2 channels. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.
  • No Thumbnail Available
    PublicationMetadata only
    Occupational therapists’ experiences and perspectives towards occupation-based practice in Thailand: A mixed-methods study
    (2020-01-01) Anuchart Kaunnil; Supalak Khemthong; Sarinya Sriphetcharawut; Peeradech Thichanpiang; Veerawat Sansri; Surachart Thongchoomsin; Kannika Permpoonputtana; Cristina R. Smith; Medical University of South Carolina; Mahidol University; Chiang Mai University
    © The Author(s) 2020. Introduction: Occupation-based practice is a core tenet of occupational therapy. This study explores perspectives and experiences with occupation-based practice among Thai occupational therapists. Method: Using mixed methods, a focus group was conducted with eight occupational therapists, and the results were interpreted using thematic analysis. A questionnaire survey was also completed concerning practitioner perspectives (n = 216). Findings: Three major themes were identified: (a) perspectives on occupation-based practice were related to practice areas and felt to strengthen the identity of occupational therapy (52% strongly agree), leading to improved services and better outcomes for clients (44% strongly agree); (b) approaches focused on activities of daily living were appropriate for cross-practice areas; and (c) occupation-based practice is consistent with integrated medical sciences and occupations for clients (52% strongly agree). Conclusion: Implementing occupation-based practice will be of value to clients, provide benefits as a compass to direct processes, and enhance clinical reasoning and outcomes.
  • No Thumbnail Available
    ItemMetadata only
    Playgroup intervention in young children with autistic spectrum disorders : a series of 6 boys
    (Mahidol University. Mahidol University Library and Knowledge Center, 2006) Kannika Permpoonputtana; Nittaya J. Kotchabhakdi; Niphinich Kotchabhakdi; Nalinee Cherwanitchakorn; Vitharon Boon-yasidhi; Kaewta Nopmaneejumruslers
  • No Thumbnail Available
    PublicationMetadata only
    Protective Effects of Melatonin on Methamphetamine-Induced Blood–Brain Barrier Dysfunction in Rat Model
    (2020-01-01) Jatuporn Namyen; Kannika Permpoonputtana; Chutikorn Nopparat; Jiraporn Tocharus; Chainarong Tocharus; Piyarat Govitrapong; Mahidol University; Chiang Mai University; Chulabhorn Royal Academy
    © 2020, Springer Science+Business Media, LLC, part of Springer Nature. The specialized brain endothelial cells interconnected by unique junctions and adhesion molecules are distinctive features of the blood–brain barrier (BBB), maintaining the homeostasis of the cerebral microenvironment. This study was designed to investigate the protective effects of melatonin on methamphetamine (METH)-induced alterations of BBB integrity. Wistar rats were randomly distributed into groups and underwent melatonin pretreatment and escalating-high doses of METH treatment. Immunohistochemistry was performed to demonstrate the BBB leakage. Protein and RNA samples were isolated from hippocampal and prefrontal cortical tissues and measured expression levels of molecular markers associated with BBB structural components and inflammatory processes. METH provoked the loss of zonula occludens (ZO)-1, occludin, and claudin-5 tight junction proteins. Furthermore, METH caused an excessive increase in matrix metalloproteinase-9 (MMP-9) enzyme, intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) and the increase in NAD(P)H oxidase 2 (NOX2). Melatonin exerted the protective effects by recovering tight junction loss; attenuating excessive MMP-9, NOX2, and cell adhesion molecule expression; and reducing serum albumin in the brain. Our results also showed the protective effects of melatonin against METH neurotoxic profiles, characterized by reactive gliosis: microglia (integrin-αM) and astrocyte (GFAP); an excessive upregulation of primary pro-inflammatory cytokines: interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α); activation of neuroinflammatory signaling: nuclear factor-kappa B (NF-κB); and suppression of anti-oxidative signaling: nuclear factor erythroid 2-related factor (Nrf2), that may exacerbate BBB structural impairment. Our results provide insights into the beneficial effects of melatonin against METH-induced BBB disruption and mechanisms that play detrimental roles in BBB impairment by in vivo design.