Limboonreung, Tanapol

Preferred name

Main Affiliation

School of Dentistry

tanapol.li@kmitl.ac.th

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Quinazolinedione Derivatives as Potential Anticancer Agents Through Apoptosis Induction in MCF-7
(2025-07-01)
Limboonreung, Tanapol
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Suansilpong, Teetat
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Jumjitvi, Panitan
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Lohawittayanan, Duangporn
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Krobthong, Sucheewin
Breast cancer remains a leading cause of mortality among women worldwide. Surgery, radiation therapy, chemotherapy, and hormone-based treatments are standard therapeutic approaches, but drug resistance and adverse effects necessitate the search for novel anticancer agents. Quinazolinedione derivatives have emerged as potential anticancer compounds due to their cytotoxic and apoptosis-inducing properties. This study aimed to evaluate the apoptotic induction of previously reported quinazolinedione derivatives on MCF-7 breast cancer cells. The cytotoxic effect was assessed using the MTT assay, apoptosis was quantified by Annexin V-PE/7AAD staining and flow cytometry, and apoptosis-related protein expression was analyzed via multiplexed bead-based immunoassays. These findings indicate that two derivatives in the series significantly reduced the cell viability in a dose-dependent manner. Apoptosis was induced primarily through the intrinsic apoptotic pathway as evidenced by the upregulation of caspase-9 and p53 and the downregulation of Bcl-2 and p-Akt. These results highlight quinazolinedione derivatives as promising candidates for breast cancer therapy prompting further investigation into their molecular mechanisms and potential clinical applications.
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17β-estradiol mitigates the inhibition of SH-SY5Y cell differentiation through WNT1 expression
(2023-12-01)
Shakya, Rubina
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Amonruttanapun, Prateep
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Limboonreung, Tanapol
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Chongthammakun, Sukumal
17β-estradiol (E2) and canonical WNT-signaling represent crucial regulatory pathways for microtubule dynamics and synaptic formation. However, it is unclear yet whether E2-induced canonical WNT ligands have significant impact on neurogenic repair under inflammatory condition. In this study, first, we prepared the chronic activated-microglial-conditioned media, known to be comprised of neuro-inflammatory components. Long term exposure of microglial conditioned media to SH-SY5Y cells showed a negative impact on differentiation markers, microtubule associated protein-2 (MAP2) and synaptophysin (SYP), which was successfully rescued by pre and co-treatment of 10 nM 17β-estradiol. The inhibition of estrogen receptors, ERα and ERβ significantly blocked the E2-mediated recovery in the expression of differentiation marker, SYP. Furthermore, the inflammatory inhibition of canonical signaling ligand, WNT1 was also found to be rescued by E2. To our surprise, E2 was unable to replicate this success with β-catenin, which is considered to be the intracellular transducer of canonical WNT signaling. However, WNT antagonist - Dkk1 blocked the E2-mediated recovery in the expression of the differentiation marker, MAP2. Therefore, our data suggests that E2-mediated recovery in SH-SY5Y differentiation follows a divergent pathway from the conventional canonical WNT signaling pathway, which seems to regulate microtubule stability without the involvement of β-catenin. This mechanism provides fresh insight into how estradiol contributes to the restoration of differentiation marker proteins in the context of chronic neuroinflammation.
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Corrigendum to “Diterpene glycosides from Holothuria scabra exert the α-synuclein degradation and neuroprotection from α-synuclein-mediated neurodegeneration in C. elegans model” [J. Ethnopharmacol. 279 (2021) 114347](S0378874121005766)(10.1016/j.jep.2021.114347)
(2023-01-30)
Chalorak, Pawanrat
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Sornkaew, Nilubon
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Manohong, Preeyanuch
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Niamnont, Nakorn
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Malaiwong, Nawapaht
The authors regret that two images on Figs. 6A and 7A were inadvertently duplicated during the assembly of the figures. The authors reviewed the original data and reorganized the correct representative images. The correct Figs. 6A and 7A are shown below. As described in the article, the images displayed in the figures were representative from each experimental group which were taken from the confocal microscopy, while the data represented in the graph were analysed from many images collected by using fluorescence microscopy. Therefore, the authors confirmed that the corrections of the images made in this erratum do not affect the figure legends, results, and conclusion of the study.[Formula presented][Formula presented] The authors would like to apologise for any inconvenience caused.
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Neurorescue effects of frondoside a and ginsenoside rg3 in c. Elegans model of parkinson’s disease
(2021-08-02)
Chalorak, Pawanrat
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Sanguanphun, Tanatcha
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Limboonreung, Tanapol
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Meemon, Krai
Parkinson’s disease (PD) is a currently incurable neurodegenerative disorder characterized by the loss of dopaminergic (DAergic) neurons in the substantia nigra pars compacta and αsynuclein aggregation. Accumulated evidence indicates that the saponins, especially from ginseng, have neuroprotective effects against neurodegenerative disorders. Interestingly, saponin can also be found in marine organisms such as the sea cucumber, but little is known about its effect in neurodegenerative disease, including PD. In this study, we investigated the anti-Parkinson effects of frondoside A (FA) from Cucumaria frondosa and ginsenoside Rg3 (Rg3) from Panax notoginseng in C. elegans PD model. Both saponins were tested for toxicity and optimal concentration by food clearance assay and used to treat 6-OHDA-induced BZ555 and transgenic α-synuclein NL5901 strains in C. elegans. Treatment with FA and Rg3 significantly attenuated DAergic neurodegeneration induced by 6-OHDA in BZ555 strain, improved basal slowing rate, and prolonged lifespan in the 6-OHDAinduced wild-type strain with downregulation of the apoptosis mediators, egl-1 and ced-3, and upregulation of sod-3 and cat-2. Interestingly, only FA reduced α-synuclein aggregation, rescued lifespan in NL5901, and upregulated the protein degradation regulators, including ubh-4, hsf-1, hsp16.1 and hsp-16.2. This study indicates that both FA and Rg3 possess beneficial effects in rescuing DAergic neurodegeneration in the 6-OHDA-induced C. elegans model through suppressing apoptosis mediators and stimulating antioxidant enzymes. In addition, FA could attenuate α-synuclein aggregation through the protein degradation process.
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Suppression of PI3K/Akt/mTOR pathway in chrysoeriol-induced apoptosis of rat C6 glioma cells
(2022-01-01)
Wongkularb, Suppanut
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Limboonreung, Tanapol
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Tuchinda, Patoomratana
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Chongthammakun, Sukumal
Chrysoeriol, a dietary methoxyflavonoid which is found in tropical medicinal plants, has been shown to have antioxidant, anti-inflammatory, and antineoplastic properties. The present study aimed to investigate the effects of chrysoeriol and its related mechanisms in rat C6 glioma cells. Cell viability in rat C6 glioma cells were measured by MTT assay. The protein expression levels of cleaved caspase-3, caspase-3, pro-apoptotic (Bax), anti-apoptotic protein (Bcl-2), and Annexin V were detected by Western blot analysis and immunocytochemical staining. Results showed that chrysoeriol significantly decreased cell viability and induced apoptosis in rat C6 glioma cells. Chrysoeriol significantly increased the levels of Bax/Bcl-2 ratio and cleaved caspase-3/caspase-3 ratio. Moreover, treatment with chrysoeriol significantly reduced the phosphorylation of PI3K, Akt, and mTOR expression in ratios. These results suggest that chrysoeriol promote apoptosis in rat C6 glioma cells via suppression of the PI3K/Akt/mTOR signaling pathway, thereby demonstrating the potential antineoplastic effects of chrysoeriol on glioma cells.
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Diterpene glycosides from Holothuria scabra exert the α-synuclein degradation and neuroprotection against α-synuclein-Mediated neurodegeneration in C. elegans model
(2021-10-28)
Chalorak, Pawanrat
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Sornkaew, Nilubon
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Manohong, Preeyanuch
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Niamnont, Nakorn
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Malaiwong, Nawaphat
Ethnopharmacological relevance: Holothuria (Metriatyla) scabra Jaeger (H. scabra), sea cucumber, is the marine organism that has been used as traditional food and medicine to gain the health benefits since ancient time. Although our recent studies have shown that crude extracts from H. scabra exhibited neuroprotective effects against Parkinson's disease (PD), the underlying mechanisms and bioactive compounds are still unknown. Aim of the study: In the present study, we examined the efficacy of purified compounds from H. scabra and their underlying mechanism on α-synuclein degradation and neuroprotection against α-synuclein-mediated neurodegeneration in a transgenic Caenorhabditis elegans PD model. Material and methods: The H. scabra compounds (HSEA-P1 and P2) were purified and examined for their toxicity and optimal dose-range by food-clearance and lifespan assays. The α-synuclein degradation and neuroprotection against α-synuclein-mediated neurodegeneration were determined using transgenic C. elegans model, Punc-54
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Influence of fluoride on neuronal differentiation in dopaminergic differentiation SH-SY5Y cells
(2022-01-01)
Limboonreung, Tanapol
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Chansiri, Sirirat
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Tsao, Stephany
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Khwanraj, Kawinthra
Fluoride is widely used in dentistry to prevent dental caries by increasing the fluoride content in saliva and aiding enamel remineralization. Excessive fluoride in the blood can cause adverse health effects such as fluorosis, which alter cerebral function. The influence of fluoride on dopaminergic neurons however, remains largely unclear. The present study examined the effect of sodium fluoride toxicity on dopaminergic neurons in retinoic acid-induced differentiation in SH-SY5Y cells. Cell viability was reduced by fluoride in both time- and concentration-dependent manners. Moreover, immunoblot analysis showed that fluoride decreased neuronal marker microtubule-associated protein-2 expression and levels of tyrosine hydroxylase, a rate-determining step enzyme in dopamine synthesis, even at a nonlethal dose. These results suggest that fluorosis may adversely affect dopaminergic neurons and may have harmful effects in individuals with degenerative dopaminergic neuron conditions, such as Parkinson's disease.
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Rational Design and Lead Optimisation of Potent Antimalarial Quinazolinediones and Their Cytotoxicity against MCF-7
(2023-04-01)
Charoensutthivarakul, Sitthivut
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Lohawittayanan, Duangporn
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Kanjanasirirat, Phongthon
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Jearawuttanakul, Kedchin
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Seemakhan, Sawinee
Quinazolinedione is one of the most outstanding heterocycles in medicinal chemistry thanks to its wide ranges of biological activities including antimalarial, anticancer, and anti-inflammatory. TCMDC-125133 containing a quinazolinedione pharmacophore displays promising antimalarial activity and low toxicity, as described in the GlaxoSmithKline (GSK) report. Herein, the design and synthesis of novel quinazolinedione derivatives is described on the basis of our previous work on the synthesis of TCMDC-125133, where low-cost chemicals and greener alternatives were used when possible. The initial SAR study focused on the replacement of the valine linker moiety; according to the in silico prediction using SwissADME, concise four-step syntheses toward compounds 4–10 were developed. The in-house synthesized compounds 4–10 were assayed for antimalarial activity against P. falciparum 3D7, and the result revealed that only the compound 2 containing a valine linker was tolerated. Another round of lead optimization focused on the replacement of the m-anisidine moiety in compound 2. A library of 12 derivatives was prepared, and the antimalarial assay showed that potent antimalarial activity could be maintained by replacing the methoxy group in the meta position of the phenyl side chain with a fluorine or chlorine atom (21: IC<inf>50</inf> = 36 ± 5 nM, 24: IC<inf>50</inf> = 22 ± 5 nM). Further lead optimization is underway to enhance the antimalarial activity of this class of compound. The compounds included in the study possess little to no antiproliferative activity against MCF-7 cells.

Limboonreung, Tanapol

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