Browsing by Author "Chittipong Tipbunjong"

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    Diarylheptanoid 1-(4-hydroxyphenyl)-7-phenyl-(6E)-6-hepten-3-one enhances C2C12 myoblast differentiation by targeting membrane estrogen receptors and activates Akt-mTOR and p38 MAPK-NF-κB signaling axes
    (2019-09-13) Chittipong Tipbunjong; Pissared Khuituan; Yindee Kitiyanant; Apichart Suksamrarn; Chumpol Pholpramool; Ramkhamhaeng University; Mahidol University; Prince of Songkla University
    © 2019, The Japanese Society of Pharmacognosy. Diarylheptanoid, 1-(4-hydroxyphenyl)-7-phenyl(6E)-6-hepten-3-one (HPPH), has been reported to enhance myoblast differentiation via estrogen receptor (ER). However, the underlying signaling pathway promising this action remains unknown. The present study thus aimed to investigate the signaling pathway of HPPH that enhances myoblast differentiation. Confluence C2C12 myoblasts were induced to differentiate in the absence or presence of HPPH (10 nM). Differentiation markers (myosin heavy chain (MHC) and myogenin) and other signaling molecules implicated in myogenic differentiation were analyzed by immunostaining and western blotting methods. To identify the location of ER and the signaling molecules, specific inhibitors were applied targeting these molecules. Nuclear factor-κB (NF-κB) DNA binding activity was measured using the electrophoresis mobility shift assay. The results showed that HPPH enhanced myoblast differentiation by increasing MHC and myogenin levels, number, and size as well as the fusion index of myotubes. These actions occurred via membrane ER. Several MAPK proteins were activated at the early stage of differentiation. However, only Akt and p38 MAPK, but not ERK, were implicated in these effects. The underlying signaling molecules of Akt to enhance myogenic differentiation by HPPH, at least in part, were mTOR/P70S6K and GSK-3β. On the other hand, the downstream signaling molecule of p38 MAPK was NF-κB. Our results suggested that HPPH enhanced myogenic differentiation by binding with membrane ER, which in turn recruited multiple axes including Akt-mTOR-P70S6K, Akt-GSK-3β, and p38 MAPK-NF-κB.
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    Molecular cloning and distribution of oxytocin/vasopressin-like mRNA in the blue swimming crab, Portunus pelagicus, and its inhibitory effect on ovarian steroid release
    (2018-04-01) Jirawat Saetan; Thanapong Kruangkum; Phetcharat Phanthong; Chittipong Tipbunjong; Wandee Udomuksorn; Prasert Sobhon; Prapee Sretarugsa; Mahidol University; Burapha University; Prince of Songkla University
    © 2018 Elsevier Inc. This study was aimed to characterize the full length of mRNA of oxytocin/vasopressin (OT/VP)-like mRNA in female Portunus pelagicus (PpelOT/VP-like mRNA) using a partial PpelOT/VP-like sequence obtained previously in our transcriptome analysis (Saetan, 2014) to construct the primers. The PpelOT/VP-like mRNA was 626 bp long and it encoded the preprohormones containing 158 amino acids. This preprohormone consisted of a signal peptide, an active nonapeptide (CFITNCPPG) followed by the dibasic cleavage site (GKR), and the neurophysin domain. Sequence alignment of the PpelOT/VP-like peptide with those of other animals revealed strong molecular conservation. Phylogenetic analysis of encoded proteins revealed that the PpelOT/VP-like peptide was clustered within the group of crustacean OT/VP-like peptide. Analysis by RT-PCR revealed the expression of mRNA transcripts in the eyestalk, brain, ventral nerve cord (VNC), ovary, intestine and gill. The in situ hybridization demonstrated the cellular localizations of the transcripts in the central nervous system (CNS) and ovary tissues. In the eyestalk, the mRNA expression was observed in the neuronal clusters 1–5 but not in the sinus gland complex. In the brain and the VNC, the transcripts were detected in all neuronal clusters but not in the glial cell. In the ovary, the transcripts were found in all stages of oocytes (Oc1, Oc2, Oc3, and Oc4). In addition, synthetic PpelOT/VP-like peptide could inhibit steroid release from the ovary. The knowledge gained from this study will provide more understanding on neuro-endocrinological controls in this crab species.
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    Natural diarylheptanoid compounds from Curcuma comosa Roxb. promote differentiation of mouse myoblasts C2C12 cells selectively via ER alpha receptors
    (2017-01-01) Chittipong Tipbunjong; Yindee Kitiyanant; Ganyapong Chaturapanich; Nilubon Sornkaew; Apichart Suksamrarn; Narisorn Kitiyanant; Karyn A. Esser; Chumpol Pholpramool; Mahidol University; Ramkhamhaeng University; University of Kentucky
    © 2016, Springer Science+Business Media New York. Diarylheptanoids exhibit numerous biological activities and have been used as traditional medicine in Asian countries. However, their effects on myogenesis are still unknown. This study determined the effects of eight different diarylheptanoid compounds including 1,7-diphenyl-(6E)-6-hepten-3-one (compound 1) and its analogs (compounds 2–8) isolated and purified from Curcuma comosa Roxb. on mouse myoblasts (C2C12 cells) proliferation and differentiation. All compounds (10−9–10−5M) were non-toxic to C2C12 cells, and had no anti-oxidant activity except (3S)-1-(3,4–dihydroxyphenyl)-7-phenyl-(6E)-6-hepten-3-ol (compound 8), which showed higher activity compared to that of ascorbic acid. Additionally, this compound (10−8M) effectively prevented the toxic effect of H2O2 on C2C12 cells. Proliferation of C2C12 cells was significantly increased by all compounds except compound 1 and (3R)-1,7-diphenyl-(4E,6E)-4,6-heptadien-3-ol (compound 4), whereas differentiation of myoblasts was enhanced by all compounds. The effect on proliferation was not blocked by ICI 182,780, but this blocker completely inhibited the effects of diarylheptanoids on differentiation. In addition, silencing the transcription of oestrogen receptor α (ERα), but not estrogen receptor β (ERβ), completely abolished the enhancement of differentiation. Together, the results indicate that diarylheptanoids enhance proliferation of C2C12 cells by a non-estrogenic mechanism, but induce differentiation selectively via ERα. These compounds may have potential for further development as therapeutic agents for treatment of muscle injury and/or diseases.
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    Styrene Oxide Caused Cell Cycle Arrest and Abolished Myogenic Differentiation of C2C12 Myoblasts
    (2020-01-01) Piyaporn Surinlert; Nitchamon Kongthong; Mariam Watthanard; Thannicha Sae-Lao; Piyawat Sookbangnop; Chumpol Pholpramool; Chittipong Tipbunjong; Siam University; Mahidol University; Thammasat University; Prince of Songkla University; Hatyaiwittayalai School
    © 2020 Piyaporn Surinlert et al. Contaminations of chemicals in foods and drinks are raising public concerns. Among these, styrene, a monomer for plastic production, receives increasing interest due to its ability to leach from the packaging and contaminate in foods and drinks causing many health problems. The present study was designed to investigate the effects of styrene monomer (STR) and its metabolite styrene oxide (STO) on C2C12 myoblast proliferation and differentiation. Based on an MTT assay, both STR and STO showed no cytotoxic effect at 10-100 μM. However, at 50-100 μM STO, but not STR, significantly inhibited cell proliferation. The STO-treated cells were accumulated in S-phase of cell cycles as revealed by flow cytometry. The antioxidant enzyme (catalase and superoxide dismutase) activities and the gene expressing these enzymes of the arrested cells were decreased and ultimately led to nuclear condensation and expression of apoptotic markers such as cleaved caspase-3 and-9, but not cleaved caspase-8. In addition, STO significantly suppressed myogenic differentiation by decreasing both the number and size of differentiated myotubes. Biochemical analysis showed attenuations of total protein synthesis and myosin heavy chain (MHC) protein expression. In conclusion, a metabolite of styrene, STO, leached from plastic packaging of foods and beverages suppressed both myoblast proliferation and differentiation, which would affect skeletal muscle development and regeneration.
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    Synthetic curcuminoid analogues abrogate oxidation-induced cell death and promote myogenic differentiation of C2C12 mouse myoblasts
    (2018-08-01) Chittipong Tipbunjong; Piyawat Sookbangnop; Vachiraporn Ajavakom; Apichart Suksamrarn; Yindee Kitiyanant; Chumpol Pholpramool; Ramkhamhaeng University; Mahidol University; Prince of Songkla University
    © Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, 300001 Nigeria and 2018 The authors. Purpose: To investigate the ability of two synthetic curcuminoid analogues, 6-(4-hydroxy-3-methoxyphenethyl)-5-(3-(4-hydroxy-3-methoxyphenyl)propanoyl)-4-phenyl-3,4-dihydropyrimidin-2(1H)-one (compound A) and 6-(4-hydroxy-3-methoxyphenethyl)-4-(4-hydroxy-3-methoxyphenyl)-5-(3-(4-hydroxy-3-methoxyphenyl)propanoyl)-3,4-dihydropyrimidin-2(1H)-one (compound B), to protect against oxidation-induced cell death and the potential to enhance proliferation and differentiation of C2C12 myoblast cells. Methods: Antioxidant activity of curcuminoid analogues was evaluated by DPPH assay. The cytotoxic activity of the compounds (0-25 mM) on C2C12 myoblasts was determined by MTT assay while the effect on cell proliferation was assessed by BrdU uptake. Myoblast cell differentiation was measured by the formation of myotubes and myosin heavy chain (MHC) protein expression using immunofluorescence staining and Western blotting, respectively. Results: Both curcuminoid analogues exhibited strong anti-oxidant activity of up to 3-fold greater than that of ascorbic acid, and were non-toxic to C2C12 myoblasts at concentrations up to 25 mM. Furthermore, these curcuminoid analogues mitigated myoblast cell death induced by oxidative stress. Notably, both analogues (10 nM) had no effect on cell proliferation. However, only compound A significantly enhanced myoblast differentiation comparable to the effects of dihydrotestosterone (1 µM) and estradiol (10 nM). Conclusion: The results suggest that compound A may serve as a lead compound for the development of suitable therapeutic agents for muscle injuries and diseases.