Sirithanakorn, Chaiyos

Preferred name

Main Affiliation

Faculty of Medicine

chaiyos.si@kmitl.ac.th

Now showing 1 - 7 of 7

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Evidence for endogenous hydrogen peroxide production by E. coli fatty acyl-CoA dehydrogenase
(2024-10-01)
Sirithanakorn, Chaiyos
;
Imlay, James A.
Aerobic organisms continuously generate internal superoxide and hydrogen peroxide, which can damage enzymes and impair growth. To avoid this problem cells maintain high levels of superoxide dismutases, catalases, and peroxidases. Surprisingly, we do not know the primary sources of these reactive oxygen species (ROS) in living cells. However, in vitro studies have shown that flavoenzymes can inadvertently transfer electrons to oxygen. Therefore, it seems plausible that substantial ROS may be generated when large metabolic fluxes flow through flavoproteins. Such a situation may arise during the catabolism of fatty acids. Acyl-CoA dehydrogenase (FadE) is a flavoprotein involved in each turn of the beta-oxidation cycle. In the present study the catabolism of dodecanoic acid specifically impaired the growth of strains that lack enzymes to scavenge hydrogen peroxide. The defect was absent from fadE mutants. Direct measurements confirmed that the beta-oxidation pathway amplified the rate of intracellular hydrogen peroxide formation. Scavenging-proficient cells did not display the FadE-dependent growth defect. Those cells also did not induce the peroxide stress response during dodecanoate catabolism, indicating that the basal defenses are sufficient to cope with moderately elevated peroxide formation. In vitro work still is needed to test whether the ROS evolve specifically from the FadE flavin site and to determine whether superoxide as well as peroxide is released. At present such experiments are challenging because the natural redox partner of FadE has not been identified. This study supports the hypothesis that the degree of internal ROS production can depend upon the type of active metabolism inside cells.
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Biosynthetic sericin 1-like protein skews dendritic cells to tolerogenic-like phenotype
(2021-12-01)
Ritprajak, Patcharee
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Sirithanakorn, Chaiyos
;
Nguyen, Thu N.Y.
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Sereemaspun, Amornpun
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Aramwit, Pornanong
Silkworm sericin has been widely exploited in biomaterials due to its favorable biological activities. However, the extraction processes of sericin from silkworm cocoons can alter the biological and biophysical properties, including a structural diversity of natural sericin. In addition, extracted natural sericin is often contaminated with fibroin that may be harmful to human cells. Induction of tolerogenic dendritic cell (DC) has become a strategy in biomaterial fields because this cell type plays a key role in immune modulation and wound healing. To overcome undesired effects of extracted natural sericin and to improve its biological properties, we biosynthesized sericin 1-like protein that contained only functional motifs and tested its biological activity and immunomodulatory properties in fibroblasts and DCs, respectively. In comparison to natural sericin, biosynthetic sericin 1 promoted collagen production in fibroblasts at a late time point. Furthermore, DCs treated with biosynthetic sericin 1 exhibited a tolerogenic-like phenotype with semimaturation and low production of proinflammatory cytokines, but high production of anti-inflammatory cytokine, IL-10. Biosynthetic sericin 1 might be developed as immunomodulator or immunosuppressant.
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The role of the phosphate groups of trinitrophenyl adenosine 5′-triphosphate (TNP-ATP) in allosteric activation of pyruvate carboxylase and the inhibition of acetyl CoA-dependent activation
(2021-10-30)
Rattanapornsompong, Khanti
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Sirithanakorn, Chaiyos
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Jitrapakdee, Sarawut
;
Attwood, Paul V.
A previous study showed that 2′-3′-O-(2,4,6-trinitrophenyl) adenosine 5′-triphosphate (TNP-ATP) was a weak allosteric activator of Rhizobium etli pyruvate carboxylase (RePC) in the absence of acetyl-CoA. On the other hand, TNP-ATP inhibited the allosteric activation of RePC by acetyl-CoA. Here, we aimed to study the role of triphosphate group of TNP-ATP on its allosteric activation of the enzyme and inhibition of acetyl-CoA-dependent activation of RePC using TNP-ATP and its derivatives, including TNP-ADP, TNP-AMP and TNP-adenosine. The pyruvate carboxylation activity was assayed to determine the effect of reducing the number of phosphate groups in TNP-ATP derivatives on allosteric activation and inhibition of acetyl-CoA activation of RePC and chicken liver pyruvate carboxylase (CLPC). Reducing the number of phosphate groups in TNP-ATP derivatives decreased the activation efficacy for both RePC and CLPC compared to TNP-ATP. The apparent binding affinity and inhibition of activation of the enzymes by acetyl-CoA were also diminished when the number of phosphate groups in the TNP-ATP derivatives was reduced. Whilst TNP-AMP activated RePC, it did not activate CLPC, but it did inhibit acetyl-CoA activation of both RePC and CLPC. Similarly, TNP-adenosine did not activate RePC; however, it did inhibit acetyl-CoA activation using a different mechanism compared to phosphorylated TNP-derivatives. These findings indicate that mechanisms of PC activation and inhibition of acetyl-CoA activation by TNP-ATP and its derivatives are different. This study provides the basis for possible drug development for treatment of metabolic diseases and cancers with aberrant expression of PC.
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Cannabidiol Lipid Nanoparticles Stabilize Gut–Brain–Bone Axis Integrity and Enhance Neuroplasticity in Stressed Rats: A Comparison with Atomoxetine and Escitalopram
(2025-10-01)
Lapmanee, Sarawut
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Lumsutti, Jitpatima
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Charoenphon, Natthawut
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Inchan, Anjaree
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Boonmuen, Nittaya
Chronic stress induces mood disturbances, disrupts gut barrier function, and promotes low-grade systemic inflammation. This study assessed the therapeutic effects of atomoxetine (ATX), escitalopram (ESC), cannabidiol (CBD), and CBD-loaded lipid nanoparticles (CBD/LNP) in male rats exposed to repeated restraint stress. Stressed rats exhibited a 2.03-fold increase in interleukin-6 and a 1.89-fold increase in TNF-α, a 1.20-fold decrease in brain-derived neurotrophic factor, a 1.36-fold decrease in osteocalcin, accompanied by alterations in gut metabolites, particularly short-chain fatty acids (SCFAs; from 155.3 to 94.83 μmol/L), polyamines (from 273.6 to 192.4 μmol/L), and bile acids (BAs; from 21.19 to 14.53 μmol/L), compared with the control group. Protein analysis revealed gut barrier disruption and microglial/macrophage activation, accompanied by reduced synaptic plasticity. ATX improved gut permeability and reduced glial activation but did not restore osteocalcin. ESC provided neuroimmune benefits with limited and BA gut restoration and modulated the gut–brain axis and improved anxiety-like behaviors, partly by altering gut microbiota and metabolites. CBD and CBD/LNP treatment restored intestinal barrier function, as indicated by intestinal permeability in the range of 1.15–1.61-fold. These treatments also normalized bile acids (1.0–1.38-fold) and osteocalcin (1.0–1.28-fold) and significantly reduced glial activation (0.63–1.12-fold) as opposed to the non-treated stressed group. All treatments were found to be effective in correcting SCFA and polyamine levels. Histological analysis confirmed that CBD/LNP, ATX, and ESC ameliorated tissue alterations. These findings highlight CBD/LNP as a promising intervention for stress-induced gut–brain–bone axis disruption, supporting its potential as a therapeutic alternative through modulation of microbiota-driven gut–brain communication in stress-associated disorders.
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Mucoadhesive Andrographolide-Loaded Liposomes for Nasal Delivery Modulate Inflammatory Responses in Tumor Necrosis Factor Alpha-Induced Acute Lung Injury in Mice
(2025-08-12)
Khongkow, Mattaka
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Rimsueb, Natchanon
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Namdee, Katawut
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Bunwatcharaphansakun, Phichaporn
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Saenmuangchin, Rattaporn
Inflammatory lung injury from a fever or sepsis can impair pulmonary function. While anti-inflammatory agents are commonly used, side effects could occur. Andrographolide (AGP) exhibits potent anti-inflammatory activity, making it a promising alternative treatment. Nevertheless, AGP has low solubility and absorption, and drug-delivery liposomes (Lip) improve site-specific targeting and controlled release. This study aimed to develop and evaluate the physicochemical properties, safety, and therapeutic efficacy of AGP-Lip through both in vitro and in vivo studies. The characteristics of AGP-Lip included an average size of 139.7 ± 2.00 nm, a polydispersity index of 0.16 ± 0.02, and a zeta potential of 34.5 ± 0.80 mV, with strong mucoadhesive properties. AGP-Lip exhibited no cytotoxicity in IMR-90 lung fibroblast cells while effectively reducing inflammation by decreasing nitric oxide production in RAW 264.7 murine macrophage cells exposed to lipopolysaccharide. In the animal study, adult male C57BL/6 mice received a single intraperitoneal dose of 100 μg/kg of tumor necrosis factor-α (TNF-α)-induced acute pulmonary systemic inflammation. Mice were randomly assigned to six groups (9 mice per group): control, PBS (negative control), Blank-Lip, AGP-Lip, dexamethasone (POS), and AGP-Lip+POS. All treatments (20 to 25 μL with AGP-Lip, AGP-Lip, and/or POS at 1 mg/kg) were administered via nasal delivery daily for 7 days. The vehicle-treated mice exhibited signs of sickness and systemic inflammation, including reduced body weight gain, hyperlocomotion, decreased exploratory activity, elevated total white blood cell counts, serum IL-6 and TNF-α, and upregulation of targeted mRNA expression of lung inflammatory markers. Histological analysis showed an increase in inflammatory scores, and secretory cells were also observed in the vehicle-treated group. AGP-Lip improved body weight and stress-related behaviors, restored mRNA expression levels of IFN-γ, IL-1α/β, IL-6, IL-10, NF-κBp65, and TNF-α, and alleviated mucus secretion in lung histological analysis. Notably, AGP-Lip effectively mitigated the detrimental effects compared to POS alone, showing significant differences in serum IL-6, lung inflammation-related gene expression (i.e., IFN-γ, IL-1α, NF-κBp50, and VEGF), and PAS staining relative to the combined treatment. These findings suggest that AGP-Lip could serve as a potential alternative treatment for acute respiratory infections, warranting further consideration for long-term administration and clinical trials.
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Stress-induced changes in cognitive function and intestinal barrier integrity can be ameliorated by venlafaxine and synbiotic supplementations
(2024-01-01)
Lapmanee, Sarawut
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Supkamonseni, Nattapon
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Bhubhanil, Sakkarin
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Treesaksrisakul, Nattakan
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Sirithanakorn, Chaiyos
Stress profoundly impacts various aspects of both physical and psychological well-being. Our previous study demonstrated that venlafaxine (Vlx) and synbiotic (Syn) treatment attenuated learned fear-like behavior and recognition memory impairment in immobilized-stressed rats. In this study, we further investigated the physical, behavior, and cellular mechanisms underlying the effects of Syn and/or Vlx treatment on brain and intestinal functions in stressed rats. Adult male Wistar rats, aged 8 weeks old were subjected to 14 days of immobilization stress showed a decrease in body weight gain and food intake as well as an increase in water consumption, urinary corticosterone levels, and adrenal gland weight. Supplementation of Syn and/or Vlx in stressed rats resulted in mitigation of weight loss, restoration of normal food and fluid intake, and normalization of corticosterone levels. Behavioral analysis showed that treatment with Syn and/or Vlx enhanced depressive-like behaviors and improved spatial learning-memory impairment in stressed rats. Hippocampal dentate gyrus showed stress-induced neuronal cell death, which was attenuated by Syn and/or Vlx treatment. Stress-induced ileum inflammation and increased intestinal permeability were both effectively reduced by the supplementation of Syn. In addition, Syn and Vlx partly contributed to affecting the expression of the glial cell-derived neurotrophic factor in the hippocampus and intestines of stressed rats, suggesting particularly protective effects on both the gut barrier and the brain. This study highlights the intricate interplay between stress physiological responses in the brain and gut. Syn intervention alleviate stress-induced neuronal cell death and modulate depression- and memory impairment-like behaviors, and improve stress-induced gut barrier dysfunction which were similar to those of Vlx. These findings enhance our understanding of stress-related health conditions and suggest the synbiotic intervention may be a promising approach to ameliorate deleterious effects of stress on the gut-brain axis.
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Smart colorimetric label based on chitosan-grafted cresol red for early detection of catheter blockage and infection through urinary pH monitoring
(2025-12-01)
Keawdoungdee, Anchisa
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Chalitangkoon, Jongjit
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Sirithanakorn, Chaiyos
;
Kamolvit, Witchuda
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Detsri, Ekarat
This study presents a smart, non-invasive colorimetric sensor designed for the early detection of catheter-associated urinary tract infections (CAUTIs) and impending catheter blockage. The sensor was developed by covalently grafting cresol red onto chitosan (CS-g-CR) via a Mannich reaction, producing a biocompatible, pH-responsive material exhibiting strong dye retention and stable, visible color transitions across the urinary pH range. The material was formulated into a water-based screen-printable ink and applied to cotton fabric, yielding flexible labels capable of detecting alkaline shifts associated with Proteus mirabilis infection. In an in vitro bladder model, the printed labels provided up to 20 h of advance warning prior to complete catheter blockage. Color changes were quantified using smartphone-based RGB analysis, enabling objective and real-time monitoring. This low-cost sensing platform holds promise for point-of-care applications aimed at improving early diagnosis and reducing complications in long-term catheterized patients.

Sirithanakorn, Chaiyos

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