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Article ; Online: Antrodia camphorata and coenzyme Q

Yang, Hsin-Ling / Chang, Yao-Hsien / Pandey, Sudhir / Bhat, Asif Ali / Vadivalagan, Chithravel / Lin, Kai-Yuan / Hseu, You-Cheng

Environmental toxicology

2023 Volume 38, Issue 7, Page(s) 1548–1564

Abstract: Antrodia camphorata (AC) and Coenzyme ... ...

Abstract	Antrodia camphorata (AC) and Coenzyme Q
MeSH term(s)	Humans ; Animals ; Mice ; beta Catenin/metabolism ; Ubiquinone/pharmacology ; Vimentin/metabolism ; Epithelial-Mesenchymal Transition ; Glioblastoma/drug therapy ; Neoplasm Invasiveness/pathology ; Cadherins/genetics ; Cell Line, Tumor ; Hypoxia-Inducible Factor 1, alpha Subunit ; Cell Movement
Chemical Substances	beta Catenin ; Ubiquinone (1339-63-5) ; Vimentin ; Cadherins ; quinone (3T006GV98U) ; Hypoxia-Inducible Factor 1, alpha Subunit
Language	English
Publishing date	2023-03-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	1463449-1
ISSN	1522-7278 ; 1520-4081
ISSN (online)	1522-7278
ISSN	1520-4081
DOI	10.1002/tox.23785
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Article ; Online: The in vitro and in vivo depigmentation activity of coenzyme Q

Hseu, You-Cheng / Yeh, Jou-Tsen / Vadivalagan, Chithravel / Chen, Siang-Jyun / Gowrisankar, Yugandhar Vudhya / Pandey, Sudhir / Hsu, Yuan-Tai / Yen, Hung-Rong / Huang, Hui-Chi / Hseu, Jhih-Hsuan / Yang, Hsin-Ling

Cell communication and signaling : CCS

2024 Volume 22, Issue 1, Page(s) 151

Abstract: Background: Coenzyme Q: Methods: We resolved the depigmenting efficiency of CoQ: Results: CoQ: Conclusions: Our results showed that ... ...

Abstract	Background: Coenzyme Q Methods: We resolved the depigmenting efficiency of CoQ Results: CoQ Conclusions: Our results showed that CoQ
MeSH term(s)	Animals ; Humans ; Ubiquinone/pharmacology ; Ubiquinone/metabolism ; Melanins/metabolism ; Zebrafish/metabolism ; Monophenol Monooxygenase/metabolism ; alpha-MSH/metabolism ; Beclin-1/metabolism ; Melanocytes/metabolism ; Keratinocytes/metabolism ; Autophagy ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Cell Line, Tumor ; Benzoquinones ; Polyporales
Chemical Substances	Ubiquinone (1339-63-5) ; Melanins ; Monophenol Monooxygenase (EC 1.14.18.1) ; alpha-MSH (581-05-5) ; Beclin-1 ; quinone (3T006GV98U) ; Proto-Oncogene Proteins c-bcl-2 ; Benzoquinones
Language	English
Publishing date	2024-02-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2126315-2
ISSN	1478-811X ; 1478-811X
ISSN (online)	1478-811X
ISSN	1478-811X
DOI	10.1186/s12964-024-01537-6
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Article ; Online: Coenzyme Q

Yang, Hsin-Ling / Lin, Ping-Yu / Vadivalagan, Chithravel / Lin, Yi-An / Lin, Kai-Yuan / Hseu, You-Cheng

Archives of toxicology

2023 Volume 97, Issue 4, Page(s) 1047–1068

Abstract: ... Coenzyme ... ...

Abstract	Coenzyme Q
MeSH term(s)	Humans ; Adenosine Triphosphate ; Cadherins/genetics ; Cell Line, Tumor ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Inflammasomes ; Inflammation ; Interleukin-18 ; Lactate Dehydrogenase 5 ; Lactates ; Lipopolysaccharides ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism ; Triple Negative Breast Neoplasms/pathology ; Ubiquinone/pharmacology
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE) ; Cadherins ; cobaltous chloride (EVS87XF13W) ; Hypoxia-Inducible Factor 1, alpha Subunit ; Inflammasomes ; Interleukin-18 ; Lactate Dehydrogenase 5 (EC 1.1.1.27.-) ; Lactates ; Lipopolysaccharides ; NLR Family, Pyrin Domain-Containing 3 Protein ; Ubiquinone (1339-63-5) ; NLRP3 protein, human ; HIF1A protein, human
Language	English
Publishing date	2023-02-27
Publishing country	Germany
Document type	Journal Article
ZDB-ID	124992-7
ISSN	1432-0738 ; 0340-5761
ISSN (online)	1432-0738
ISSN	0340-5761
DOI	10.1007/s00204-023-03456-w
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Article ; Online: Intra-species variation and geographic differentiation among the populations of the quarantine agricultural pest

Karthika, Pushparaj / Vadivalagan, Chithravel / Thirumurugan, Durairaj / Murugan, Kadarkarai

Mitochondrial DNA. Part A, DNA mapping, sequencing, and analysis

2019 Volume 30, Issue 4, Page(s) 682–693

Abstract: Leucinodes ... ...

Abstract	Leucinodes orbonalis
MeSH term(s)	Animals ; DNA Barcoding, Taxonomic ; Genetic Variation/genetics ; Geographic Mapping ; Lepidoptera/classification ; Lepidoptera/genetics ; Pest Control ; Quarantine ; Species Specificity
Language	English
Publishing date	2019-06-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2881313-3
ISSN	2470-1408 ; 2470-1394
ISSN (online)	2470-1408
ISSN	2470-1394
DOI	10.1080/24701394.2019.1622691
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Article ; Online: Tranexamic acid improves psoriasis-like skin inflammation: Evidence from in vivo and in vitro studies.

Hseu, Jhih-Hsuan / Chan, Chon-I / Vadivalagan, Chithravel / Chen, Siang-Jyun / Yen, Hung-Rong / Hseu, You-Cheng / Yang, Hsin-Ling / Wu, Po-Yuan

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2023 Volume 166, Page(s) 115307

Abstract: The chronic disease psoriasis is associated with severe inflammation and abnormal keratinocyte propagation in the skin. Tranexamic acid (TXA), a plasmin inhibitor, is used to cure serious bleeding. We investigated whether TXA ointment mitigated Imiquimod ...

Abstract	The chronic disease psoriasis is associated with severe inflammation and abnormal keratinocyte propagation in the skin. Tranexamic acid (TXA), a plasmin inhibitor, is used to cure serious bleeding. We investigated whether TXA ointment mitigated Imiquimod (IMQ)-induced psoriasis-like inflammation. Furthermore, this study investigated the effect of noncytotoxic concentrations of TXA on IL-17-induced human keratinocyte (HaCaT) cells to determine the status of proliferative psoriatic keratinocytes. We found that TXA reduced IMQ-induced psoriasis-like erythema, thickness, scaling, and cumulative scores (erythema plus thickness plus scaling) on the back skin of BALB/c mice. Additionally, TXA decreased ear thickness and suppressed hyperkeratosis, hyperplasia, and inflammation of the ear epidermis in IMQ-induced BALB/c mice. Furthermore, TXA inhibited IMQ-induced splenomegaly in BALB/c mouse models. In IL-17-induced HaCaT cells, TXA inhibited ROS production and IL-8 secretion. Interestingly, TXA suppressed the IL-17-induced NFκB signaling pathway via IKK-mediated IκB degradation. TXA inhibited IL-17-induced activation of the NLRP3 inflammasome through caspase-1 and IL1β expression. TXA inhibited IL-17-induced NLRP3 inflammasome activation by enhancing autophagy, as indicated by LC3-II accumulation, p62/SQSTM1 expression, ATG4B inhibition, and Beclin-1/Bcl-2 dysregulation. Notably, TXA suppressed IL-17-induced Nrf2-mediated keratin 17 expression. N-acetylcysteine pretreatment reversed the effects of TXA on NFκB, NLRP3 inflammasomes, and the Nrf2-mediated keratin 17 pathway in IL-17-induced HaCaT cells. Results further confirmed that in the ear skin of IMQ-induced mice, psoriasis biomarkers such as NLRP3, IL1β, Nrf2, and keratin 17 expression were downregulated by TXA treatment. TXA improves IMQ-induced psoriasis-like inflammation in vivo and psoriatic keratinocytes in vitro. Tranexamic acid is a promising future treatment for psoriasis.
MeSH term(s)	Humans ; Animals ; Mice ; Interleukin-17/metabolism ; Tranexamic Acid/pharmacology ; Tranexamic Acid/therapeutic use ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Keratin-17 ; NF-E2-Related Factor 2 ; Psoriasis/chemically induced ; Psoriasis/drug therapy ; Psoriasis/metabolism ; Dermatitis ; Skin ; Keratinocytes ; Inflammation/drug therapy ; Inflammation/chemically induced ; Imiquimod/pharmacology ; NF-kappa B/metabolism ; Mice, Inbred BALB C ; Disease Models, Animal
Chemical Substances	Interleukin-17 ; Tranexamic Acid (6T84R30KC1) ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Keratin-17 ; NF-E2-Related Factor 2 ; Imiquimod (P1QW714R7M) ; NF-kappa B
Language	English
Publishing date	2023-08-11
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2023.115307
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Article ; Online: Coenzyme Q0, a quinone derivative from Antrodia camphorata, inhibits epithelial-mesenchymal transition by activating the Nrf2 signaling pathway in TGF-β-stimulated adult retinal pigment epithelial cells to improve age-related macular degeneration and proliferative vitreoretinopathy

Hsin-Ling Yang / Hung-Rong Yen / I-Chen Chang / Chithravel Vadivalagan / Siang-Jyun Chen / Chuan-Chen Lee / Wei-Chen Jane / Jhih-Hsuan Hseu / You-Cheng Hseu

Journal of Functional Foods, Vol 112, Iss , Pp 105978- (2024)

2024

Abstract: We investigated the anti-EMT and antifibrotic effects of coenzyme Q0 (CoQ0), a quinone derivative from Antrodia camphorata, in TGF-β-stimulated adult retinal pigment epithelial 19 (ARPE-19) cells. Results showed that CoQ0 treatment reversed TGF-β- ... ...

Abstract	We investigated the anti-EMT and antifibrotic effects of coenzyme Q0 (CoQ0), a quinone derivative from Antrodia camphorata, in TGF-β-stimulated adult retinal pigment epithelial 19 (ARPE-19) cells. Results showed that CoQ0 treatment reversed TGF-β-stimulated morphological changes from an epithelial to a fibroblastic phenotype in ARPE-19 cells. CoQ0 exhibited anti-EMT effects by impeding TGF-β-stimulated migration and invasion in ARPE-19 cells. Notably, CoQ0 triggered the epithelial marker E-cadherin and suppressed the mesenchymal marker N-cadherin expression in nonstimulated or TGF-β-stimulated ARPE-19 cells. Moreover, CoQ0 attenuated EMT and fibrotic Vimentin, MMP-9/-2, Slug, α-SMA, and VEGF expression in nonstimulated or TGF-β-stimulated ARPE-19 cells. Interestingly, CoQ0 inhibited TGF-β-induced intracellular ROS production by activating Nrf2 nuclear translocation and upregulating the HO-1, γ-GCLC, and NQO-1 enzymes in ARPE-19 cells. Moreover, Nrf2 silencing reversed TGF-β-induced ROS-mediated anti-EMT (E-cadherin/N-cadherin/Slug) and antifibrotic (α-SMA) effects in CoQ0-treated ARPE-19 cells. Therefore, CoQ0 could be utilized to treat age-related macular degeneration and proliferative vitreoretinopathy.
Keywords	Coenzyme Q0 ; ARPE-19 ; TGF-β ; ROS ; EMT ; Nutrition. Foods and food supply ; TX341-641
Language	English
Publishing date	2024-01-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Coenzyme Q0 defeats NLRP3-mediated inflammation, EMT/metastasis, and Warburg effects by inhibiting HIF-1α expression in human triple-negative breast cancer cells

Yang, Hsin-Ling / Lin, Ping-Yu / Vadivalagan, Chithravel / Lin, Yi'an / Lin, Kai-Yuan / Hseu, You-Cheng

Arch Toxicol 2023 Apr., v. 97, no. 4, p. 1047-1068

2023 , Page(s) 1047–1068

Abstract: Coenzyme Q₀ (CoQ₀) is a derivative quinone from Antrodia camphorata (AC) that exerts anticancer activities. This study examined the anticancer attributes of CoQ₀ (0–4 µM) on inhibited anti-EMT/metastasis and NLRP3 inflammasome, and altered Warburg ... ...

Abstract	Coenzyme Q₀ (CoQ₀) is a derivative quinone from Antrodia camphorata (AC) that exerts anticancer activities. This study examined the anticancer attributes of CoQ₀ (0–4 µM) on inhibited anti-EMT/metastasis and NLRP3 inflammasome, and altered Warburg effects via HIF-1α inhibition in triple-negative breast cancer (MDA-MB-231 and 468) cells. MTT assay, cell migration/invasion assays, Western blotting, immunofluorescence, metabolic reprogramming, and LC–ESI-MS were carried out to assess the therapy potential of CoQ₀. CoQ₀ inhibited HIF-1α expression and suppressed the NLRP3 inflammasome and ASC/caspase-1 expression, followed by downregulation of IL-1β and IL-18 expression in MDA-MB-231 and 468 cells. CoQ₀ ameliorated cancer stem-like markers by decreasing CD44 and increasing CD24 expression. Notably, CoQ₀ modulated EMT by upregulating the epithelial marker E-cadherin and downregulating the mesenchymal marker N-cadherin. CoQ₀ inhibited glucose uptake and lactate accumulation. CoQ₀ also inhibited HIF-1α downstream genes involved in glycolysis, such as HK-2, LDH-A, PDK-1, and PKM-2 enzymes. CoQ₀ decreased extracellular acidification rate (ECAR), glycolysis, glycolytic capacity, and glycolytic reserve in MDA-MB-231 and 468 cells under normoxic and hypoxic (CoCl₂) conditions. CoQ₀ inhibited the glycolytic intermediates lactate, FBP, and 2/3-PG, and PEP levels. CoQ₀ increased oxygen consumption rate (OCR), basal respiration, ATP production, maximal respiration, and spare capacity under normoxic and hypoxic (CoCl₂) conditions. CoQ₀ increased TCA cycle metabolites, such as citrate, isocitrate, and succinate. CoQ0 inhibited aerobic glycolysis and enhanced mitochondrial oxidative phosphorylation in TNBC cells. Under hypoxic conditions, CoQ₀ also mitigated HIF-1α, GLUT1, glycolytic-related (HK-2, LDH-A, and PFK-1), and metastasis-related (E-cadherin, N-cadherin, and MMP-9) protein or mRNA expression in MDA-MB-231 and/or 468 cells. Under LPS/ATP stimulation, CoQ₀ inhibited NLRP3 inflammasome/procaspase-1/IL-18 activation and NFκB/iNOS expression. CoQ₀ also hindered LPS/ATP-stimulated tumor migration and downregulated LPS/ATP-stimulated N-cadherin and MMP-2/-9 expression. The present study revealed that suppression of HIF-1α expression caused by CoQ₀ may contribute to inhibition of NLRP3-mediated inflammation, EMT/metastasis, and Warburg effects of triple-negative breast cancers.
Keywords	Taiwanofungus camphoratus ; acidification ; breast neoplasms ; breasts ; cadherins ; cell movement ; citrates ; epithelium ; fluorescent antibody technique ; gene expression ; glucose ; glycolysis ; humans ; inflammasomes ; inflammation ; interleukin-18 ; lactic acid ; metabolites ; metastasis ; mitochondria ; oxidative phosphorylation ; oxygen consumption ; quinones ; succinic acid ; therapeutics ; toxicity testing ; tricarboxylic acid cycle
Language	English
Dates of publication	2023-04
Size	p. 1047-1068
Publishing place	Springer Berlin Heidelberg
Document type	Article ; Online
ZDB-ID	124992-7
ISSN	1432-0738 ; 0340-5761
ISSN (online)	1432-0738
ISSN	0340-5761
DOI	10.1007/s00204-023-03456-w
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: In vitro and in vivo anti-tumor activity of Coenzyme Q

Yang, Hsin-Ling / Chiu, Li-Wen / Lin, Yi-An / Pandey, Sudhir / Vadivalagan, Chithravel / Liao, Jiunn-Wang / Gowrisankar, Yugandhar Vudhya / Chen, Hui-Jye / Lin, Hui-Yi / Hseu, You-Cheng

Toxicology and applied pharmacology

2023 Volume 465, Page(s) 116453

Abstract: HNSCC (Head and Heck Squamous Cell Carcinoma) is a reasonably prevalent cancer with a high mortality rate. In this study, we tried to examine the anti-metastasis and apoptosis/autophagy actions of Coenzyme ... ...

Abstract	HNSCC (Head and Heck Squamous Cell Carcinoma) is a reasonably prevalent cancer with a high mortality rate. In this study, we tried to examine the anti-metastasis and apoptosis/autophagy actions of Coenzyme Q
MeSH term(s)	Humans ; Animals ; Mice ; Ubiquinone/pharmacology ; Ubiquinone/therapeutic use ; Reactive Oxygen Species/metabolism ; Mice, Nude ; Squamous Cell Carcinoma of Head and Neck ; Cell Death ; Apoptosis ; Cell Line, Tumor ; Autophagy ; Head and Neck Neoplasms/drug therapy ; Xenograft Model Antitumor Assays ; Nuclear Proteins ; Twist-Related Protein 1
Chemical Substances	Ubiquinone (1339-63-5) ; Reactive Oxygen Species ; TWIST1 protein, human ; Nuclear Proteins ; Twist-Related Protein 1
Language	English
Publishing date	2023-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2023.116453
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Article ; Online: The Warburg effect in osteoporosis: Cellular signaling and epigenetic regulation of energy metabolic events to targeting the osteocalcin for phenotypic alteration.

Vadivalagan, Chithravel / Krishnan, Anand / Chen, Siang-Jyun / Hseu, You-Cheng / Muthu, Sathish / Dhar, Rajib / Aljabali, Alaa A A / Tambuwala, Murtaza M

Cellular signalling

2022 Volume 100, Page(s) 110488

Abstract: Osteoporosis is a silent disease of skeletal morphology that induces fragility and fracture risk in aged persons irrespective of gender. Juvenile secondary osteoporosis is rare and is influenced by familial genetic abnormalities. Despite the currently ... ...

Abstract	Osteoporosis is a silent disease of skeletal morphology that induces fragility and fracture risk in aged persons irrespective of gender. Juvenile secondary osteoporosis is rare and is influenced by familial genetic abnormalities. Despite the currently available therapeutic options, more-acute treatments are in need. Women suffer from osteoporosis after menopause, which is characterized by a decline in the secretion of sex hormones in the later phase of life. Several studies in the past two decades emphasized hormone-related pathways to combat osteoporosis. Some studies partially examined energy-related pathways, but achieving a more vivid picture of metabolism and bone remodeling in terms of the Warburg phenomenon is still warranted. Each cell requires sufficient energy for cellular propagation and growth; in particular, osteoporosis is an energy-dependent mechanism affected by a decreased cellular mass of the bone morphology. Energy utilization is the actual propagation of such diseases, and narrowing down these criteria will hopefully provide clues to formulate better therapeutic strategies. Oxidative glycolysis is a particular type of energy metabolic pathway in cancer cells that influences cellular proliferation. Therefore, the prospect of utilizing collective glucose metabolism by inducing the Warburg effect may improve cell propagation. The benefits of utilizing the energy from the Warburg effect may be a difficult task. However, it seems to improve their effectiveness in the osteoblast phenotype by connecting the selected pathways such as WNT, Notch, AKT, and Insulin signaling by targeting osteocalcin resulting in phenotypic alteration. Osteocalcin directs ATP utilization through the sclerostin SOST gene in the bone microenvironment. Thus, selective activation of ATP production involved in osteoblast maturation remains a prime strategy to fight osteoporosis.
Language	English
Publishing date	2022-10-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2022.110488
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Article ; Online: Clinical Theragnostic Signature of Extracellular Vesicles in Traumatic Brain Injury (TBI).

Dey, Anuvab / Ghosh, Subhrojyoti / Bhuniya, Tiyasa / Koley, Madhurima / Bera, Aishi / Guha, Sudeepta / Chakraborty, Kashmira / Muthu, Sathish / Gorai, Sukhamoy / Vorn, Rany / Vadivalagan, Chithravel / Anand, Krishnan

ACS chemical neuroscience

2023 Volume 14, Issue 17, Page(s) 2981–2994

Abstract: Traumatic brain injury (TBI) is a common cause of disability and fatality worldwide. Depending on the clinical presentation, it is a type of acquired brain damage that can be mild, moderate, or severe. The degree of patient's discomfort, prognosis, ... ...

Abstract	Traumatic brain injury (TBI) is a common cause of disability and fatality worldwide. Depending on the clinical presentation, it is a type of acquired brain damage that can be mild, moderate, or severe. The degree of patient's discomfort, prognosis, therapeutic approach, survival rates, and recurrence can all be strongly impacted by an accurate diagnosis made early on. The Glasgow Coma Scale (GCS), along with neuroimaging (MRI (Magnetic Resonance Imaging) and CT scan), is a neurological assessment tools used to evaluate and categorize the severity of TBI based on the patient's level of consciousness, eye opening, and motor response. Extracellular vesicles (EVs) are a growing domain, explaining neurological complications in a more detailed manner. EVs, in general, play a role in cellular communication. Its molecular signature such as DNA, RNA, protein, etc. contributes to the status (health or pathological stage) of the parental cell. Brain-derived EVs support more specific screening (diagnostic and prognostic) in TBI research. Therapeutic impact of EVs are more promising for aiding in TBI healing. It is nontoxic, biocompatible, and capable of crossing the blood-brain barrier (BBB) to transport therapeutic molecules. This review has highlighted the relationships between EVs and TBI theranostics, EVs and TBI-related clinical trials, and related research domain-associated challenges and solutions. This review motivates further exploration of associations between EVs and TBI and develops a better approach to TBI management.
MeSH term(s)	Humans ; Brain Injuries, Traumatic ; Brain Injuries ; Brain ; Blood-Brain Barrier ; Extracellular Vesicles
Language	English
Publishing date	2023-08-25
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ISSN	1948-7193
ISSN (online)	1948-7193
DOI	10.1021/acschemneuro.3c00386
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