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Article: NRICM101 ameliorates SARS-CoV-2-S1-induced pulmonary injury in K18-hACE2 mice model.

Wei, Wen-Chi / Tsai, Keng-Chang / Liaw, Chia-Ching / Chiou, Chun-Tang / Tseng, Yu-Hwei / Liao, Geng-You / Lin, Yu-Chi / Chiou, Wen-Fei / Liou, Kuo-Tong / Yu, I-Shing / Shen, Yuh-Chiang / Su, Yi-Chang

Frontiers in pharmacology

2023 Volume 14, Page(s) 1125414

Abstract: The coronavirus disease 2019 (COVID-19) pandemic continues to represent a challenge for public health globally since transmission of different variants of the virus does not seem to be effectively affected by the current treatments and vaccines. During ... ...

Abstract	The coronavirus disease 2019 (COVID-19) pandemic continues to represent a challenge for public health globally since transmission of different variants of the virus does not seem to be effectively affected by the current treatments and vaccines. During COVID-19 the outbreak in Taiwan, the patients with mild symptoms were improved after the treatment with NRICM101, a traditional Chinese medicine formula developed by our institute. Here, we investigated the effect and mechanism of action of NRICM101 on improval of COVID-19-induced pulmonary injury using S1 subunit of the SARS-CoV-2 spike protein-induced diffuse alveolar damage (DAD) of hACE2 transgenic mice. The S1 protein induced significant pulmonary injury with the hallmarks of DAD (strong exudation, interstitial and intra-alveolar edema, hyaline membranes, abnormal pneumocyte apoptosis, strong leukocyte infiltration, and cytokine production). NRICM101 effectively reduced all of these hallmarks. We then used next-generation sequencing assays to identify 193 genes that were differentially expressed in the S1+NRICM101 group. Of these, three (
Language	English
Publishing date	2023-06-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2023.1125414
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Article ; Online: The protective role of Achyranthes aspera extract against cisplatin-induced nephrotoxicity by alleviating oxidative stress, inflammation, and PANoptosis.

Lin, Song-Yi / Chang, Chia-Lin / Liou, Kuo-Tong / Kao, Yao-Kai / Wang, Yea-Hwey / Chang, Cher-Chia / Kuo, Terry B J / Huang, Hung-Tse / Yang, Cheryl C H / Liaw, Chia-Ching / Shen, Yuh-Chiang

Journal of ethnopharmacology

2023 Volume 319, Issue Pt 1, Page(s) 117097

Abstract: Ethnopharmacological relevance: Achyranthes aspera, a widely recognized medicinal plant, is used in various cultures for treating different ailments, including renal dysfunction; however, there is a lack of comprehensive understanding of its protective ... ...

Abstract	Ethnopharmacological relevance: Achyranthes aspera, a widely recognized medicinal plant, is used in various cultures for treating different ailments, including renal dysfunction; however, there is a lack of comprehensive understanding of its protective effects and the underlying signaling networks involved. Aim of the study: This study aimed to investigate the molecular mechanisms of the action of A. aspera by employing an integrative approach including functional and tissue imaging as well as comprehensive genomics analysis. Materials and methods: Cisplatin-induced nephrotoxicity is a well-established animal model for acute kidney injury (AKI). In this study, we investigated the protective effects and underlying mechanisms of the action of A. aspera water-soluble extract (AAW) on a murine model of cisplatin-induced AKI. The evaluation includes measurements of blood urea nitrogen (BUN) and serum creatinine (SCr) levels, histology examination, and transcriptome analysis using RNA sequencing. Results: In male ICR mice, oral administration of AAW at doses of 0.5-1.0 g/kg significantly reduced cisplatin-induced nephrotoxicity. This effect included the amelioration of tubular injury, renal fibrosis, and the lowering of BUN and SCr levels. AAW also effectively decreased oxidative markers, such as malondialdehyde (MDA) and nitrotyrosine (NT), along with inflammation markers, including COX-2, iNOS, NLRP3, and pP65NFκB. Moreover, AAW administration induced a dose-dependent increase in the expression of two protective factors, Nrf2 and BcL2, and suppressed apoptosis, as evidenced by reduced levels of truncated caspase 3 (t-Casp3). To explore the underlying molecular mechanisms and signaling networks, next-generation sequencing (NGS) analysis was employed. The results revealed that AAW mitigated apoptosis, necroptosis, and PANoptosis pathways by inhibiting inflammation signaling pathways, such as the TNFα-, NFκB-, NETs-, and leukocyte transendothelial migration pathways. Additionally, AAW was found to enhance protective signaling pathways, including the cGMP/PKG-, cAMP-, AMPK-, and mTOR-dependent activation of autophagy and mitophagy pathways. The primary bioactive compound found in AAW was identified as 20-hydroxyecdysone (0.36%). Conclusion: Our study demonstrates that AAW reduces cisplatin-induced nephrotoxicity. The protective effects of AAW are attributed to its modulation of multiple molecular signaling networks. Specifically, AAW downregulates genes and signaling pathways associated with oxidative stress and endoplasmic reticulum (ER) stress, inflammation, and PANoptosis. Simultaneously, it upregulates genes and signaling pathways associated with cell survival, including autophagy and mitophagy pathways.
MeSH term(s)	Mice ; Animals ; Cisplatin/pharmacology ; Kidney ; Achyranthes ; Mice, Inbred ICR ; Oxidative Stress ; Inflammation/chemically induced ; Inflammation/drug therapy ; Inflammation/metabolism ; Acute Kidney Injury/chemically induced ; Acute Kidney Injury/drug therapy ; Acute Kidney Injury/metabolism ; Apoptosis ; Plant Extracts/pharmacology ; Plant Extracts/therapeutic use ; Plant Extracts/metabolism
Chemical Substances	Cisplatin (Q20Q21Q62J) ; Plant Extracts
Language	English
Publishing date	2023-08-28
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2023.117097
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Article ; Online: Medicarpin isolated from Radix Hedysari ameliorates brain injury in a murine model of cerebral ischemia.

Chern, Chang-Ming / Lu, Chung-Kuang / Liou, Kuo-Tong / Wang, Yea-Hwey / Tsai, Keng-Chang / Chang, Chia-Lin / Chang, Chia-Che / Shen, Yuh-Chiang

Journal of food and drug analysis

2021 Volume 29, Issue 4, Page(s) 581–605

Abstract: The development of effective post-stroke therapy is highly demanded. Medicarpin is a key active component of a famous Chinese herbal prescription used for post-stroke treatment in Taiwan; however, little is known about its biological effects and ... ...

Abstract	The development of effective post-stroke therapy is highly demanded. Medicarpin is a key active component of a famous Chinese herbal prescription used for post-stroke treatment in Taiwan; however, little is known about its biological effects and mechanisms of action. Herein, we implemented a murine model of cerebral ischemic/reperfusional injury-related stroke to elucidate medicarpin's neuroprotective effect. In male ICR mice 24 h after stroke induction, treatment with medicarpin (0.5 and 1.0 mg/kg, i.v.) markedly enhanced the survival rates, improved moving distance and walking area coverage, reduced brain infarction, and preserved the blood-brain barrier, supporting medicarpin's protective effect on stroke-induced injury. Immunohistochemistry analysis further revealed that medicarpin treatment decreased the expression/activation of p65NF-κB and caspase 3, especially near the infarct cortex, while promoting the expression of neurogenesis-associated proteins, including doublecortin (DCX), brain-derived neurotrophic factor (BDNF), and tyrosine receptor kinase B (TrkB). These changes of expression levels were accompanied by GSK-3 inactivation and β-catenin upregulation. Notably, pretreatment with LY294002, a PI3K inhibitor, abolished the aforementioned beneficial effects of medicarpin, illustrating an essential role of PI3K/Akt activation in medicarpin's neuroprotective and reparative activities. In vitro studies revealed that medicarpin displayed strong anti-inflammatory activity by reducing nitric oxide (NO) production in lipopolysaccharide-stimulated microglial cells (BV2) with an IC
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Brain Injuries ; Brain Ischemia/drug therapy ; Brain Ischemia/genetics ; Brain Ischemia/metabolism ; Brain-Derived Neurotrophic Factor/metabolism ; Brain-Derived Neurotrophic Factor/therapeutic use ; Caspase 3 ; Disease Models, Animal ; Glycogen Synthase Kinase 3/therapeutic use ; Male ; Mice ; Mice, Inbred ICR ; Neuroprotective Agents/pharmacology ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Pterocarpans ; Stroke/drug therapy ; Stroke/genetics ; Stroke/metabolism ; beta Catenin/therapeutic use
Chemical Substances	Anti-Inflammatory Agents ; Brain-Derived Neurotrophic Factor ; Neuroprotective Agents ; Pterocarpans ; beta Catenin ; medicarpin (6TX086I6IG) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2021-12-15
Publishing country	China (Republic : 1949- )
Document type	Journal Article
ISSN	2224-6614
ISSN (online)	2224-6614
DOI	10.38212/2224-6614.3377
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Article ; Online: Ergostatrien-7,9(11),22-trien-3β-ol from Antrodia camphorata ameliorates ischemic stroke brain injury via downregulation of p65NF-κ-B and caspase 3, and activation of Akt/GSK3/catenin-associated neurogenesis.

Wang, Yea-Hwey / Chern, Chang-Ming / Liou, Kuo-Tong / Kuo, Yueh-Hsiung / Shen, Yuh-Chiang

Food & function

2019 Volume 10, Issue 8, Page(s) 4725–4738

Abstract: Antrodia camphorata is a well-known traditional Chinese mushroom used as a functional food and nutraceutical in Taiwan and China. The aim of this study was to explore the protective effects and mechanism(s) of the ethyl acetate crude extract of A. ... ...

Abstract	Antrodia camphorata is a well-known traditional Chinese mushroom used as a functional food and nutraceutical in Taiwan and China. The aim of this study was to explore the protective effects and mechanism(s) of the ethyl acetate crude extract of A. camphorata (EtOAc-AC) and its active constituent ergostatrien-7,9(11),22-trien-3β-ol (EK100) in an acute ischemic stroke (AIS) murine model. Treating mice with induced AIS injury by using EtOAc-AC (0.3-0.6 g kg
MeSH term(s)	Animals ; Anti-Inflammatory Agents/administration & dosage ; Anti-Inflammatory Agents/chemistry ; Antrodia/chemistry ; Apoptosis/drug effects ; Brain Ischemia/drug therapy ; Brain Ischemia/genetics ; Brain Ischemia/metabolism ; Brain Ischemia/physiopathology ; Caspase 3/genetics ; Caspase 3/metabolism ; Catenins/genetics ; Catenins/metabolism ; Down-Regulation/drug effects ; Drugs, Chinese Herbal/administration & dosage ; Drugs, Chinese Herbal/chemistry ; Ergosterol/administration & dosage ; Ergosterol/analogs & derivatives ; Glycogen Synthase Kinase 3/genetics ; Glycogen Synthase Kinase 3/metabolism ; Humans ; Male ; Mice ; Mice, Inbred ICR ; Neurogenesis/drug effects ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects ; Stroke/drug therapy ; Stroke/genetics ; Stroke/metabolism ; Stroke/physiopathology ; Transcription Factor RelA/genetics ; Transcription Factor RelA/metabolism
Chemical Substances	Anti-Inflammatory Agents ; Catenins ; Drugs, Chinese Herbal ; Transcription Factor RelA ; ergostatrien-3-ol ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; Caspase 3 (EC 3.4.22.-) ; Ergosterol (Z30RAY509F)
Language	English
Publishing date	2019-07-15
Publishing country	England
Document type	Journal Article
ZDB-ID	2612033-1
ISSN	2042-650X ; 2042-6496
ISSN (online)	2042-650X
ISSN	2042-6496
DOI	10.1039/c9fo00908f
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Article: Ergostatrien-7,9(11),22-trien-3β-ol from Antrodia camphorata ameliorates ischemic stroke brain injury via downregulation of p65NF-κ-B and caspase 3, and activation of Akt/GSK3/catenin-associated neurogenesis

Wang, Yea-Hwey / Chern, Chang-Ming / Kuo, Yueh-Hsiung / Liou, Kuo-Tong / Shen, Yuh-Chiang

Food & function. 2019 Aug. 14, v. 10, no. 8

2019

Abstract	Antrodia camphorata is a well-known traditional Chinese mushroom used as a functional food and nutraceutical in Taiwan and China. The aim of this study was to explore the protective effects and mechanism(s) of the ethyl acetate crude extract of A. camphorata (EtOAc-AC) and its active constituent ergostatrien-7,9(11),22-trien-3β-ol (EK100) in an acute ischemic stroke (AIS) murine model. Treating mice with induced AIS injury by using EtOAc-AC (0.3–0.6 g kg−1, p.o.) and EK100 (60 and 120 mg kg−1, p.o.) 2 h after AIS induction significantly increased the tracking distance and reduced brain infarction. Both EtOAc-AC and EK-100 reduced the expression levels of p65NF-κB and caspase 3 near the peri-infarct cortex and promoted the expression of neurogenesis-associated protein doublecortin (DCX) near the hippocampus, accompanied by glycogen synthase kinase 3 (GSK-3) inhibition and β-catenin upregulation. Signaling pathway analysis revealed that the advantageous effects of EtOAc-AC and EK-100 involved triggering the activation of PI3K/Akt and inhibition of GSK-3. Our findings suggest that EtOAc-AC and its active constituent EK100 display anti-inflammatory and anti-apoptotic activities. Both EtOAc-AC and EK100 reduce ischemic brain injury by decreasing p65NF-κB and caspase 3 expression, and they promote neurogenesis (DCX) and neuroprotection (Bcl2) by activating the PI3k/Akt-associated GSK3 inhibition and β-catenin activation.
Keywords	animal models ; beta catenin ; brain damage ; caspase-3 ; cortex ; dietary supplements ; ethyl acetate ; functional foods ; hippocampus ; infarction ; mice ; mushrooms ; neurogenesis ; neuroprotective effect ; phosphatidylinositol 3-kinase ; signal transduction ; stroke ; Taiwanofungus camphoratus ; tau-protein kinase ; China ; Taiwan
Language	English
Dates of publication	2019-0814
Size	p. 4725-4738.
Publishing place	The Royal Society of Chemistry
Document type	Article
ZDB-ID	2612033-1
ISSN	2042-650X ; 2042-6496
ISSN (online)	2042-650X
ISSN	2042-6496
DOI	10.1039/c9fo00908f
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Targeting spike protein-induced TLR/NET axis by COVID-19 therapeutic NRICM102 ameliorates pulmonary embolism and fibrosis.

Wei, Wen-Chi / Liaw, Chia-Ching / Tsai, Keng-Chang / Chiou, Chun-Tang / Tseng, Yu-Hwei / Chiou, Wen-Fei / Lin, Yu-Chi / Tsai, Chia-I / Lin, Chen-Shien / Lin, Chen-Sung / Liou, Kuo-Tong / Yu, I-Shing / Shen, Yuh-Chiang / Su, Yi-Chang

Pharmacological research

2022 Volume 184, Page(s) 106424

Abstract: The global COVID-19 pandemic remains a critical public health threat, as existing vaccines and drugs appear insufficient to halt the rapid transmission. During an outbreak from May to August 2021 in Taiwan, patients with severe COVID-19 were administered ...

Abstract	The global COVID-19 pandemic remains a critical public health threat, as existing vaccines and drugs appear insufficient to halt the rapid transmission. During an outbreak from May to August 2021 in Taiwan, patients with severe COVID-19 were administered NRICM102, which was a traditional Chinese medicine (TCM) formula developed based on its predecessor NRICM101 approved for treating mild cases. This study aimed to explore the mechanism of NRICM102 in ameliorating severe COVID-19-related embolic and fibrotic pulmonary injury. NRICM102 was found to disrupt spike protein/ACE2 interaction, 3CL protease activity, reduce activation of neutrophils, monocytes and expression of cytokines (TNF-α, IL-1β, IL-6, IL-8), chemokines (MCP-1, MIP-1, RANTES) and proinflammatory receptor (TLR4). NRICM102 also inhibited the spread of virus and progression to embolic and fibrotic pulmonary injury through reducing prothrombotic (vWF, PAI-1, NET) and fibrotic (c-Kit, SCF) factors, and reducing alveolar type I (AT1) and type II (AT2) cell apoptosis. NRICM102 may exhibit its protective capability via regulation of TLRs, JAK/STAT, PI3K/AKT, and NET signaling pathways. The study demonstrates the ability of NRICM102 to ameliorate severe COVID-19-related embolic and fibrotic pulmonary injury in vitro and in vivo and elucidates the underlying mechanisms.
MeSH term(s)	Angiotensin-Converting Enzyme 2 ; COVID-19/drug therapy ; Chemokine CCL5 ; Cytokines ; Fibrosis ; Humans ; Interleukin-6/metabolism ; Interleukin-8 ; Lung Injury/drug therapy ; Pandemics ; Phosphatidylinositol 3-Kinases ; Plasminogen Activator Inhibitor 1 ; Proto-Oncogene Proteins c-akt ; Pulmonary Embolism/drug therapy ; Spike Glycoprotein, Coronavirus ; Toll-Like Receptor 4/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; von Willebrand Factor
Chemical Substances	Chemokine CCL5 ; Cytokines ; Interleukin-6 ; Interleukin-8 ; Plasminogen Activator Inhibitor 1 ; Spike Glycoprotein, Coronavirus ; Toll-Like Receptor 4 ; Tumor Necrosis Factor-alpha ; spike protein, SARS-CoV-2 ; von Willebrand Factor ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2022-09-05
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2022.106424
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Article ; Online: Ameliorative effects of caffeic acid phenethyl ester on an eccentric exercise-induced skeletal muscle injury by down-regulating NF-κb mediated inflammation.

Shen, Yuh-Chiang / Yen, Jiin-Cherng / Liou, Kuo-Tong

Pharmacology

2013 Volume 91, Issue 3-4, Page(s) 219–228

Abstract: Background and purpose: Caffeic acid phenethyl ester (CAPE), a phenolic compound isolated from propolis, displays a variety of biological activities. The aim is to examine the protective effect and mechanisms of CAPE on an eccentric exercise-induced ... ...

Abstract	Background and purpose: Caffeic acid phenethyl ester (CAPE), a phenolic compound isolated from propolis, displays a variety of biological activities. The aim is to examine the protective effect and mechanisms of CAPE on an eccentric exercise-induced muscle injury model. Experimental approach: An intermittent downhill eccentric exercise protocol was used. The oxidative tissue injury and expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β), monocyte chemotactic protein-1 (MCP-1), and activation of nuclear factor-κB (NF-κB) were examined. CAPE was applied in a dose of 5 and 10 mg/kg/day, p.o. Key results: The eccentric exercise induced remarkable skeletal muscle damage uncovered by a dramatic elevation of creatine kinase in the serum and severe degenerative myopathy. These pathophysiological changes were accompanied by an upregulation of the inflammatory responses including protein nitrotyrosylation, poly-ADP-ribose-polymerase (PARP) upregulation, lipid peroxidation as measured by malondialdehyde (MDA) formation, and leukocyte infiltration as measured by myeloperoxidase (MPO). The inflammatory responses primarily resulted from enhanced expression of COX2, iNOS, and production of IL-1β and MCP-1, possibly through activation of NF-κB. All these pathological changes were suppressed by treatment of CAPE. Conclusions and implications: Our results indicate that CAPE exhibits protective effects against eccentric exercise-induced skeletal muscle damage in rats by blocking the NF-κB-dependent activation of the inflammatory responses.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Caffeic Acids/pharmacology ; Caffeic Acids/therapeutic use ; Creatine Kinase/blood ; Cyclooxygenase 2/metabolism ; Down-Regulation ; Inflammation/drug therapy ; Inflammation/metabolism ; Inflammation/pathology ; Male ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/injuries ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; NF-kappa B/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Oxidative Stress/drug effects ; Phenylethyl Alcohol/analogs & derivatives ; Phenylethyl Alcohol/pharmacology ; Phenylethyl Alcohol/therapeutic use ; Physical Conditioning, Animal/adverse effects ; Poly(ADP-ribose) Polymerases/metabolism ; Rats ; Rats, Wistar
Chemical Substances	Anti-Inflammatory Agents ; Caffeic Acids ; NF-kappa B ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, rat (EC 1.14.13.39) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Ptgs2 protein, rat (EC 1.14.99.1) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30) ; Creatine Kinase (EC 2.7.3.2) ; caffeic acid phenethyl ester (G960R9S5SK) ; Phenylethyl Alcohol (ML9LGA7468)
Language	English
Publishing date	2013
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	206671-3
ISSN	1423-0313 ; 0031-7012
ISSN (online)	1423-0313
ISSN	0031-7012
DOI	10.1159/000348412
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Article: Suppression of Inflammatory and Fibrotic Signals by Cinnamon (

Chen, Lih-Lian / Lee, Mei-Hsien / Chang, Chia-Lin / Liou, Kuo-Tong / Liu, Shu-Hsiang / Chern, Chang-Ming / Chen, Hui-I / Shen, Yuh-Chiang / Wang, Yea-Hwey

Evidence-based complementary and alternative medicine : eCAM

2021 Volume 2021, Page(s) 5205759

Abstract: Cinnamon ( ...

Abstract	Cinnamon (
Language	English
Publishing date	2021-12-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2171158-6
ISSN	1741-4288 ; 1741-427X
ISSN (online)	1741-4288
ISSN	1741-427X
DOI	10.1155/2021/5205759
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Article ; Online: GSK-3 inhibition through GLP-1R allosteric activation mediates the neurogenesis promoting effect of P7C3 after cerebral ischemic/reperfusional injury in mice.

Wang, Yea-Hwey / Liou, Kuo-Tong / Tsai, Keng-Chang / Liu, Hui-Kang / Yang, Li-Ming / Chern, Chang-Ming / Shen, Yuh-Chiang

Toxicology and applied pharmacology

2018 Volume 357, Page(s) 88–105

Abstract: An aminopropyl carbazole compound, P7C3, has been shown to be a potent neurogenesis promoting agent; however, its fundamental signaling action has yet to be elucidated. A cerebral ischemic/reperfusional (CI/R) injury model in mice was implemented to ... ...

Abstract	An aminopropyl carbazole compound, P7C3, has been shown to be a potent neurogenesis promoting agent; however, its fundamental signaling action has yet to be elucidated. A cerebral ischemic/reperfusional (CI/R) injury model in mice was implemented to elucidate the neuronal protective mechanism(s) of P7C3. Treating CI/R mice using P7C3 (50-100 μg/kg, i.v.) significantly improved tracking distance and walking behavior, and reduced brain damage. Specifically, P7C3 promoted the expression of neurogenesis-associated proteins, including doublecortin, beta tubulin III (β-tub3), adam11 and adamts20, near the peri-infarct cortex, accompanied by glycogen synthase kinase 3 (GSK-3) inhibition and β-catenin upregulation. The application of a specific inhibitor against glucagon-like peptide 1 receptor (GLP-1R), exendin(9-39), revealed that the beneficial effects of P7C3 involved triggering the activation of GLP-1R-associated PKA/Akt signaling. P7C3 elicited the GLP-1R-dependent intracellular cAMP increment and the insulin secretion in cellular models. Surface plasmon resonance assay of P7C3 showed a Kd value of 0.53 μM for GLP-1R binding, and the docking of P7C3 to the putative active site on GLP-1R was successfully predicted by molecular modeling. Our findings indicate that P7C3 promotes the expression of neurogenesis proteins by activation of the cAMP/PKA-dependent and Akt/GSK3-associated β-catenin through positive allosteric stimulation of GLP-1R. Within the P7C3 class of neuroprotective molecules, this mechanism appears to be unique to the prototypical P7C3 molecule, as other active derivatives such as P7C2-A20 and P7C3-S243 they do not engage this same pathway and have been shown to work by nicotinamide phosphoribosyltransferase (NAMPT) stimulation.
MeSH term(s)	Animals ; Blood-Brain Barrier ; Brain Ischemia ; Carbazoles/chemistry ; Carbazoles/pharmacology ; Gene Expression Regulation/drug effects ; Glucagon-Like Peptide-1 Receptor/genetics ; Glucagon-Like Peptide-1 Receptor/metabolism ; Glycogen Synthase Kinase 3/antagonists & inhibitors ; Glycogen Synthase Kinase 3/genetics ; Glycogen Synthase Kinase 3/metabolism ; Male ; Mice ; Molecular Structure ; Neurogenesis/drug effects ; Reperfusion Injury/drug therapy ; Surface Plasmon Resonance
Chemical Substances	Carbazoles ; Glucagon-Like Peptide-1 Receptor ; P7C3 compound ; Glycogen Synthase Kinase 3 (EC 2.7.11.26)
Language	English
Publishing date	2018-09-04
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.2018.08.023
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Article ; Online: Osthole ameliorates cartilage degradation by downregulation of NF-κB and HIF-2α pathways in an osteoarthritis murine model.

Chern, Chang-Ming / Zhou, Han / Wang, Yea-Hwey / Chang, Chia-Lin / Chiou, Wen-Fei / Chang, Wen-Te / Yao, Chun-Hsu / Liou, Kuo-Tong / Shen, Yuh-Chiang

European journal of pharmacology

2019 Volume 867, Page(s) 172799

Abstract: Osteoarthritis (OA) is a common and disabling joint disease mainly characterized by cartilage degradation, with the knees most commonly affected. No effective treatment for the cartilage degradation of OA exists. Preliminary studies have revealed the ... ...

Abstract	Osteoarthritis (OA) is a common and disabling joint disease mainly characterized by cartilage degradation, with the knees most commonly affected. No effective treatment for the cartilage degradation of OA exists. Preliminary studies have revealed the protective and osteogenic effects of osthole, a natural coumarin first isolated from Cnidium monnieri (Fructus Cnidii); however, no evidence of osthole in an OA-related model has been published to date. This study further explored the effects of osthole in a monoiodoacetate (MIA)-induced OA-related animal model and focused on the molecular mechanism(s) behind the anti-inflammatory and cartilage protective effects of osthole. This study revealed that the cartilage protective effect of osthole in a MIA-induced osteoarthritis (OA) murine model can be explained by downregulation of COX-2 and RUNX2 by inhibition of NF-κB and HIF-2α up-regulated by OA induction, resulting in downregulation of MMP-13, Syndecan IV and ADAMTS-5. In addition, osthole might have anti-inflammatory and analgesic effects due to COX-2 inhibition. Osthole can be considered as a potential component of the treatment of OA, for it possesses a cartilage protective effect, as well as anti-inflammation, analgesic, and movement improving effects. Further preclinical and human clinical studies are needed to examine the efficacy and safety profile of long-term therapy.
MeSH term(s)	Administration, Oral ; Animals ; Arthritis, Experimental/chemically induced ; Arthritis, Experimental/drug therapy ; Arthritis, Experimental/pathology ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Cartilage, Articular/drug effects ; Cartilage, Articular/pathology ; Coumarins/administration & dosage ; Down-Regulation/drug effects ; Drug Evaluation, Preclinical ; Humans ; Iodoacetic Acid/toxicity ; Male ; Mice ; Mice, Inbred ICR ; NF-kappa B/metabolism ; Osteoarthritis/chemically induced ; Osteoarthritis/drug therapy ; Osteoarthritis/pathology ; Protective Agents/administration & dosage ; Signal Transduction/drug effects
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors ; Coumarins ; NF-kappa B ; Protective Agents ; endothelial PAS domain-containing protein 1 (1B37H0967P) ; Iodoacetic Acid (WF5188V710) ; osthol (XH1TI1759C)
Language	English
Publishing date	2019-11-22
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2019.172799
Database	MEDical Literature Analysis and Retrieval System OnLINE

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