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Start Over Author "Jiang, Fan" Journal acta pharmacologica sinica
9 results on '"Jiang, Fan"'

3. Z16b, a natural compound from Ganoderma cochlear is a novel RyR2 stabilizer preventing catecholaminergic polymorphic ventricular tachycardia

Author

Jiang-fan Wan, Gang Wang, Fu-ying Qin, Dan-ling Huang, Yan Wang, Ai-ling Su, Hai-ping Zhang, Yang Liu, Shao-yin Zeng, Chao-liang Wei, Yong-xian Cheng, and Jie Liu

Subjects
Pharmacology, Arrhythmias, Cardiac, Ganoderma, Ryanodine Receptor Calcium Release Channel, General Medicine, Molecular Docking Simulation, Mice, Mutation, Tachycardia, Ventricular, Animals, Humans, Pharmacology (medical), Calcium, Myocytes, Cardiac
Abstract

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited, lethal ventricular arrhythmia triggered by catecholamines. Mutations in genes that encode cardiac ryanodine receptor (RyR2) and proteins that regulate RyR2 activity cause enhanced diastolic Ca

Published
2021

4. Adenosine A2A receptor deficiency attenuates the somnogenic effect of prostaglandin D2 in mice

Author

Yoshihiro Urade, Zhi-Li Huang, Bin-Jia Zhang, Jiang-Fan Chen, and Wei-Min Qu

Subjects
0301 basic medicine, medicine.medical_specialty, Prostaglandin, Adenosine A2A receptor, Endogeny, Non-rapid eye movement sleep, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Internal medicine, medicine, Pharmacology (medical), Receptor, Pharmacology, integumentary system, business.industry, General Medicine, Sleep in non-human animals, Adenosine, 030104 developmental biology, Endocrinology, chemistry, lipids (amino acids, peptides, and proteins), Prostaglandin D2, business, 030217 neurology & neurosurgery, medicine.drug
Abstract

Prostaglandin D2 (PGD2) is one of the most potent endogenous sleep promoting substances. PGD2 activates the PGD2 receptor (DPR) and increases the extracellular level of adenosine in wild-type (WT) mice but not DPR knockout (KO) mice, suggesting that PGD2-induced sleep is DPR-dependent, and adenosine may be the signaling molecule that mediates the somnogenic effect of PGD2. The aim of this study was to determine the involvement of the adenosine A2A receptor (A2AR) in PGD2-induced sleep. We infused PGD2 into the lateral ventricle of WT and A2AR KO mice between 20:00 and 2:00 for 6 h, and electroencephalograms and electromyograms were simultaneously recorded. In WT mice, PGD2 infusion dose-dependently increased non-rapid eye movement (non-REM, NREM) sleep, which was 139.1%, 145.0% and 202.7% as large as that of vehicle-treated mice at doses of 10, 20 and 50 pmol/min, respectively. PGD2 infusion at doses of 20 and 50 pmol/min also increased REM sleep during the 6-h PGD2 infusion and 4-h post-dosing periods in WT mice to 148.9% and 166.7%, respectively. In A2AR KO mice, however, PGD2 infusion at 10 pmol/min did not change the sleep profile, whereas higher doses at 20 and 50 pmol/min increased the NREM sleep during the 6-h PGD2 infusion to 117.5% and 155.6%, respectively, but did not change the sleep in the post-dosing period. Moreover, PGD2 infusion at 50 pmol/min significantly increased the episode number in both genotypes but only enhanced the episode duration in WT mice. The results demonstrate that PGD2-induced sleep in mice is mediated by both adenosine A2AR-dependent and -independent systems.

Published
2017

5. Z16b, a natural compound from Ganoderma cochlearis a novel RyR2 stabilizer preventing catecholaminergic polymorphic ventricular tachycardia

Author

Wan, Jiang-fan, Wang, Gang, Qin, Fu-ying, Huang, Dan-ling, Wang, Yan, Su, Ai-ling, Zhang, Hai-ping, Liu, Yang, Zeng, Shao-yin, Wei, Chao-liang, Cheng, Yong-xian, and Liu, Jie

Abstract

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited, lethal ventricular arrhythmia triggered by catecholamines. Mutations in genes that encode cardiac ryanodine receptor (RyR2) and proteins that regulate RyR2 activity cause enhanced diastolic Ca2+release (leak) through the RyR2 channels, resulting in CPVT. Current therapies for CPVT are limited. We found that Z16b, a meroterpenoid isolated from Ganoderma cochlear, inhibited Ca2+spark frequency (CaSF) in R2474S/ + cardiomyocytes in a dose-dependent manner, with an IC50of 3.2 μM. Z16b also dose-dependently suppressed abnormal post-pacing Ca2+release events. Intraperitoneal injection (i.p.) of epinephrine and caffeine stimulated sustained ventricular tachycardia in all R2474S/+ mice, while pretreatment with Z16b (0.5 mg/kg, i.p.) prevented ventricular arrhythmia in 9 of 10 mice, and Z16b administration immediately after the onset of VT abolished sVT in 9 of 12 mice. Of translational significance, Z16b significantly inhibited CaSF and abnormal Ca2+release events in human CPVT iPS-CMs. Mechanistically, Z16b interacts with RyR2, enhancing the “zipping” state of the N-terminal and central domains of RyR2. A molecular docking simulation and point mutation and pulldown assays identified Z16b forms hydrogen bonds with Arg626, His1670, and Gln2126 in RyR2 as a triangle shape that anchors the NTD and CD interaction and thus stabilizes RyR2 in a tight “zipping” conformation. Our findings support that Z16b is a novel RyR2 stabilizer that can prevent CPVT. It may also serve as a lead compound with a new scaffold for the design of safer and more efficient drugs for treating CPVT.

Published
2022
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6. Adenosine A

Author

Bin-Jia, Zhang, Zhi-Li, Huang, Jiang-Fan, Chen, Yoshihiro, Urade, and Wei-Min, Qu

Subjects
Male, Mice, Knockout, Infusions, Intraventricular, integumentary system, Receptor, Adenosine A2A, Prostaglandin D2, Animals, lipids (amino acids, peptides, and proteins), Original Article, Wakefulness, Sleep
Abstract

Prostaglandin D2 (PGD2) is one of the most potent endogenous sleep promoting substances. PGD2 activates the PGD2 receptor (DPR) and increases the extracellular level of adenosine in wild-type (WT) mice but not DPR knockout (KO) mice, suggesting that PGD2-induced sleep is DPR-dependent, and adenosine may be the signaling molecule that mediates the somnogenic effect of PGD2. The aim of this study was to determine the involvement of the adenosine A2A receptor (A2AR) in PGD2-induced sleep. We infused PGD2 into the lateral ventricle of WT and A2AR KO mice between 20:00 and 2:00 for 6 h, and electroencephalograms and electromyograms were simultaneously recorded. In WT mice, PGD2 infusion dose-dependently increased non-rapid eye movement (non-REM, NREM) sleep, which was 139.1%, 145.0% and 202.7% as large as that of vehicle-treated mice at doses of 10, 20 and 50 pmol/min, respectively. PGD2 infusion at doses of 20 and 50 pmol/min also increased REM sleep during the 6-h PGD2 infusion and 4-h post-dosing periods in WT mice to 148.9% and 166.7%, respectively. In A2AR KO mice, however, PGD2 infusion at 10 pmol/min did not change the sleep profile, whereas higher doses at 20 and 50 pmol/min increased the NREM sleep during the 6-h PGD2 infusion to 117.5% and 155.6%, respectively, but did not change the sleep in the post-dosing period. Moreover, PGD2 infusion at 50 pmol/min significantly increased the episode number in both genotypes but only enhanced the episode duration in WT mice. The results demonstrate that PGD2-induced sleep in mice is mediated by both adenosine A2AR-dependent and -independent systems.

Published
2016

8. Adenosine A2Areceptor deficiency attenuates the somnogenic effect of prostaglandin D2in mice

Author

Zhang, Bin-jia, Huang, Zhi-li, Chen, Jiang-fan, Urade, Yoshihiro, and Qu, Wei-min

Abstract

Prostaglandin D2(PGD2) is one of the most potent endogenous sleep promoting substances. PGD2activates the PGD2receptor (DPR) and increases the extracellular level of adenosine in wild-type (WT) mice but not DPR knockout (KO) mice, suggesting that PGD2-induced sleep is DPR-dependent, and adenosine may be the signaling molecule that mediates the somnogenic effect of PGD2. The aim of this study was to determine the involvement of the adenosine A2Areceptor (A2AR) in PGD2-induced sleep. We infused PGD2into the lateral ventricle of WT and A2AR KO mice between 20:00 and 2:00 for 6 h, and electroencephalograms and electromyograms were simultaneously recorded. In WT mice, PGD2infusion dose-dependently increased non-rapid eye movement (non-REM, NREM) sleep, which was 139.1%, 145.0% and 202.7% as large as that of vehicle-treated mice at doses of 10, 20 and 50 pmol/min, respectively. PGD2infusion at doses of 20 and 50 pmol/min also increased REM sleep during the 6-h PGD2infusion and 4-h post-dosing periods in WT mice to 148.9% and 166.7%, respectively. In A2AR KO mice, however, PGD2infusion at 10 pmol/min did not change the sleep profile, whereas higher doses at 20 and 50 pmol/min increased the NREM sleep during the 6-h PGD2infusion to 117.5% and 155.6%, respectively, but did not change the sleep in the post-dosing period. Moreover, PGD2infusion at 50 pmol/min significantly increased the episode number in both genotypes but only enhanced the episode duration in WT mice. The results demonstrate that PGD2-induced sleep in mice is mediated by both adenosine A2AR-dependent and -independent systems.

Published
2017
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9. Adenosine A 2A receptor deficiency attenuates the somnogenic effect of prostaglandin D 2 in mice.

Author

Zhang BJ, Huang ZL, Chen JF, Urade Y, and Qu WM

Subjects
Animals, Infusions, Intraventricular, Male, Mice, Knockout, Prostaglandin D2 administration & dosage, Receptor, Adenosine A2A metabolism, Wakefulness drug effects, Prostaglandin D2 pharmacology, Receptor, Adenosine A2A deficiency, Sleep drug effects
Abstract

Prostaglandin D 2 (PGD 2 ) is one of the most potent endogenous sleep promoting substances. PGD 2 activates the PGD 2 receptor (DPR) and increases the extracellular level of adenosine in wild-type (WT) mice but not DPR knockout (KO) mice, suggesting that PGD 2 -induced sleep is DPR-dependent, and adenosine may be the signaling molecule that mediates the somnogenic effect of PGD 2 . The aim of this study was to determine the involvement of the adenosine A 2A receptor (A 2A R) in PGD 2 -induced sleep. We infused PGD 2 into the lateral ventricle of WT and A 2A R KO mice between 20:00 and 2:00 for 6 h, and electroencephalograms and electromyograms were simultaneously recorded. In WT mice, PGD 2 infusion dose-dependently increased non-rapid eye movement (non-REM, NREM) sleep, which was 139.1%, 145.0% and 202.7% as large as that of vehicle-treated mice at doses of 10, 20 and 50 pmol/min, respectively. PGD 2 infusion at doses of 20 and 50 pmol/min also increased REM sleep during the 6-h PGD 2 infusion and 4-h post-dosing periods in WT mice to 148.9% and 166.7%, respectively. In A 2A R KO mice, however, PGD 2 infusion at 10 pmol/min did not change the sleep profile, whereas higher doses at 20 and 50 pmol/min increased the NREM sleep during the 6-h PGD 2 infusion to 117.5% and 155.6%, respectively, but did not change the sleep in the post-dosing period. Moreover, PGD 2 infusion at 50 pmol/min significantly increased the episode number in both genotypes but only enhanced the episode duration in WT mice. The results demonstrate that PGD 2 -induced sleep in mice is mediated by both adenosine A 2A R-dependent and -independent systems.

Published
2017
Full Text
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