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Article ; Online: The activation of spliced X-box binding protein 1 by isorhynchophylline therapy improves diabetic encephalopathy.

Wang, Jian / Wang, Xuebao / Zhang, Minxue / Lang, Yan / Chen, Baihui / Ye, Yiru / Bai, Yongheng / Ding, Saidan

2023 Volume 39, Issue 6, Page(s) 2587–2613

Abstract: The primary symptom of diabetic encephalopathy (DE), a kind of central diabetic neuropathy caused by diabetes mellitus (DM), is cognitive impairment. In addition, the tetracyclic oxindole alkaloid isorhynchophylline (IRN) helps lessen cognitive ... ...

Abstract	The primary symptom of diabetic encephalopathy (DE), a kind of central diabetic neuropathy caused by diabetes mellitus (DM), is cognitive impairment. In addition, the tetracyclic oxindole alkaloid isorhynchophylline (IRN) helps lessen cognitive impairment. However, it is still unclear how IRN affects DM and DE and what mechanisms are involved. The effectiveness of IRN on brain insulin resistance was carefully examined in this work, both in vitro and in vivo. We found that IRN accelerates spliced form of X-box binding protein 1 (sXBP1) translocation into the nucleus under high glucose conditions in vitro. IRN also facilitates the nuclear association of pCREB with sXBP1 and the binding of regulatory subunits of phosphatidylinositol 3-kinase (PI3K) p85α or p85β with XBP1 to restore high glucose impairment. Also, IRN treatment improves high glucose-mediated impairment of insulin signaling, endoplasmic reticulum stress, and pyroptosis/apoptosis by depending on sXBP1 in vitro. In vivo studies suggested that IRN attenuates cognitive impairment, ameliorating peripheral insulin resistance, activating insulin signaling, inactivating activating transcription factor 6 (ATF6) and C/EBP homology protein (CHOP), and mitigating pyroptosis/apoptosis by stimulation of sXBP1 nuclear translocation in the brain. In summary, these data indicate that IRN contributes to maintaining insulin homeostasis by activating sXBP1 in the brain. Thus, IRN is a potent antidiabetic agent as well as an sXBP1 activator that has promising potential for the prevention or treatment of DE.
MeSH term(s)	Humans ; Oxindoles/pharmacology ; X-Box Binding Protein 1 ; Insulin Resistance ; Phosphatidylinositol 3-Kinases ; Endoplasmic Reticulum Stress ; Insulin ; Glucose ; Diabetes Mellitus/drug therapy
Chemical Substances	rhyncophylline (46BQ79VJ8D) ; Oxindoles ; X-Box Binding Protein 1 ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Insulin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-01-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	48824-0
ISSN	1573-6822 ; 0742-2091
ISSN (online)	1573-6822
ISSN	0742-2091
DOI	10.1007/s10565-022-09789-z
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Article ; Online: Autocrine S100B in astrocytes promotes VEGF-dependent inflammation and oxidative stress and causes impaired neuroprotection.

Ding, Saidan / Wang, Chengde / Wang, Weikan / Yu, He / Chen, Baihui / Liu, Leping / Zhang, Minxue / Lang, Yan

Cell biology and toxicology

2021 Volume 39, Issue 5, Page(s) 1–25

Abstract: Minimal hepatic encephalopathy (MHE) is strongly associated with neuroinflammation. Nevertheless, the underlying mechanism of the induction of inflammatory response in MHE astrocytes remains not fully understood. In the present study, we investigated the ...

Abstract	Minimal hepatic encephalopathy (MHE) is strongly associated with neuroinflammation. Nevertheless, the underlying mechanism of the induction of inflammatory response in MHE astrocytes remains not fully understood. In the present study, we investigated the effect and mechanism of S100B, a predominant isoform expressed and released from mature astrocytes, on MHE-like neuropathology in the MHE rat model. We discovered that S100B expressions and autocrine were significantly increased in MHE rat brains and MHE rat brain-derived astrocytes. Furthermore, S100B stimulates VEGF expression via the interaction between TLR2 and RAGE in an autocrine manner. S100B-facilitated VEGF autocrine expression further led to a VEGFR2 and COX-2 interaction, which in turn induced the activation of NFƙB, eventually resulting in inflammation and oxidative stress in MHE astrocytes. MHE astrocytes supported impairment of neuronal survival and growth in a co-culture system. To sum up, a comprehensive understanding of the role of S100B-overexpressed MHE astrocyte in MHE pathogenesis may provide insights into the etiology of MHE.
MeSH term(s)	Animals ; Rats ; Astrocytes/metabolism ; Inflammation/metabolism ; Neuroprotection ; Oxidative Stress ; S100 Calcium Binding Protein beta Subunit/metabolism ; S100 Calcium Binding Protein beta Subunit/pharmacology ; Vascular Endothelial Growth Factors
Chemical Substances	S100 Calcium Binding Protein beta Subunit ; S100b protein, rat ; Vascular Endothelial Growth Factors
Language	English
Publishing date	2021-11-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	48824-0
ISSN	1573-6822 ; 0742-2091
ISSN (online)	1573-6822
ISSN	0742-2091
DOI	10.1007/s10565-021-09674-1
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Article ; Online: Insulin Resistance Disrupts the Interaction Between AKT and the NMDA Receptor and the Inactivation of the CaMKIV/CREB Pathway in Minimal Hepatic Encephalopathy.

Ding, Saidan / Zhuge, Weishan / Yang, Jianjing / Wen, Fangfang / Xu, Zhu / Wang, Xuebao / Zhuge, Qichuan

Toxicological sciences : an official journal of the Society of Toxicology

2017 Volume 161, Issue 1, Page(s) 208

Language	English
Publishing date	2017-12-07
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/kfx256
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Article: Pathogenesis of hepatic fibrosis analyzed at the proteome level.

Ding, Saidan / Chen, Bicheng

Saudi medical journal

2012 Volume 33, Issue 2, Page(s) 123–127

Abstract: Proteomic technologies have provided effective approaches to the analysis of the pathogenesis of hepatic fibrosis. A large number of proteins that have been revealed by this technology play a critical role in various aspects of pathological liver ... ...

Abstract	Proteomic technologies have provided effective approaches to the analysis of the pathogenesis of hepatic fibrosis. A large number of proteins that have been revealed by this technology play a critical role in various aspects of pathological liver fibrosis. Comprehensive evaluations of these proteins have led to the understanding that the mechanisms of hepatic fibrosis can be stratified into several broad classifications. Here, we describe the mechanisms of action that are defined as being related to 1) oxidative stress and mitochondrial damage, 2) inflammatory response and immune injury, 3) abnormal cell proliferation and apoptosis, 4) abnormal metabolism, 5) abnormal cellular signal transduction, and 6) abnormal extracellular matrix metabolism.
MeSH term(s)	Humans ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Proteome/physiology
Chemical Substances	Proteome
Language	English
Publishing date	2012-02
Publishing country	Saudi Arabia
Document type	Journal Article ; Review
ZDB-ID	392302-2
ISSN	1658-3175 ; 0379-5284
ISSN (online)	1658-3175
ISSN	0379-5284
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Article: [Dopamine inhibits glutamate-uptake ability of astrocytes via TAAR1-EAAT2 pathway].

Wen, Fangfang / Liu, Leping / Xu, Zhu / Yang, Janjing / Ding, Saidan

Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology

2017 Volume 33, Issue 7, Page(s) 930–935

Abstract: Objective To investigate the effect of dopamine (DA) on the glutamate (Glu)-uptake ability of astrocytes, and the role of trace amine-associated receptor 1-excitatory amino acid transporter 2 (TAAR1-EAAT2) signaling pathway in Glu uptake by astrocytes. ... ...

Abstract	Objective To investigate the effect of dopamine (DA) on the glutamate (Glu)-uptake ability of astrocytes, and the role of trace amine-associated receptor 1-excitatory amino acid transporter 2 (TAAR1-EAAT2) signaling pathway in Glu uptake by astrocytes. Methods In the primary cultured astrocytes pretreated with DA, extracellular Glu levels were measured by the Amplex Red glutamic acid assay kit. The levels of TAAR1 and EAAT2 transcriptions were detected by reverse transcription PCR and their protein levels were analyzed by Western blotting. After TAAR1 plasmid and TAAR1 siRNA were separately transfected into the primary astrocytes pretreated by DA, Western blotting was performed to determine the level of EAAT2 and Amplex Red glutamic acid assay kit was used to analyze Glu uptake in primary cultured astrocyte supernatants. Results The expression of EAAT2 in the primary cultured astrocytes significantly decreased in response to DA, and the level of TAAR1 increased. DA significantly enhanced the Glu uptake in primary cultured astrocyte supernatants. After TAAR1 siRNA transfection, EAAT2 expression was upregulated by DA treatment and Glu content in the supernatants was downregulated. On the contrary, after TAAR1 plasmid transfection, EAAT2 expression descended and Glu level ascended in the supernatants. Conclusion DA reduces the Glu-uptake ability of astrocytes through TAAR1-EAAT2 signaling pathway, causes extracellular Glu accumulation, and ultimately destroys the function of astrocytes.
MeSH term(s)	Animals ; Astrocytes/drug effects ; Astrocytes/metabolism ; Dopamine/pharmacology ; Excitatory Amino Acid Transporter 2/physiology ; Glutamic Acid/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled/physiology ; Signal Transduction/physiology
Chemical Substances	Excitatory Amino Acid Transporter 2 ; Receptors, G-Protein-Coupled ; Slc1a2 protein, rat ; Glutamic Acid (3KX376GY7L) ; Dopamine (VTD58H1Z2X) ; Trace amine-associated receptor 1 (XMC8VP6RI2)
Language	Chinese
Publishing date	2017-07-20
Publishing country	China
Document type	Journal Article
ISSN	1007-8738
ISSN	1007-8738
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Article ; Online: Dopamine induces glutamate accumulation in astrocytes to disrupt neuronal function leading to pathogenesis of minimal hepatic encephalopathy.

Ding, Saidan / Wang, Xuebao / Zhuge, Weishan / Yang, Jianjing / Zhuge, Qichuan

Neuroscience

2017 Volume 365, Page(s) 94–113

Abstract: Minimal hepatic encephalopathy (MHE) is induced by elevated intracranial dopamine (DA). Glutamate (Glu) toxicity is known to be involved in many neurological disorders. In this study, we investigated whether DA increased Glu levels and collaborated with ... ...

Abstract	Minimal hepatic encephalopathy (MHE) is induced by elevated intracranial dopamine (DA). Glutamate (Glu) toxicity is known to be involved in many neurological disorders. In this study, we investigated whether DA increased Glu levels and collaborated with Glu to impair memory. We found that DA upregulated TAAR1, leading to reduced EAAT2 expression and Glu clearance in primary cortical astrocytes (PCAs). High DA increased TAAR1 expression, and high Glu increased AMPAR expression, inducing the activation of CaN/NFAT signaling and a decrease in the production of BDNF (Brain Derived Nerve Growth Factor)/NT3 (neurotrophin-3) in primary cortical neurons (PCNs). DA activated TAAR1 to downregulate EAAT2 and increase extracellular Glu levels in MHE. Additionally, DA together with Glu caused decreased production of neuronal BDNF/NT3 and memory impairment through the activation of CaN/NFAT signaling in MHE. From these findings, we conclude that DA increases Glu levels via interaction with TAAR1 and disruption of EAAT2 signaling in astrocytes, and DA interacting with TAAR1 and Glu interacting with AMPAR synergistically decreased the production of BDNF by activation of CaN/NFAT signaling to impair memory in MHE rats.
MeSH term(s)	Animals ; Astrocytes/drug effects ; Brain-Derived Neurotrophic Factor/genetics ; Brain-Derived Neurotrophic Factor/metabolism ; Cells, Cultured ; Cerebral Cortex/cytology ; Disease Models, Animal ; Dopamine/pharmacology ; Excitatory Amino Acid Transporter 2/genetics ; Excitatory Amino Acid Transporter 2/metabolism ; Glial Fibrillary Acidic Protein/metabolism ; Glutamic Acid/metabolism ; Hepatic Encephalopathy/chemically induced ; Hepatic Encephalopathy/complications ; Hepatic Encephalopathy/pathology ; Maze Learning/drug effects ; Microdialysis ; Nerve Growth Factors/genetics ; Nerve Growth Factors/metabolism ; Neurons/drug effects ; Neurons/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Thioacetamide/toxicity
Chemical Substances	Brain-Derived Neurotrophic Factor ; Excitatory Amino Acid Transporter 2 ; Glial Fibrillary Acidic Protein ; Nerve Growth Factors ; RNA, Small Interfering ; Thioacetamide (075T165X8M) ; Glutamic Acid (3KX376GY7L) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2017-12-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/j.neuroscience.2017.09.040
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Article: Dopamine Burden Induced the Inactivation of Sonic Hedgehog Signaling to Cognitive Decline in Minimal Hepatic Encephalopathy.

Ding, Saidan / Yang, Jianjing / Huang, Xueli / Liu, Leping / Hu, Jiangnan / Xu, Zhu / Zhuge, Qichuan

Aging and disease

2017 Volume 8, Issue 4, Page(s) 442–457

Abstract: Minimal hepatic encephalopathy (MHE) is induced by elevated intracranial dopamine (DA). The relationship of the Shh pathway with memory loss in MHE, however, is elusive. In the current study, rats with MHE induced with DA displayed downregulation of the ... ...

Abstract	Minimal hepatic encephalopathy (MHE) is induced by elevated intracranial dopamine (DA). The relationship of the Shh pathway with memory loss in MHE, however, is elusive. In the current study, rats with MHE induced with DA displayed downregulation of the Shh pathway. Additionally, injection of Shh into MHE/DA-treated rats reversed downregulation of BDNF/NT3, whereas administration of cyclopamine (Cyc) enhanced the inhibition of expression of BDNF/NT3. Furthermore, naringin (Nrg) substantially prevented cognitive impairment in MHE/DA-treated rats and upregulated the Shh pathway, paralleling the elevated expression of BDNF/NT3. Overall, our results indicate that the Shh pathway can induce the expression of BDNF/NT3, and DA causes memory loss by inactivation of Shh pathway signaling to BDNF/NT3 in MHE rats, which is reversed by Nrg. Our study may provide new theory basis of pathogenesis and therapeutic target of MHE.
Language	English
Publishing date	2017-07-21
Publishing country	United States
Document type	Journal Article
ISSN	2152-5250
ISSN	2152-5250
DOI	10.14336/AD.2016.1123
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Article ; Online: Oridonin prevents insulin resistance-mediated cognitive disorder through PTEN/Akt pathway and autophagy in minimal hepatic encephalopathy.

Wen, Fangfang / Zhuge, Weishan / Wang, Jian / Lu, Xiaoai / You, Ruimin / Liu, Leping / Zhuge, Qichuan / Ding, Saidan

Journal of cellular and molecular medicine

2019 Volume 24, Issue 1, Page(s) 61–78

Abstract: Minimal hepatic encephalopathy (MHE) was characterized for cognitive dysfunction. Insulin resistance (IR) has been identified to be correlated with the pathogenesis of MHE. Oridonin (Ori) is an active terpenoid, which has been reported to rescue synaptic ...

Abstract	Minimal hepatic encephalopathy (MHE) was characterized for cognitive dysfunction. Insulin resistance (IR) has been identified to be correlated with the pathogenesis of MHE. Oridonin (Ori) is an active terpenoid, which has been reported to rescue synaptic loss and restore insulin sensitivity. In this study, we found that intraperitoneal injection of Ori rescued IR, reduced the autophagosome formation and synaptic loss and improved cognitive dysfunction in MHE rats. Moreover, in insulin-resistant PC12 cells and N2a cells, we found that Ori blocked IR-induced synaptic deficits via the down-regulation of PTEN, the phosphorylation of Akt and the inhibition of autophagy. Taken together, these results suggested that Ori displays therapeutic efficacy towards memory deficits via improvement of IR in MHE and represents a novel bioactive therapeutic agent for treating MHE.
MeSH term(s)	Animals ; Autophagy ; Cognitive Dysfunction/etiology ; Cognitive Dysfunction/metabolism ; Cognitive Dysfunction/pathology ; Cognitive Dysfunction/prevention & control ; Diterpenes, Kaurane/pharmacology ; Hepatic Encephalopathy/complications ; Hepatic Encephalopathy/pathology ; Insulin Resistance ; Memory Disorders/etiology ; Memory Disorders/metabolism ; Memory Disorders/pathology ; Memory Disorders/prevention & control ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Diterpenes, Kaurane ; oridonin (0APJ98UCLQ) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; Pten protein, rat (EC 3.1.3.67)
Language	English
Publishing date	2019-09-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.14546
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Article ; Online: Dopamine Burden Triggers Cholesterol Overload Following Disruption of Synaptogenesis in Minimal Hepatic Encephalopathy.

Zhuge, Weishan / Wen, Fangfang / Ni, Zhihui / Zheng, Zhao / Zhu, Xiaohong / Lin, Jianting / Wang, Jian / Zhuge, Qichuan / Ding, Saidan

Neuroscience

2019 Volume 410, Page(s) 1–15

Abstract: The contribution of Dopamine (DA) to minimal hepatic encephalopathy (MHE) has been demonstrated. However, recent studies have revealed that cholesterol (CHO) treatment substantially increased the risk of dementia. The objectives of this study were to ... ...

Abstract	The contribution of Dopamine (DA) to minimal hepatic encephalopathy (MHE) has been demonstrated. However, recent studies have revealed that cholesterol (CHO) treatment substantially increased the risk of dementia. The objectives of this study were to investigate whether CHO was induced by DA overload and its involvement in DA-induced cognitive impairment in MHE. Our study showed that DA treatment triggered CHO biosynthesis via the activation of JNK3/SREBP2 signaling pathway in primary cultured astrocytes. Conditioned media from DA-treated astrocytes increased CHO uptake by primary cultured neurons and disrupted synaptic formations; at the same time, inhibition of CHO synthesis and transportation from astrocytes diminished the disruption of synaptogenesis, which indicates the involvement of CHO in the perturbation of neural synaptogenesis in vitro. Secondary secretion of DA from primary cultured neurons was stimulated by CHO secreted from astrocytes. DA induced synergistic decreases of PPARγ/pERK/pCREB expressions in the presence of CHO in neurons, leading to synergistic synaptic impairment. Memory impairments were observed in MHE/DA-treated rats, which were partially rescued by atorvastatin (ATVS) treatment, confirming the involvement of CHO burden in vivo. Overall, our study suggests that DA overload triggers obvious CHO production from astrocytes. Excessive CHO in turn triggered neurons to secrete abundant DA and DA burden in combination with CHO overload elicit the cognitive decline and memory loss via PPARγ/ERK/CREB pathway in MHE.
MeSH term(s)	Animals ; Astrocytes/drug effects ; Astrocytes/metabolism ; Astrocytes/pathology ; Brain/drug effects ; Brain/metabolism ; Brain/pathology ; Cells, Cultured ; Cholesterol/metabolism ; Dopamine/administration & dosage ; Dopamine/toxicity ; Hepatic Encephalopathy/metabolism ; Hepatic Encephalopathy/pathology ; Injections, Intraventricular ; Lipogenesis/drug effects ; Lipogenesis/physiology ; Neurogenesis/drug effects ; Neurogenesis/physiology ; Rats ; Rats, Sprague-Dawley ; Synapses/drug effects ; Synapses/metabolism ; Synapses/pathology
Chemical Substances	Cholesterol (97C5T2UQ7J) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2019-05-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/j.neuroscience.2019.04.056
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Article ; Online: New Measures for the Coronavirus Disease 2019 Response: A Lesson From the Wenzhou Experience.

Ruan, Linhui / Wen, Min / Zeng, Qingrun / Chen, Chengshui / Huang, Shengwei / Yang, Su / Yang, Jianjing / Wang, Jingqiang / Hu, Yuhuan / Ding, Saidan / Zhang, Ying / Zhang, Hongxia / Feng, Yuanjing / Jin, Kunlin / Zhuge, Qichuan

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America

2020 Volume 71, Issue 15, Page(s) 866–869

Abstract: As the outbreak of coronavirus disease 2019 (COVID-19) has spread globally, determining how to prevent the spread is of paramount importance. We reported the effectiveness of different responses of 4 affected cities in preventing the COVID-19 spread. We ... ...

Abstract	As the outbreak of coronavirus disease 2019 (COVID-19) has spread globally, determining how to prevent the spread is of paramount importance. We reported the effectiveness of different responses of 4 affected cities in preventing the COVID-19 spread. We expect the Wenzhou anti-COVID-19 measures may provide information for cities around the world that are experiencing this epidemic.
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Betacoronavirus/pathogenicity ; COVID-19 ; Child ; Child, Preschool ; China/epidemiology ; Cities/epidemiology ; Coronavirus Infections/epidemiology ; Coronavirus Infections/virology ; Disease Outbreaks ; Female ; Humans ; Male ; Middle Aged ; Pandemics ; Pneumonia, Viral/epidemiology ; Pneumonia, Viral/virology ; SARS-CoV-2 ; Young Adult
Keywords	covid19
Language	English
Publishing date	2020-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1099781-7
ISSN	1537-6591 ; 1058-4838
ISSN (online)	1537-6591
ISSN	1058-4838
DOI	10.1093/cid/ciaa386
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