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The Chinese patent medicine, Jin-tang-ning, ameliorates hyperglycemia through improving β cell function in pre-diabetic KKAy mice

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Chinese Journal of natural medicines 2020年第11期18卷 827-836页

作者： LIU Shuai-Nan LIU Quan LEI Lei SUN Su-Juan LI Cai-Na HUAN Yi HOU Shao-Cong SHEN Zhu-Fang State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Key laboratory of Polymorphic Drugs of BejingInstitute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical CollegeBejing 100050China

Jin-tang-ning(JTN), a Chinese patent medicine, mainly comprised of Bombyx mori L., has been proved to show α-glucosidase inhibitory efficacy and clinically effective for the treatment of type 2 diabetes(T2 DM). Recently, we have reported that JTN could ameliorate postprandial hyperglycemia and improved β cell function in monosodium glutamate(MSG)-induced obese mice,suggesting that JTN might play a potential role in preventing the conversion of impaired glucose tolerance(IGT) to T2 DM. In this study, we evaluated the effect of JTN on the progression of T2 DM in the pre-diabetic KKAy mice. During the 10 weeks of treatment,blood biochemical analysis and oral glucose tolerance tests were performed to evaluate glucose and lipid profiles. The β cell function was quantified using hyperglycemic clamp at the end of the study. JTN-treated groups exhibited slowly raised fasting and postprandial blood glucose levels, and also ameliorated lipid profile. JTN improved glucose intolerance after 8 weeks of treatment. Meanwhile, JTN restored glucose-stimulated first-phase of insulin secretion and induced higher maximum insulin levels in the hyperglycemic ***, to investigate the underlying mechanisms of JTN in protecting β cell function, the morphologic changes of the pancreatic islets were observed by optical microscope and immunofluorescence of hormones(insulin and glucagon). Pancreatic protein expression levels of key factors involving in insulin secretion-related pathway and ER stress were also detected by Western blot. Pre-diabetic KKAy mice exhibited a compensatory augment in β cell mass and abnormal α cell distribution. Long-term treatment of JTN recovered islet morphology accompanied by reducing α cell area in KKAy mice. JTN upregulated expression levels of glucokinase(GCK), pyruvate carboxylase(PCB) and pancreas duodenum homeobox-1(PDX-1), while down-regulating C/EBP homologous protein(Chop)expression in pancreas of the hyperglycemic clamp, which indicated the improvem

关键词： Jin-tang-ning(JTN) Pre-diabetes βCell function Type 2 diabetes ER stress

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Inflammasomes in neurodegenerative diseases

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Translational Neurodegeneration 2024年第1期13卷 71-92页

作者： Qianchen Wang Songwei Yang Xuan Zhang Shanshan Zhang Liping Chen Wanxue Wang Naihong Chen Jiaqing Yan Department of Pharmacy The First Affiliated Hospital of China Medical UniversityShenyang 110001China Hunan Engineering Technology Center of Standardization and Function of Chinese Herbal Decoction Pieces School of PharmacyHunan University of Chinese MedicineChangsha 410208China Department of Pharmacy National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China China Three Gorges University College of Medicine and Health Sciences Yichang 443002China State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Institute of Materia Medica and Neuroscience CenterChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100050China

Inflammasomes represent a crucial component of the innate immune system,which respond to threats by recognizing different *** are known as pathogen-associated molecular patterns(PAMPs)or host-derived damage-associated molecular patterns(DAMPs).In neurodegenerative diseases and neuroinflammation,the accumulation of misfolded proteins,such as beta-amyloid and alpha-synuclein,can lead to inflammasome activation,resulting in the release of interleukin(IL)-1βand *** activation also induces pyroptosis,the release of inflammatory mediators,and exacerbates *** evidence suggests that inflammasomes play a pivotal role in neurodegenerative ***,elucidating and investigating the activation and regulation of inflammasomes in these diseases is of paramount *** review is primarily focused on evidence indicating that inflammasomes are activated through the canonical pathway in these *** as potential targets for treating neurodegenerative diseases are also discussed.

关键词： Inflammasome Neurodegenerative diseases Neurodegeneration Neuroinflammation Microglia

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Long noncoding RNA GAS5 acts as a competitive endogenous RNA to regulate GSK-3β and PTEN expression by sponging miR-23b-3p in Alzheimer's disease

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Neural Regeneration Research 2026年第1期21卷 392-405页

作者： Li Zeng Kaiyue Zhao Jianghong Liu Mimin Liu Zhongdi Cai Ting Sun Zhuorong Li Rui Liu Institute of Medicinal Biotechnology Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Institute of Medicinal BiotechnologyPeking Union Medical College and Chinese Academy of Medical SciencesBeijingChina Department of Neurology Xuanwu HospitalCapital Medical UniversityBeijingChina

Long noncoding RNA and microRNA are regulatory noncoding RNAs that are implicated in Alzheimer's disease, but the role of long noncoding RNA-associated competitive endogenous RNA has not been fully elucidated. The long noncoding RNA growth arrest-specific 5(GAS5) is a member of the 5′-terminal oligopyrimidine gene family that may be involved in neurological disorders, but its role in Alzheimer's disease remains unclear. This study aimed to investigate the function of GAS5 and construct a GAS5-associated competitive endogenous RNA network comprising potential targets. RNA sequencing results showed that GAS5 was upregulated in five familial Alzheimer's disease(5×FAD) mice, APPswe/PSEN1dE9(APP/PS1) mice, Alzheimer's disease-related APPswe cells, and serum from patients with Alzheimer's disease. Functional experiments with targeted overexpression and silencing demonstrated that GAS5 played a role in cognitive dysfunction and multiple Alzheimer's disease-associated pathologies, including tau hyperphosphorylation, amyloid-beta accumulation, and neuronal apoptosis. Mechanistic studies indicated that GAS5 acted as an endogenous sponge by competing for microRNA-23b-3p(miR-23b-3p) binding to regulate its targets glycogen synthase kinase 3beta(GSK-3β) and phosphatase and tensin homologue deleted on chromosome 10(PTEN) expression in an Argonaute 2-induced RNA silencing complex(RISC)-dependent manner. GAS5 inhibited miR-23b-3p-mediated GSK-3β and PTEN cascades with a feedforward PTEN/protein kinase B(Akt)/GSK-3β linkage. Furthermore, recovery of GAS5/miR-23b-3p/GSK-3β/PTEN pathways relieved Alzheimer's disease-like symptoms in vivo, indicated by the amelioration of spatial cognition, neuronal degeneration, amyloid-beta load, and tau phosphorylation. Together, these findings suggest that GAS5 promotes Alzheimer's disease pathogenesis. This study establishes the functional convergence of the GAS5/miR-23b-3p/GSK-3β/PTEN pathway on multiple pathologies, suggesting a candidate therap

关键词： Alzheimer's disease amyloid-beta peptide accumulation cognitive dysfunction competitive endogenous RNA glycogen synthase kinase 3beta lncRNA growth arrest-specific 5 microRNA-23b-3p neuronal apoptosis phosphatase and tensin homologue deleted on chromosome 10 tau phosphorylation

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Author correction to"YPD-30,a prodrug of YPD-29B,is an oral small-molecule inhibitor targeting PD-L1 for the treatment of human cancer"[Acta Pharmaceutica Sinica B 12(2022)2845-2858]

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Acta Pharmaceutica Sinica B 2023年第7期13卷 3178-3179页

作者： Fangfang Lai Ming Ji Lei Huang Yunchen Wang Nina Xue Tingting Du Kai Dong Xiaoqing Yao Jing Jin Zhiqiang Feng Xiaoguang Chen Department of Pharmacology State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Institute of Materia Medica Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100050 China Tianjin Chase Sun Pharmaceutical Co. Ltd. Tianjin 300170 China Department of Pharmacochemistry Institute of Materia Medica Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100050 China

[This corrects the article DOI: 10.1016/***.2022.02.031.].

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Ganoderic acid A protects neural cells against NO stress injury in vitro via stimulating β adrenergic receptors

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中国药理学报（英文版） 2020年第4期41卷 516-522页

作者： Zi-ru Yu Wei-hua Jia Chao Liu Hong-qing Wang Hai-guang Yang Guo-rong He Ruo-yun Chen Guan-hua Du State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Beijing Key Laboratory of Drug Target and Screening Research Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College Beijing 100050 China

Excessive nitric oxide (NO) causes extensive damage to the nervous system,and the adrenergic system is disordered in many neuropsychiatric ***,the role of the adrenergic system in protection of the nervous system against sodium nitroprusside (SNP) injury remains *** this study,we investigated the effect of ganoderic acid A (GA A) against SNP injury in neural cells and the role of adrenergic receptors in GA A *** found that SNP (0.125-2 mM) dosedependently decreased the viability of both SH-SYSY and PC12 cells and markedly increased NO *** with GA A (10 μM) significantly attenuated SNP-induced cytotoxicity and NO increase in SH-SY5Y cells,but not in PC12 ***,pretreatment with GA A caused significantly higher adrenaline content in SH-SYSY cells than in PC12 *** order to elucidate the mechanism of GA A-protecting SH-SYSY cells,we added adrenaline,phentolamine,metoprolol,or ICI 118551 1 h before GA A was added to the culture *** found that addition of adrenaline (10 μM) significantly improved GA A protection in PC12 *** addition of β1-adrenergic receptor antagonist metoprolol (10 μM) or β2-adrenergic receptor antagonist ICI 118551 (0.1 μM) blocked the protective effect of GA A,whereas the addition of α-adrenergic receptor antagonist phentolamine (0.1 μM) did not affect GA A protection in SH-SYSY *** results suggest that β-adrenergic receptors play an important role in the protection of GA A in SH-SYSY cells against SNP injuries,and excessive adrenaline system activation caused great damage to the nervous system.

关键词： β-adrenergic receptors sodium nitroprusside (SNP) SH-SY5Y cells PC12 cells ganoderic acid A adrenaline norepinephrine phentolamine metoprolol ICI 118551

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Identification ACTA2 and KDR as key proteins for prognosis of PD-1/PD-L1 blockade therapy in melanoma

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Animal Models and Experimental Medicine 2021年第2期4卷 138-150页

作者： Yuchen Wang Zhaojun Li Zhihui Zhang Xiaoguang Chen State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina Beijing Key Laboratory of New Drug Mechanisms and Pharmacological Evaluation Study Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina

Programmed cell death protein 1(PD-1)/programmed cell death ligand 1(PD-L1)blockade is an important therapeutic strategy for melanoma,despite its low clinical *** is important to identify genes and pathways that may reflect the clinical outcomes of this therapy in *** analyzed clinical dataset GSE96619,which contains clinical information from five melanoma patients before and after anti-PD-1 therapy(five pairs of data).We identified 704 DEGs using these five pairs of data,and then the number of DEGs was narrowed down to 286 in patients who responded to ***,we performed KEGG pathway enrichment and constructed a DEG-associated protein-protein interaction *** muscle actin 2(ACTA2)and tyrosine kinase growth factor receptor(KDR)were identified as the hub genes,which were significantly downregulated in the tumor tissue of the two patients who re-sponded to *** confirm our analysis,we demonstrated similar expression tendency to the clinical data for the two hub genes in a B16F10 subcutaneous xeno-graft *** study demonstrates that ACTA2 and KDR are valuable responsive markers for PD-1/PD-L1 blockade therapy.

关键词： expression profiling data hub genes melanoma PD-1/PD-L1 blockade therapy

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Four Pairs of Meroterpenoid Enantiomers with Coumarin- and Chromone-Monoterpene Skeletons from Gerbera Piloselloides and Their bioactive Activities

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SSRN 2024年

作者： Zou, Zhong-Mei Chen, Shi-Lin Zhao, Chen-Xu Gao, Ha Zhang, Tao State Key Laboratory of Bioactive Substance and Function of Natural Medicines Institute of Medicinal Plant Development Chinese Academy of Medical Sciences Peking Union Medical College Beijing100193 China Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine Ministry of Education Beijing100193 China

Phytochemical investigations of the extracts from the whole plant of Gerbera piloselloides resulted in the isolation and identification of four pairs of previously unreported meroterpenoid enantiomers with coumarin- and chromone-monoterpene skeletons (1a/1b–4a/4b), including two pairs of 5-methylcoumarin monoterpenes and two pairs of 5-methylchromone monoterpenes. The structures and absolute configurations of these compounds were definitively determined through NMR and MS data, electronic circular dichroism (ECD) data, and X-ray diffraction analysis. Structurally, compounds 1–4 feature 5-methylphenylpropanoid-substituted monoterpene frameworks. All compounds were evaluated for neuroprotective activity and cytotoxicity against the human cancer cell line SGC-7901 in vitro. Compounds 1, 1a, and 1b exhibited inhibitory effects with IC50 values ranging from 12.07 to 12.44 μM against SGC-7901. Furthermore, the hypothetical biogenetic pathways for these compounds were discussed. © 2024, The Authors. All rights reserved.

关键词： Enantiomers

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Author Correction: Ginsenoside Rg1 protects against ischemic/reperfusion-induced neuronal injury through miR-144/Nrf2/ARE pathway

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Acta pharmacologica Sinica 2024年第9期45卷 1995-1996页

作者： Shi-Feng Chu Zhao Zhang Xin Zhou Wen-Bin He Chen Chen Piao Luo Dan-Dan Liu Qi-di Ai Hai-Fan Gong Zhen-Zhen Wang Hong-Shuo Sun Zhong-Ping Feng Nai-Hong Chen State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Institute of Materia Medica Neuroscience Center Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100050 China. Shanxi Key Laboratory of Chinese Medicine Encephalopathy Shanxi University of Chinese Medicine Jinzhong 030619 China. Hunan University of Chinese Medicine Changsha 410208 China. Department of Physiology Faculty of Medicine University of Toronto Toronto ON M5S 1A8 Canada. State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Institute of Materia Medica Neuroscience Center Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100050 China. chennh@***. Hunan University of Chinese Medicine Changsha 410208 China. chennh@***.

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Luteolin alleviates cognitive impairment in Alzheimer's disease mouse model via inhibiting endoplasmic reticulum stress-dependent neuroinflammation

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中国药理学报（英文版） 2022年第4期43卷 840-849页

作者： Jie-jian Kou Jun-zhuo Shi Yang-yang He Jiao-jiao Hao Hai-yu Zhang Dong-mei Luo Jun-ke Song Yi Yan Xin-mei Xie Guan-hua Du Xiao-bin Pang School of Pharmacy Henan UniversityKaifeng 475004China State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Institute of Materia MedicaChinese Academy of Medical Science and Peking Union Medical CollegeBeijing 100050China Beijing Key Laboratory of Drug Target Identification and Drug Screening National Center for Pharmaceutical ScreeningInstitute of Materia MedicaChinese Academy of Medical Science and Peking Union Medical CollegeBeijing 100050China Institute for Cardiovascular Prevention(IPEK) Ludwig-Maximilians-University MunichMunich 80336Germany DZHK(German Centre for Cardiovascular Research) Partner Site Munich Heart AllianceMunich 80336Germany

Luteolin is a flavonoid in a variety of fruits,vegetables,and herbs,which has shown anti-inflammatory,antioxidant,and anti-cancer neuroprotective *** this study,we investigated the potential beneficial effects of luteolin on memory deficits and neuroinflammation in a triple-transgenic mouse model of Alzheimer's disease(AD)(3×Tg-AD).The mice were treated with luteolin(20,40 mg·kg-1·d-1,ip)for 3 *** showed that luteolin treatment dose-dependently improved spatial learning,ameliorated memory deficits in 3×Tg-AD mice,accompanied by inhibiting astrocyte overactivation(GFAP)and neuroinflammation(TNF-α,IL-1 β,IL-6,NO,COX-2,and iNOS protein),and decreasing the expression of endoplasmic reticulum(ER)stress markers GRP78 and IRE1α in brain *** rat C6 glioma cells,treatment with luteolin(1,10 μM)dose-dependently inhibited LPS-induced cell proliferation,excessive release of inflammatory cytokines,and increase of ER stress marker *** conclusion,luteolin is an effective agent in the treatment of learning and memory deficits in 3×Tg-AD mice,which may be attributable to the inhibition of ER stress in astrocytes and subsequent *** results provide the experimental basis for further research and development of luteolin as a therapeutic agent for AD.

关键词： Alzheimer’s disease luteolin neuroinflammation endoplasmic reticulum stress astrocyte 3 × Tg-AD mice C6 cells

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Construction of a Library of Fully Protected Oligosaccharide for Preparing Various Subtypes of Chondroitin Sulfate

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SSRN 2023年

作者： Jin, Longlong Liu, Qi Yang, Shuang Sun, Huimin Zhao, Zhehui Lu, Yong Wu, Xianfu National Institutes for Food and Drug Control Beijing102629 China State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Department of Medicinal Chemistry Institute of Materia Medica Chinese Academy of Medical Sciences Peking Union Medical College Beijing100050 China

Chondroitin sulfate (CS) regulates a wide range of biological processes, including cell differentiation and division, cancer development, and viral infections. We herein explored and established the method to selectively remove the 4,6-benzyl protective group of galactosamine, selectively introduced different types of protecting groups at positions 4 and 6, and synthesized four different subtypes of CS oligosaccharide modules—CS-O, A, C, and E—and a small library of 16 fully protected tetrasaccharides with different subtypes of CS disaccharides, which could be converted into the final corresponding CS product according to the literature. This work will be helpful for the research of structure–activity relationship and pharmacological mechanism of CS in the future and unlocking the "sulfation code." © 2023, The Authors. All rights reserved.

关键词： Oligosaccharides

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