Tengyue Zhang

Zhejiang Sci-Tech University

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Pingsheng Fan

University of Science and Technology of China

Kelong Ma

Anhui University of Traditional Chinese Medicine

Yabei Liu

University of Science and Technology of China

Niansheng Yang

Sun Yat-sen University

Guangshan Yang

Huazhong University of Science and Technology

Yuefang Huang

Washington University in St. Louis

Mianjing Zhou

The First Affiliated Hospital, Sun Yat-sen University

Jun‐Min He

Shaanxi Normal University

Chaozhao Liang

First Affiliated Hospital of Anhui Medical University

Miao Liu

Renmin Hospital of Wuhan University

Cooperative Institutions

Chinese Academy of Sciences

Anhui Medical University

University of Chinese Academy of Sciences

University of Science and Technology of China

Sun Yat-sen University

Peking University

Shanghai Jiao Tong University

Sichuan University

Chinese Academy of Medical Sciences & Peking Union Medical College

Nanjing Medical University

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RIP3 dependent NLRP3 inflammasome activation is implicated in acute lung injury in mice

Journal of Translational Medicine (2018)

Jingxian Chen Shuang Wang Rong Fu Mianjing Zhou Tengyue Zhang

NLRP3 inflammasome is involved in the inflammatory responses during acute lung injury (ALI). RIP3 triggered NLRP3 inflammasome activation independent of necroptosis induction has recently been documented. In this study, the role of RIP3 in the activation of NLRP3 inflammasome in the development of ALI was investigated. A selective RIP3 inhibitor GSK872 was used to investigate the roles of RIP3 in NLRP3 inflammasome activation in the lipopolysaccharide (LPS) induced ALI mouse model. The mechanism of NLRP3 inflammasome activation was investigated in the human monocytic cell line THP-1. NLRP3 inflammasome and necroptosis were measured by flow cytometry or western blot. RIP3–NLRP3 interaction was interrogated using immunoprecipitation and the Duolink® In situ detection. Significant upregulation of both necroptosis and NLRP3 inflammasome pathways were observed in the lungs of mice with LPS induced ALI. GSK872 significantly suppressed the activation of necroptosis and NLRP3 activation with reduction of IL-1β and IL-18 production and inflammatory cells infiltration, resulting in a significant amelioration of lung injury. These two processes were shown to be active in interstitial macrophages and CD11b+ monocyte–macrophages/dendritic cells. In THP-1 cells, RIP3 and NLRP3 interaction was enhanced by LPS/ATP stimulation resulting in IL-1β and IL-18 production. This RIP3–NLRP3 interaction was significantly inhibited by GSK872. Taking together, these results show that RIP3 participates in the NLRP3 inflammasome activation in infiltrating macrophages in ALI induced by LPS. This process plays a significant pathogenic role in LPS-induced lung injury.

THP1 cell line

10.1186/s12967-018-1606-4

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Deciphering the pharmacological mechanisms of Fraxini Cortex for ulcerative colitis treatment based on network pharmacology and in vivo studies

BMC Complementary Medicine and Therapies (2023)

Tianming Wang Xuyang Su Jing Peng Xiaofen Tan Guangshan Yang

Abstract Background Ulcerative colitis (UC) is a common type of inflammatory bowel disease. Due to the elusive pathogenesis, safe and effective treatment strategies are still lacking. Fraxini Cortex (FC) has been widely used as a medicinal herb to treat some diseases. However, the pharmacological mechanisms of FC for UC treatment are still unclear. Methods An integrated platform combining network pharmacology and experimental studies was introduced to decipher the mechanism of FC against UC. The active compounds, therapeutic targets, and the molecular mechanism of action were acquired by network pharmacology, and the interaction between the compounds and target proteins were verified by molecular docking. Dextran sulfate sodium (DSS)-induced colitis model was employed to assess the therapeutic effect of FC on UC, and validate the molecular mechanisms of action predicted by network pharmacology. Results A total of 20 bioactive compounds were retrieved, and 115 targets were predicted by using the online databases. Ursolic acid, fraxetin, beta-sitosterol, and esculetin were identified as the main active compounds of FC against UC. PPI network analysis identified 28 FC-UC hub genes that were mainly enriched in the IL-17 signaling pathway, the TNF signaling pathway, and pathways in cancer. Molecular docking confirmed that the active compounds had high binding affinities to the predicted target proteins. GEO dataset analysis showed that these target genes were highly expressed in the UC clinical samples compared with that in the healthy controls. Experimental studies showed that FC alleviated DSS-induced colitis symptoms, reduced inflammatory cytokines release, and suppressed the expression levels of IL1β, COX2, MMP3, IL-17 and RORγt in colon tissues. Conclusion FC exhibits anti-UC properties through regulating multi-targets and multi-pathways with multi-components. In vivo results demonstrated that FC alleviated DSS-induced colitis.

10.1186/s12906-023-03983-0

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CaMK4 Promotes Acute Lung Injury Through NLRP3 Inflammasome Activation in Type II Alveolar Epithelial Cell

Frontiers in Immunology (2022)

Tengyue Zhang Mengyuan Li Siyuan Zhao Mianjing Zhou Huai Liao

Background Type II alveolar epithelial cell (AEC II), in addition to its roles in maintaining lung homeostasis, takes an active role in inflammatory response during acute lung injury (ALI). Ca 2+ /calmodulin-dependent protein kinase IV (CaMK4) activated by Ca 2+ /calmodulin signaling, has been implicated in immune responses. This study was to investigate the roles of CaMK4 in the development of ALI and the underlying mechanisms. Methods CaMK4 inhibitor KN-93 was used to investigate the effects of CaMK4 on NLRP3 inflammasome activation. The effects of KN-93 on disease development of lipopolysaccharide (LPS)-induced ALI were also evaluated. The role of CaMK4 on NLRP3 inflammasome activation was explored in human AEC II cell line A549 using KN-93 or CaMK4 siRNA. NLRP3 inflammasome activation was measured by histology immunofluorescence and Western blot. IL-1β and IL-18 were measured by ELISA. Results Phosphorylation of CaMK4 and the expression of NLRP3 and Caspase-1 p20 were increased in the lungs of LPS-induced ALI mice, which was suppressed by KN-93 as measured by Western blot. Further, the activation of NLRP3 inflammasome was detected in AEC II from patients with acute respiratory distress syndrome (ARDS) and LPS-induced ALI mice. In vitro , inhibition or silencing CaMK4 in AEC II significantly inhibited NLRP3 inflammasome activation, resulting in reduced IL-1β production. The inhibition of NLRP3 inflammasome and decreased IL-1β/IL-18 production by KN-93 led to reduced inflammatory infiltration and ameliorated lung injury in LPS-induced ALI mice. Conclusion CaMK4 controls the activation of NLRP3 inflammasome in AEC II during LPS-induced ALI. CaMK4 inhibition could be a novel therapeutic approach for the treatment of ALI.

10.3389/fimmu.2022.890710

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Citations (19)

Verapamil enhances the sensitivity of oxaliplatin to tumor cells by influencing the PARP pathway.

PubMed (2019)

Tengyue Zhang Guangshan Yang Yabei Liu Pingsheng Fan

PARP is a DNA damage-modifying enzyme present in most eukaryotic cells. In this study, reverse docking showed that verapamil (Vera), which can effectively bind PARP1/2, could significantly inhibit PARP1/2 activity inside and outside the system. Moreover, it could enhance the sensitivity of oxaliplatin to low-expression P-glycoprotein (P-gP) tumor cells and strengthen its apoptosis-inducing effect on tumor cells under the reverse drug resistance concentration of tumor cells. Vera, which can reverse chemotherapy resistance of tumor cells, showed no simple correlations with oxaliplatin drug resistance or P-gP expression and could enhance the anti-tumor effect of platinum chemotherapeutic agents by influencing the PARP pathway.

PARP1

10.1691/ph.2019.9715

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Citations (1)

Acid-sensing ion channel 1a mediates acid-induced increases in intracellular calcium in rat articular chondrocytes

Molecular and Cellular Biochemistry (2010)

Feng‐Lai Yuan Feihu Chen Weiguo Lü Xia Li Fan‐Rong Wu

Acid-sensing ion channel

Calcium in biology

10.1007/s11010-010-0412-y

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Citations (61)

Evaluating the roles of lipopolysaccharide, fimbria and colanic acid in the attachment of Escherichia coli strains on inert surfaces by a quantitative method via atomic force microscopy

Yi Chao Tengyue Zhang

Inert

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Effects of plant growth regulators and endogenous phytohormone profiles on the rooting of tissue culture raised shoots of persimmon (Diospyros kaki Thunb.)

Scientia Horticulturae (2024)

Jiaying Yuan Tengyue Zhang Yinfeng Hu Lu Bai Lu Zhang

Diospyros kaki

Diospyros

10.1016/j.scienta.2024.113917

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Reconsideration of the taxonomy of the marine ciliate Neobakuella aenigmatica Moon et al., 2019 (Protozoa, Ciliophora, Hypotrichia)

Marine Life Science & Technology (2020)

Tengyue Zhang Jingyi Dong Ting Cheng Lili Duan Chen Shao

10.1007/s42995-020-00032-4

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Biological Evaluation of 3-Sulfonate-Substituted Icariin Derivatives as Reversal Agents of P-Glycoprotein-Mediated Multidrug Resistance

Tengyue Zhang Pingsheng Fan Guohong Yang Lili Zhang Miao Liu

As an extension of the previous study, 14 synthesized 3-sulfonate-substituted icariin derivatives, which served as P-gp-mediated MDR reversal agents, were assessed. The biological assessment showed that all icariin derivatives can reverse the drug resistance of MCF-7/ADR cells against ADR, and the reversal index is in the range of 1.77-9.57. At the concentration of 10 μM, the most effective compound ZTY9 could significantly increase the accumulation of ADR in MCF-7/ADR cells and promote cell apoptosis. As further investigated, ZTY9 could repress P-gp-mediated drug outflow without downregulating the protein level of P-gp, thus strengthening drug residence. Molecular docking and dynamic simulation results manifested the high binding stability of ZTY9 to the NBD domain of P-gp. More importantly, ZTY9 markedly enhanced the curative effect of ADR on a xenograft model of MCF-7/ADR on the premise of unchanged body weight. Hence, 3-sulfonate-substituted icariin derivatives are promising materials for the development of MDR reversal agents applied to cancer chemotherapy.

Icariin

P-glycoprotein

10.2139/ssrn.4498607

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CDKN2B is critical for verapamil-mediated reversal of doxorubicin resistance in hepatocellular carcinoma

Oncotarget (2017)

Tengyue Zhang Kelong Ma Jin Huang Wang Shi-tang Yabei Liu

// Tengyue Zhang 1, 2, * , Kelong Ma 3, * , Jin Huang 2, * , Shitang Wang 4, * , Yabei Liu 2 , Gaofei Fan 2 , Miao Liu 2 , Guangshan Yang 2 , Cheng Wang 4 and Pingsheng Fan 1, 2 1 School of Clinical Medicine, Shan Dong University, Jinan 250100, China 2 The Cancer Hospital of Anhui Province, Provincial Hospital of Anhui Medical University, Hefei 230032, China 3 Clinical College of Integrated Traditional Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei 230032, China 4 Department of General Surgery, Provincial Hospital of Anhui Medical University, Hefei 230032, China * These authors have contributed equally to this work Correspondence to: Pingsheng Fan, email: wangal2014@sohu.com Cheng Wang, email: blackpippy@163.com Keywords: hepatocellular carcinoma (HCC); verapamil (VER); doxorubicin (ADM); CDKN2B; chemotherapy resistance Received: June 14, 2017 Accepted: October 05, 2017 Published: October 26, 2017 ABSTRACT In this study, we explored the function and mechanism of CDKN2B genes in verapamil (VER)-induced reversal of resistance to doxorubicin (ADM) chemotherapy in hepatocellular carcinoma (HCC). We examined 4 HCC cell lines and found that the expression levels of CDKN2B genes correlated with the level of apoptosis induced by ADM+VER. Overexpression of CDKN2B genes promoted apoptosis in cells treated with VER+ADM. CDKN2B knockdown using siRNA weakened the effect of ADM+VER, indicating that ADM+VER promotes HCC cell apoptosis and that CDKN2B genes participate in VER-mediated promotion in tumor cell apoptosis. Future research will further explore the functional mechanism, and the associated signal transduction pathways via which CDKN2B affects HCC drug resistance.

CDKN2B

10.18632/oncotarget.22123

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Citations (11)