Jinshui Chen

First Affiliated Hospital of Fujian Medical University

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Tianmin Wu

Shandong University

Liufang Fan

First Affiliated Hospital of Fujian Medical University

Ruxi Tong

First Affiliated Hospital of Fujian Medical University

Wenyan Xie

Guangdong Ocean University

Xuanbin Huang

First Affiliated Hospital of Fujian Medical University

Yungang Chen

Shandong University of Traditional Chinese Medicine

Ke Jin

Nanjing Medical University

Luisana Astudillo

University of Miami

Huang You-zhen

First Affiliated Hospital of Fujian Medical University

Stephan C. Schürer

University of Miami

Cooperative Institutions

Fujian Medical University

First Affiliated Hospital of Fujian Medical University

Shandong University of Traditional Chinese Medicine

Affiliated Hospital of Shandong University of Traditional Chinese Medicine

University of Miami

Zhejiang University

Sun Yat-sen University

Sylvester Comprehensive Cancer Center

University of Cincinnati

Jiangsu University

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Ruanmailing Oral Liquid Inhibit Atherosclerosis in ApoE-/- Mice by Regulation of TGF-β1/SMAD4 Signaling Pathway

Research Square (Research Square) (2021)

Tianmin Wu Xuanbin Huang Jinshui Chen Wenjuan Xue Liufang Fan

Abstract BackgroundTo investigate the effect of Ruanmailing oral liquid on atherosclerosis and TGF-β1/SMAD4 signaling pathway in ApoE knockout mice induced by high-fat diet. MethodsForty ApoE -/- mice were randomly divided into 5 groups, and mice fed with standard diets were the control group. ApoE -/- mice high-fat diet induced atherosclerotic phenotype. After grouping and treatment, they were divided into high-fat feeding model group, low-dose and high-dose of Ruanmailing groups (1.75, 4.55 ml/kg/d), Lipitor Group (3.0 mg/kg/d). After 12 weeks of administration, blood was collected from the mice orbit to determine the levels of TC, TG, LDL-C, and HDL-C, and the pathological changes of thoracic aorta atherosclerosis were observed. Enzyme-linked immunosorbent assay (ELISA) was used to detect the concentration of serum TGF-β1, and RT-PCR and Western Blot were used to detect the expression of SMAD4 and GATA2 in the thoracic aorta of ApoE -/- mice in each group. ResultsCompared with the high-fat model group, the serum lipids level of each administration group were reduced ( P <0.01 or P <0.05), and the ratio of plaque area to luminal area (W/L) was significantly reduced ( P <0.05), and pathological examination indicated atherosclerotic lesions in thoracic aorta of ApoE -/- mice were alleviated, and the high-dose Ruanmailing group had the most significant anti-atherosclerotic effect. ConclusionsRuanmailing oral liquid has an anti-atherosclerotic effect, and its mechanism may be related to the intervention of GATA2 in the TGF-β1/SMAD4 signaling pathway to reduce the differentiation and proliferation of arterial smooth muscle cells.

Apolipoprotein E

Thoracic aorta

10.21203/rs.3.rs-478536/v1

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Abstract A33: Discovery of novel anti-cancer therapeutic agents for Notch activation complex kinase (NACK) targeting the Notch pathway

Clinical Cancer Research (2017)

Xiaoxia Zhu Zhiqiang Wang Ke Jin Luisana Astudillo Wen Zhou

Abstract The Notch signaling pathway has been found to play an important role in multiple human cancers by regulating transcriptional programs. However, the mechanism by which Notch drives target gene transcription is still elusive. In our previous study, we have identified and characterized a novel Notch activation complex kinase, NACK, which acts as a Notch transcriptional co-activator and an essential regulator of Notch-mediated tumorigenesis and development. In this regard, NACK could become a putative drug target in anti-cancer therapies. The lack of three-dimensional (3D) structure of NACK hinders the designing of potential drug inhibitors. Therefore, computational methods are adopted to elucidate the structural and functional features of NACK, which further aid in designing new NACK inhibitors. Molecule docking (Glide) is utilized to obtain potential hit inhibitors for NACK, which will be validated using in-vitro and in-vivo assays. This will open avenues for the development of new therapies for Notch-dependent cancers. Citation Format: Xiaoxia Zhu, Zhiqiang Wang, Ke Jin, Luisana Astudillo, Wen Zhou, Jinshui Chen, Peter Buchwald, Stephan C. Schürer, Anthony J. Capobianco. Discovery of novel anti-cancer therapeutic agents for Notch activation complex kinase (NACK) targeting the Notch pathway. [abstract]. In: Proceedings of the AACR Precision Medicine Series: Targeting the Vulnerabilities of Cancer; May 16-19, 2016; Miami, FL. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(1_Suppl):Abstract nr A33.

NAK

10.1158/1557-3265.pmccavuln16-a33

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Circ_0001721 enhances doxorubicin resistance and promotes tumorigenesis in osteosarcoma through miR-758/TCF4 axis

Cancer Cell International (2021)

Huapeng Guan Hao Xu Jinshui Chen Weishan Wu Dongfeng Chen

Abstract Background Osteosarcoma (OS) is a common type of bone malignancy that often occurs in children and adolescents. Chemoresistance is a huge barrier to cancer therapy. This study aimed to investigate the role and potential mechanism of circ_0001721 in doxorubicin (DXR) resistance and OS development. Methods The levels of circ_0001721, miR-758 and transcription factor 4 (TCF4) were detected by quantitative real-time polymerase chain reaction or western blot assay. Cell Counting Kit-8 (CCK-8) assay was used to calculate the half inhibition concentration (IC 50 ) of DXR and assess cell viability. Cell migration and invasion were evaluated by transwell assay. Cell apoptosis was monitored by flow cytometry. The levels of multidrug resistance-related and Wnt/β-catenin pathway-related proteins were measured by western blot assay. The interaction among circ_0001721, miR-758 and TCF4 were confirmed by dual-luciferase reporter assay, RNA immunoprecipitation assay or RNA pull-down assay. The xenograft model was established to analyze tumor growth in vivo. Results Circ_0001721 and TCF4 were upregulated, whereas miR-758 was down-regulated in DXR-resistant OS tissues and cells. Circ_0001721 silence reduced DXR resistance of KHOS/DXR and MG63/DXR cells. Circ_0001721 regulated DXR resistance via sponging miR-758. Moreover, miR-758 modulated DXR resistance by targeting TCF4. Besides, circ_0001721 knockdown inhibited tumor growth in vivo. Conclusion Circ_0001721 potentiated DXR resistance and facilitated the progression of OS by regulating miR-758/TCF4 axis, which provides promising therapeutic targets for OS treatment.

Viability assay

10.1186/s12935-021-02016-5

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Effects of Ruanmailing in Blocking Early Stages of Atherosclerosis by TNF-α Regulation via Kir2.1

Evidence-based Complementary and Alternative Medicine (2022)

Liufang Fan Xuanbin Huang Wenjuan Xue Weyan Xie Ruxi Tong

Ruanmailing oral solution consists of 16 herbs, has anti-lipid peroxidation activity, protects vascular endothelial cells, and improves vascular elasticity. It is an effective drug for the treatment of atherosclerosis (AS). The objective of this study was to investigate the mechanism underlying the antiatherosclerotic effects of Ruanmailing oral solution.Macrophages were isolated, cultured, and divided into the macrophage control; macrophage foam cell; and low-, medium-, and high-concentration Ruanmailing groups. Cell proliferation was analyzed by cell counting kit-8 (CCK-8) assay, and the expression levels of inward-rectifier potassium ion channel 2.1 (Kir2.1) and tumor necrosis factor (TNF)-α were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analyses.CCK-8 assay results showed that the tested concentrations of Ruanmailing solution did not affect macrophage proliferation. RT-PCR and Western blot assays indicated that TNF-α expression increased significantly with the formation of macrophage foam cells (P < 0.05). In addition, significant decreases in Kir2.1 and TNF-α expression were observed following treatment with various concentrations of Ruanmailing (P < 0.05).Based on the results, Ruanmailing affects macrophage foam cell formation by regulating Kir2.1 expression, which in turn reduces TNF-α expression and exerts antiatherosclerotic effects. These findings provide a scientific basis for the use of traditional Chinese medicine for AS treatment.

Foam cell

10.1155/2022/2836880

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Chinese Medicine Supplementing Qi and Activating Blood Circulation Relieves the Progression of Diabetic Cardiomyopathy

Endocrine Metabolic & Immune Disorders - Drug Targets (2023)

Ruxi Tong Tianmin Wu Jinshui Chen

Diabetic cardiomyopathy (DCM) is the leading cause of diabetic death as the final occurrence of heart failure and arrhythmia. Traditional Chinese medicine is usually used to treat various diseases including diabetes.

Preload

Diabetic Cardiomyopathy

Ventricular pressure

Ventricular remodeling

Dilated Cardiomyopathy

10.2174/1871530323666230501151924

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Progress in the Study of TLR-NF-κB Signaling Pathway Associated with Myocarditis

Medical Recapitulate (2011)

Jinshui Chen

Toll-like receptor is a super family of receptors related with the recognition of microorganisms,and expressed on the surface of inflammatory cells,which plays a crucial role in natural immunity.Studies show that the activation of Toll-like receptor-nuclear factor kappa B(TLR-NF-κB)signaling transduction pathway can induce the activation of inflammatory cells to secret pro-inflammatory cytokines to trigger the inflammatory responses,mediating the conversion from innate immunity to acquired immunity,involved in the pathophysiological process of viral myocarditis(VMC).To investigate the effects of TLR-NF-κB signalingn pathway on VMC will provide a theoretical foundationfor revealing the pathogenesis of VMC and seeking effective preventive and therapeutic measures.

Pathogenesis

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Effects of Shenqi Fuzheng injection on Fas/FasL protein expression levels in the cardiomyocytes of a mouse model of viral myocarditis

Experimental and Therapeutic Medicine (2016)

Tianmin Wu Jinshui Chen Liufang Fan Wenyan Xie Changsheng Xu

The aim of the present study was to examine the effects of Shenqi Fuzheng injection (SFI) on Fas and FasL protein expression levels in the cardiomyocytes of mice with viral myocarditis (VMC) and to explore the underlying anti-apoptotic mechanisms. A total of 120 male BALB/c mice were randomly divided into five groups as follows: Blank control group, model group, ribavirin group, low‑dose SFI group and high‑dose SFI group. The VMC model was established by the injection of coxsackievirus group B type 3 and saline, ribavirin or SFI was administered 30 min later. Cardiac samples were harvested from mice in each group on days 3, 10 and 30. Apoptosis of cardiac cells was examined using terminal deoxynucleotidyl transferase dUTP nick‑end labeling, and Fas and FasL protein expression levels were detected using immunohistochemistry. Myocardial apoptosis and Fas/FasL protein expression levels were significantly increased in the model group, as compared with the blank group (P<0.01), whereas the apoptotic index (AI) and Fas/FasL protein expression levels of cardiac cells in the high‑dose SFI group were significantly decreased compared with those in the model group on day 10 (acute phase; P<0.01). The AI and Fas/FasL protein expression levels of cardiac cells in the low‑ and high‑dose SFI groups were also significantly decreased on day 30 (chronic phase; P<0.01); however, no differences between the high‑ and low‑dose groups were detected. In conclusion, SFI relieves VMC via the downregulation of Fas and FasL protein expression and the inhibition of cell apoptosis.

Fas ligand

Viral Myocarditis

Terminal deoxynucleotidyl transferase

10.3892/etm.2016.3165

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