Jing Zhang

Guangzhou University of Chinese Medicine

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Jian Liang

Zhuhai People's Hospital

Yonger Chen

Guangzhou University of Chinese Medicine

Shaozhen Hou

Guangzhou University of Chinese Medicine

Jiaying Liu

Sichuan University

Jindian Miao

Guangzhou University of Chinese Medicine

Shuoxi Xu

Guangzhou University of Chinese Medicine

Junjun Wang

Hubei University

Yuan Lin

Chongqing Medical University

Anshan Shan

Northeast Agricultural University

Mingsheng Cai

Chinese Academy of Sciences

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Guangzhou University of Chinese Medicine

Sun Yat-sen University

Chinese Academy of Medical Sciences & Peking Union Medical College

Peking Union Medical College Hospital

Guangzhou Medical University

Third Affiliated Hospital of Sun Yat-sen University

Academy of Medical Sciences

Sun Yat-sen University Cancer Center

Second Affiliated Hospital of Guangzhou Medical University

Wuhan University

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グルタミン酸が妊娠期にアルギニンを投与したラットの腸管発育とZO-1、OCCLUDIN遺伝子発現に与える影響を検討した。【JST・京大機械翻訳】

Zhongguo Shouyi Xuebao (2016)

Guochao Wu Anshan Shan Junjun Wang Di Liu Han Yu

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Design, synthesis, and evaluation of substituted 2-acylamide-1,3-benzo[d]zole analogues as agents against MDR- and XDR-MTB

European Journal of Medicinal Chemistry (2020)

Dongsheng Li Chao Liu Xinhai Jiang Yuan Lin Jing Zhang

Amide

10.1016/j.ejmech.2020.112898

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Esculin inhibits hepatic stellate cell activation and CCl4-induced liver fibrosis by activating the Nrf2/GPX4 signaling pathway

Phytomedicine (2024)

Shuoxi Xu Yonger Chen Jindian Miao Yuhua Li Jiaying Liu

Hepatic stellate cell

CCL4

Taxifolin

10.1016/j.phymed.2024.155465

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Monotropein inhibits epithelial–mesenchymal transition in chronic colitis via the mTOR/P70S6K pathway

Frontiers in Pharmacology (2025)

Yuxuan Chen Jiaying Liu Shaowen Zhong Tao Zhang Yuan Jin

Introduction Patients with chronic colitis are at risk of developing intestinal fibrosis through epithelial–mesenchymal transition (EMT). Monotropein (MON) is the main active ingredient in the traditional Chinese medicine Morinda officinalis How . It has been reported that monotropein can improve ulcerative colitis, but the mechanism remains unclear. However, whether monotropein can improve chronic colitis-associated intestinal fibrosis remains unknown. The study aimed to investigate the effect of monotropein on EMT in chronic colitis and its underlying mechanism. Methods The mice chronic colitis model was induced by dextran sodium sulfate (DSS). Cytokines were detected by ELISA. Concentrations of fluorescein isothiocyanate dextran (FITC-Dextran) in serum were detected using a fluorescein microplate analyzer. Intestinal tight junction proteins were detected by immunofluorescence. EMT marker proteins were detected by immunohistochemistry. Transforming growth factor-β1 (TGF-β1) was used to induce EMT in IEC-6 cells. Western blot, real-time quantitative PCR, and immunofluorescence were used to test the inhibitory effect of monotropein on the development of EMT and explore its mechanism. Results Results showed that monotropein significantly improved colonic injury and inhibited the expression of colonic tissue EMT marker protein. In addition, molecular docking and molecular dynamics (MD) simulation, cellular thermal shift assay (CETSA), and drug affinity responsive target stability (DARTS) assay validated monotropein targeting of mTOR. Monotropein inhibited TGF-β1-induced EMT in IEC-6 cells, inhibited the phosphorylation of mTOR and its downstream proteins, and increased the autophagy activity in chronic colitis mice and IEC-6 cells. Discussion The study indicates that monotropein inhibits the development of EMT in DSS-induced chronic colitis mice and TGF-β1-induced IEC-6 cells. Its inhibitory effect on EMT is associated with the mTOR/P70S6K pathway.

10.3389/fphar.2025.1536091

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Discovery of vitexin as a novel VDR agonist that mitigates the transition from chronic intestinal inflammation to colorectal cancer

Molecular Cancer (2024)

Yonger Chen Jian Liang Shuxian Chen Nan Lin Shuoxi Xu

Colitis-associated colorectal cancer (CAC) frequently develops in patients with inflammatory bowel disease (IBD) who have been exposed to a prolonged state of chronic inflammation. The investigation of pharmacological agents and their mechanisms to prevent precancerous lesions and inhibit their progression remains a significant focus and challenge in CAC research. Previous studies have demonstrated that vitexin effectively mitigates CAC, however, its precise mechanism of action warrants further exploration. This study reveals that the absence of the Vitamin D receptor (VDR) accelerates the progression from chronic colitis to colorectal cancer. Our findings indicate that vitexin can specifically target the VDR protein, facilitating its translocation into the cell nucleus to exert transcriptional activity. Additionally, through a co-culture model of macrophages and cancer cells, we observed that vitexin promotes the polarization of macrophages towards the M1 phenotype, a process that is dependent on VDR. Furthermore, ChIP-seq analysis revealed that vitexin regulates the transcriptional activation of phenazine biosynthesis-like domain protein (PBLD) via VDR. ChIP assays and dual luciferase reporter assays were employed to identify the functional PBLD regulatory region, confirming that the VDR/PBLD pathway is critical for vitexin-mediated regulation of macrophage polarization. Finally, in a mouse model with myeloid VDR gene knockout, we found that the protective effects of vitexin were abolished in mid-stage CAC. In summary, our study establishes that vitexin targets VDR and modulates macrophage polarization through the VDR/PBLD pathway, thereby alleviating the transition from chronic colitis to colorectal cancer.

10.1186/s12943-024-02108-6

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An Overview of Pre-expanded Perforator Flaps

Clinics in Plastic Surgery (2016)

Chunmei Wang Jing Zhang Hiko Hyakusoku Ping Song Lee L.Q. Pu

Perforator flaps

Axilla

10.1016/j.cps.2016.09.007

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Vitexin Protects against Dextran Sodium Sulfate-Induced Colitis in Mice and Its Potential Mechanisms

Journal of Agricultural and Food Chemistry (2022)

Jing Zhang Feilin Liang Zongwen Chen Yonger Chen Jun Yuan

Vitexin, one of the major active components in hawthorn, has been shown to possess multiple pharmacological activities. Here, we sought to investigate the effect of vitexin on an ameliorating dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) mouse model and further explored its potential mechanism. The results indicated that vitexin administration could significantly alleviate the signs of colitis via suppressing body weight loss, reducing disease activity index (DAI) score, and mitigating colonic damage. Also, vitexin treatment in colitis mice markedly inhibited the production of pro-inflammation cytokines (such as IL-1β, IL-6, and TNF-α). Meanwhile, vitexin also could markedly down-regulate the phosphorylation levels of p65, IκB, and STAT1. Moreover, vitexin also dose-dependently increased the expressions of muc-2, ZO-1, and occludin proteins in colonic tissues of colitis mice. Further studies revealed that vitexin dramatically modulated the disturbed intestinal flora in colitis mice. Vitexin is beneficial for regulating abundances of some certain bacteria, such as Bacteroides, Helicobacter, Alistipes, Lachnospiraceae_NK4A136_group, and Lachnospiraceae_UCG-006. Interestingly, the correlation analysis indicated that key microbes were strongly correlated with colitis features, such as pro-inflammatory cytokines and gut barrier. Collectively, these results demonstrated that vitexin treatment alleviated inflammation, intestinal barrier dysfunction, and intestinal flora dysbiosis in colitis mice. Vitexin is expected to be a promising compound for UC treatment.

Lachnospiraceae

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10.1021/acs.jafc.2c05177

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