Publications by authors named "Yiou Cao"

5 Publications

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Baicalin Inhibits Influenza A Virus Infection Promotion of M1 Macrophage Polarization.

Front Pharmacol 2020 6;11:01298. Epub 2020 Oct 6.

Department of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, Fudan University School of Pharmacy, Shanghai, China.

Background And Aims: The natural compound baicalin (BA) possesses potent antiviral properties against the influenza virus. However, the underlying molecular mechanisms of this antiviral activity and whether macrophages are involved remain unclear. In this study, we, therefore, investigated the effect of BA on macrophages.

Methods: We studied macrophage recruitment, functional phenotypes (M1/M2), and the cellular metabolism flow cytometry, qRT-PCR, immunofluorescence, a cell culture transwell system, and GC-MS-based metabolomics both in H1N1 A virus-infected mice and .

Results: BA treatment drastically reduced macrophage recruitment (CD11b, F4/80) by approximately 90% while maintaining the proportion of M1-polarized macrophages in the bronchoalveolar lavage fluid of infected mice. This BA-stimulated macrophage M1 phenotype shift was further verified in ANA-1 and primary peritoneal macrophages by measuring macrophage M1 polarization signals (CD86, iNOS, TNF-α, ratio, and IL-1β cleavage). Meanwhile, we observed an activation of the IFN pathway (upregulation of and ), an inhibition of influenza virus replication (as measured by the gene), and distinct cellular metabolic responses in BA-treated cells.

Conclusion: BA triggered macrophage M1 polarization, IFN activation, and other cellular reactions, which are beneficial for inhibition of H1N1 A virus infection.
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http://dx.doi.org/10.3389/fphar.2020.01298DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574031PMC
October 2020

Decitabine attenuates dextran sodium sulfate‑induced ulcerative colitis through regulation of immune regulatory cells and intestinal barrier.

Int J Mol Med 2020 Aug 18;46(2):583-594. Epub 2020 May 18.

Department of Surgery, Minhang Hospital, Fudan University, Shanghai 201199, P.R. China.

To investigate the effect of decitabine on the regulation of intestinal barrier function in mice with inflammatory bowel disease, an experimental model of colitis was established via drinking water with dextran sulfate sodium (DSS). Hematoxylin and eosin staining was used to observe the pathological changes of the colon. Cytokine production was measured by an ELISA assay. Flow cytometry was used to measure the level of regulatory T cells. Immunofluorescence, immunohistochemistry and western blot analyses detected the protein expression and distribution in colon tissue. Following the administration of decitabine, the symptoms of intestinal inflammation in the mice were significantly relieved; the expression of IL‑17 was decreased, and the levels of TGF‑β and IL‑10 were increased. In addition, the induction of forkhead box P3 (Foxp3) in naive T cells increased the proportion of CD4+ Foxp3+ T cells in CD4+ T cells. Furthermore, decitabine increased the levels of zonular occludens‑1 and occludin, and inhibited the phosphorylation of ERK1/2, JNK and p38. In conclusion, the present study suggested that decitabine could alleviate DSS‑induced impaired colon barrier and the weight loss, mucus and bloody stools in mice by releasing the inhibitory factor IL‑10, reducing the pro‑inflammatory factor IL‑17, activating CD4+ Foxp3+ T cells and inhibiting the activation of the MAPK pathway.
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http://dx.doi.org/10.3892/ijmm.2020.4605DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7307821PMC
August 2020

Targeting p38γ to inhibit human colorectal cancer cell progression.

Biochem Biophys Res Commun 2019 09 23;517(1):172-179. Epub 2019 Jul 23.

Department of Surgery, Minhang Hospital, Fudan University, Shanghai, China. Electronic address:

Colorectal cancer (CRC) is a common malignancy globally causing significant cancer-related mortality. Recent studies have proposed p38gamma (p38γ) as a novel cyclin-dependent kinase (CDK)-like kinase, promoting tumorigenesis and cancer progression. The current study evaluates p38γ expression and potential role in CRC. In HT-29 cells and primary human colon cancer cells, shRNA-induced p38γ silencing or CRISPR/Cas9-mediated p38γ knockout inhibited cell growth, proliferation, and migration, and induced significant apoptosis. Conversely, ectopic overexpression of p38γ further promoted the growth, proliferation, and migration of HT-29 cells and primary colon cancer cells. Retinoblastoma (Rb) phosphorylation and cyclins (E1/A) expression were decreased by p38γ silencing or KO, but increased with p38γ overexpression. p38γ mRNA and protein levels are significantly upregulated in human colon cancer tissues, when compared to levels in surrounding colon epithelial tissues. These results demonstrate that overexpression of p38γ can promote human CRC cell progression, and identify p38γ as a novel therapeutic target.
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http://dx.doi.org/10.1016/j.bbrc.2019.07.038DOI Listing
September 2019

Biological and anti-vascular activity evaluation of ethoxy-erianin phosphate as a vascular disrupting agent.

J Cell Biochem 2019 10 20;120(10):16978-16989. Epub 2019 May 20.

State Key Laboratory of Bioreactor Engineering and Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai, People's Republic of China.

The effects of ethoxy-erianin phosphate (EBTP) on cell proliferation, mitotic cell arrest, migration, infiltration, and endothelial tubular structures were evaluated in this study. The antiproliferative activity of EBTP and combretastatin A-4P (CA4P) was analyzed on several tumor cells (including MCF-7, HeLa, 2LL, and 2LL-IDO) and on an endothelial cell (human umbilical vein endothelial cells [HUVECs]) as well as a human normal liver cell (L02). The results showed that EBTP possessed antiproliferative activity in the micromole range and was relatively less toxic than CA4P. Treating HUVECs with EBTP caused cell accumulation in the G2/M phase, and wound-healing assays indicated that EBTP inhibited cell migration. Furthermore, EBTP and CA4P destroyed the vasculature in endothelial cells and showed vascular disrupting activity of the chorioallantoic membrane in fertilized chicken eggs. In addition, we found that EBTP suppressed the expression of indoleamine 2,3-dioxygenase (IDO) and significantly inhibited IDO-induced migration and infiltration of 2LL-IDO cells. Administration of EBTP blocked vasculogenic mimicry in 2LL-IDO cells, which was typically observed in tube formation assays of 2LL-IDO cells. Moreover, the results of Lewis lung carcinoma in mice showed a high inhibition rate of EBTP. EBTP is an effective vascular disrupting agent that is superior to CA4P and may prevent and treat malignancy by inhibiting the expression of IDO.
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http://dx.doi.org/10.1002/jcb.28959DOI Listing
October 2019

Erianin inhibits indoleamine 2, 3-dioxygenase -induced tumor angiogenesis.

Biomed Pharmacother 2017 Apr 24;88:521-528. Epub 2017 Jan 24.

Minhang Hospital, Fudan University, China. Electronic address:

Tumor angiogenesis is the key process in tumor growth and metastasis, and transfers essential nutrients for solid tumor. Inhibition of tumor angiogenesis has been recognized as a more effective anti-cancer strategy for NSCLC and has acquired certain therapeutic effects. IDO has non-immune functions including regulating tumor angiogenesis and IDO dysregulation in cancer pathogenesis has been valued. Erianin is a natural product isolated from Dendrobium chrysotoxum Lindl. The antitumor activity of erianin in many kinds of cancers had been demonstrated in previous studies. In this study, we demonstrated that IDO could promote the attachment of 2LL cells, the ability of migration, invasion and VM formation, as well as the tubules forming ability of HUVECs. We also find that erianin suppressed expression and enzyme ability of IDO and erianin could inhibit IDO-induced metastasis and invasion ability of 2LL cells significantly. Erianin not only blocked IDO-induced tube formation of HUVECs, but also suppressed VM formation of 2LL-IDO cells. What's more, we examined that Erianin might play its role in angiogenesis through down-regulating phosphorylation of JAK2/STAT3, inhibiting its downstream target genes MMP-2/-9 and some inflammatory mediators (COX-2, HIF-1α and IL-6), which were all induced by IDO. All these results indicated that erianin had anti-angiogenesis ability and could inhibit the expresison of IDO to prevent and treat the malignant tumors.
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http://dx.doi.org/10.1016/j.biopha.2017.01.090DOI Listing
April 2017