The purpose of this study is to assess the utility of the Modified version of VascuQol Scale as an effective biopsychosocial assessment tool for patients suffering from lower extremity peripheral arterial disease.

Start Date01 Oct 2023

Sponsor / Collaborator

Shanghai Renji Hospital

[+4]

ChiCTR2300075839 / SuspendedNot ApplicableIIT

Clinical observation on the treatment of pediatric anorexia nervosa with suppressing wood and supporting earth massage technique

Start Date18 Sep 2023

Sponsor / Collaborator

Hospital of Chengdu University of TCM

ChiCTR2300067917 / SuspendedEarly Phase 1IIT

Study on prognostic model of colon cancer syndrome” based on electronic nose exhalation fingerprint

Start Date01 Feb 2023

Sponsor / Collaborator

Hospital of Chengdu University of TCM

100 Clinical Results associated with Hospital of Chengdu University of TCM

0 Patents (Medical) associated with Hospital of Chengdu University of TCM

Literatures (Medical) associated with Hospital of Chengdu University of TCM

01 Mar 2024·Molecular Neurobiology

MiR-26b-3p Promotes Intestinal Motility Disorder by Targeting FZD10 to Inhibit GSK3β/β-Catenin Signaling and Induce Enteric Glial Cell Apoptosis

Article

Author: Tang, Xue-Gui ; Du, Li-Juan ; Wu, Rong ; Zhan, Yu ; Chen, Tai-Yu ; Wen, Yong ; Shen, Xu-Long ; Zheng, Fan

Enteric glial cells (EGCs) are the major component of the enteric nervous system and affect the pathophysiological process of intestinal motility dysfunction. MicroRNAs (miRNAs) play an important role in regulating gastrointestinal homeostasis. However, the mechanism of miRNA-mediated regulation of EGCs in intestinal dysmotility remains unclear. In this study, we investigated the effect of EGC apoptosis on intestinal dysmotility, and the effect of miR-26b-3p on EGC proliferation and apoptosis in vivo and in vitro. A loperamide hydrochloride (Lop)-induced constipated mouse model and an in vitro culture system of rat EGCs were established. The transcriptome was used to predict the differentially expressed gene miR-26b-3p and the target gene Frizzled 10 (FZD10), and their targeting binding relationship was verified by luciferase. EGCs were transfected with miR-26b-3p mimic or antagomir, and the FZD10 expression was down-regulated by siRNA. Immunofluorescence and flow cytometry were used to detect EGC apoptosis. MiR-26b-3p and FZD10 expressions were examined using quantitative real-time PCR (qRT-PCR). The CCK-8 assay was used to detect EGC proliferation. The protein levels were detected by Western blotting and enzyme-linked immunosorbent assay (ELISA). The results showed that miR-26b-3p was up-regulated in the Lop group, whereas FZD10 was down-regulated, and EGC apoptosis was increased in the colon of intestinal dysmotility mice. FZD10 down-regulation and miR-26b-3p mimic significantly increased glycogen synthase kinase-3β phosphorylation (p-GSK3β) levels, decreased β-catenin expression, and promoted EGC apoptosis. MiR-26b-3p antagomir alleviated intestinal dysmotility, promoted EGC increased activity of EGCs, and reduced EGC apoptosis in vivo. In conclusion, this study indicated that miR-26b-3p promotes intestinal motility disorders by targeting FZD10 to block GSK3β/β-catenin signaling and induces apoptosis in EGCs. Our results provide a new research target for the treatment and intervention of intestinal dysmotility.

01 Mar 2024·Chemical Biology & Drug Design

Saikosaponin D mitigate pilocarpine‐induced astrocyte injury by regulating the NLRP3/caspase‐1 signaling pathway

Article

Author: Liu, Jun-Yan ; Shen, Yu-Ling ; Zhu, Jing-Yi ; Yang, Dong-Dong

AbstractStudies have shown that saikosaponin D (SSD) has favorable neurotherapeutic effects. Therefore, the objective of this study was to explore the efficacy and possible molecular mechanisms of SSD on pilocarpine (PP)‐induced astrocyte injury. Primary astrocytes were isolated from juvenile rats and identified using immunofluorescence. The cells were treated with PP and/or SSD for 6 h and 12 h, respectively, followed by measurement of their viability through 3‐(4,5‐dimethylthiazol)‐2,5‐diphenyl‐tetrazolium bromide (MTT) assay. Next, quantitative real‐time polymerase chain reaction (qRT‐PCR) was used to measure the expression levels of Glial fibrillary acidic protein (GFAP), C3, S100 calcium binding protein A10 (S100a10), pentraxin 3 (Ptx3), toll‐like receptor 4 (TLR4), and RAG in astrocytes after different treatments. Enzyme‐linked immunosorbent assay and biochemical tests were utilized to evaluate the level of inflammatory factors [interleukin (IL)‐1β, IL‐6, and tumor necrosis factor alpha (TNF‐α)] secreted by cells and the content of oxidative stress‐related factors (malondialdehyde [MDA] and glutathione [GSH]) or enzyme activity (catalase [CAT] and glutathione peroxidase [GPX]) in cells. The JC‐1 mitochondrial membrane potential (MMP) fluorescence probe was used to measure the MMP in astrocytes. Additionally, western blot was applied to test the expression of proteins related to the nod‐like receptor protein 3 (NLRP3)/caspase‐1 signaling pathway. PP treatment (1 mM) induced cell injury by significantly reducing the viability of astrocytes and expression of cellular markers. SSD treatment (4 μM) had no toxicity to astrocytes. Besides, SSD (4 μM) treatment could significantly up‐regulate the cell viability and marker expression of PP‐induced astrocytes. Furthermore, SSD could be employed to inhibit inflammation (reduce IL‐1β, IL‐6, and TNF‐α levels) and oxidative stress (decrease MDA level, elevate GSH level, the activity of CAT and GPX), and ameliorate mitochondrial dysfunction (upregulate JC‐1 ratio) in PP‐induced astrocytes. Moreover, further mechanism exploration revealed that SSD treatment significantly reduced the activity of the NLRP3/caspase‐1 signaling pathway activated by PP induction. SSD increased cell viability, inhibited inflammation and oxidative stress response, and ameliorated mitochondrial dysfunction in PP‐induced astrocyte injury model, thus playing a neuroprotective role. The mechanism of SSD may be related to the inhibition of the NLRP3/caspase‐1 inflammasome.

01 Dec 2023·Journal of Medicinal Food

Corydalis yanhusuo Polysaccharides Ameliorate Chronic Stress-Induced Depression in Mice through Gut Microbiota-Derived Short-Chain Fatty Acid Activation of 5-Hydroxytryptamine Signaling

Article

Author: Deng, Jie ; Liang, Jingtao ; Wang, Qiannan ; Liao, Xin ; Li, Yanqing ; Fang, Yu ; Yan, Bohua

Depression, a prevalent psychiatric disorder, presents a serious health risk to humans. Increasing evidence suggested that the gut microbiota and the 5-hydroxytryptamine (5-HT) pathway both contribute significantly to depression. This research aimed to investigate how Corydalis yanhusuo polysaccharides (CYP) could potentially alleviate depression induced by chronic unpredictable mild stress in mice, as well as its underlying mechanism. The sucrose preference test, tail suspension test, and forced swimming test were employed to evaluate the behavior of mice. Enzyme-linked immunosorbent assay and PCR techniques were utilized to measure depression-related factors (dopamine [DA], 5-HT, norepinephrine [NE], brain-derived neurotrophic factor [BDNF], tryptophan hydroxylase 2 [TPH-2], 5-hydroxytryptophan [5-HTP], and tryptophan hydroxylase [TPH-1] levels). Hematoxylin and eosin staining and Nissl staining were conducted to observe histopathological changes in the hippocampus, the differences in the diversity of gut flora between groups were analyzed using 16S rRNA sequencing, and gas chromatography-mass spectrometry metabolomics was utilized to evaluate short-chain fatty acid (SCFA) concentrations. The findings indicated that CYP treatment increased the sucrose preference index, decreased the immobility time, and improved neuropathological injury. In depressed mice, CYP improved the dysregulation of the gut microbiota, and increased the SCFA levels. In addition, CYP enhanced the DA, 5-HT, NE, BDNF, and TPH-2 levels in the brain and the expression of 5-HTP and TPH-1 in the colon, while SCFAs were positively correlated with these levels. In summary, our study suggested that CYP may mitigate depression by ameliorating gut microbiota dysregulation, promoting the generation of SCFAs, and activation of 5-HT signaling expression.

100 Deals associated with Hospital of Chengdu University of TCM

100 Translational Medicine associated with Hospital of Chengdu University of TCM

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