Evidence map›Paper›PMID 39725622›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2024

[Asperosaponin VI alleviates TNBS-induced Crohn's disease-like colitis in mice by reducing intestinal epithelial cell apoptosis via inhibiting the PI3K/AKT/NF-κB signaling pathway].

Minzhu Niu, Lixia Yin, Ting Duan, Ju Huang, Jing Li, Zhijun Geng, Jianguo Hu, Chuanwang Song

Abstract readEnglish Abstract
PubMed Full text at PMC Publisher
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Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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0cells of the map it votes in
3citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Minzhu NiuDepartment of Immunology, School of Laboratory Medicine, Bengbu Medical University, Bengbu 233030, China.
Lixia YinClinical Laboratory.
Ting DuanDepartment of Emergency Medicine.
Ju HuangCentral Laboratory.
Jing LiClinical Laboratory.
Zhijun GengCentral Laboratory.
Jianguo HuClinical Laboratory.
Chuanwang SongDepartment of Immunology, School of Laboratory Medicine, Bengbu Medical University, Bengbu 233030, China.

Funding

National Natural Science Foundation of China 81902078
6 · The paper itself

Abstract

objectivesTo investigate the effects of asperosaponin VI (AVI) on intestinal epithelial cell apoptosis and intestinal barrier function in a mouse model of Crohn's disease (CD)-like colitis and explore its mechanisms.

methodsMale C57BL/6 mice with TNBS-induced CD-like colitis were treated with saline or AVI (daily dose 150 mg/kg) by gavage for 6 days. The changes in body weight, colon length, DAI scores, and colon pathologies of the mice were observed, and the expressions of inflammatory factors and tight injunction proteins were detected using ELISA and RT-qPCR. The effects of AVI on barrier function and apoptosis of mouse intestinal epithelial cells and TNF‑α‑treated Caco-2 cells were analyzed using immunofluorescence staining, TUNEL assay, and Western blotting. Network pharmacology, TUNEL assay, and Western blotting were performed to explore and validate the therapeutic mechanisms of AVI for CD.

resultsIn the mouse models of CD-like colitis, AVI significantly improved body weight loss, colon shortening and DAI and tissue inflammation scores, alleviated intestinal villi and goblet cell injuries, and lowered the expressions of inflammatory factors. AVI treatment significantly reduced the loss of tight junction proteins and apoptosis in both mouse intestinal epithelial cells and TNF‑α-stimulated Caco-2 cells. KEGG enrichment pathway analysis suggested that the therapeutic effect of AVI on CD was associated with inhibition of PI3K/AKT/NF-κB pathway activation, which was confirmed by lowered expressions of p-PI3K, p-AKT, and p-p65 in AVI-treated mouse models and Caco-2 cells. In Caco-2 cells, Recilisib significantly blocked the inhibitory effect of AVI on the PI3K/AKT/NF-κB pathway and TNF-α-induced apoptosis, and AKT1 knockdown experiment confirmed the role of the PI3K/AKT pathway for mediating the activation of downstream NF-κB signaling.

conclusionsAVI can improve TNBS-induced CD-like colitis in mice by reducing intestinal epithelial cell apoptosis and intestinal barrier damage via inhibiting the PI3K/AKT/NF-κB signaling pathway.

Indexed as

ApoptosisColitisCrohn DiseaseDisease Models, AnimalEpithelial CellsMice, Inbred C57BLNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSaponinsSignal TransductionAnimalsCaco-2 CellsHumansIntestinal MucosaMaleakebia saponin DNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSaponinsTrinitrobenzenesulfonic AcidTumor Necrosis Factor-alphaapoptosisasperosaponin VICrohn's diseaseintestinal barrierPI3K/AKT/NF-κB signaling pathway

Identifiers

PMID39725622
PMCPMC11683351

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.