Evidence map›Paper›PMID 40488849›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2025

A novel cycloastragenol-encapsulated carboxymethyl chitosan-silk fibroin hydrogel combined with sucralfate alleviates MNNG-induced chronic atrophic gastritis by targeting HIF-1α and VEGF signaling pathways.

Jianyu Ren, Qianqian Jiang, Kaiwei Wu

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Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

3 authors.

Jianyu RenTraditional Chinese Medicine Department, Dongying People's Hospital (Dongying Hospital of Shandong Provincial Hospital Group), No. 317, Dongcheng South 1 Road, Dongying, 257000, China.
Qianqian JiangTraditional Chinese Medicine Department, Dongying People's Hospital (Dongying Hospital of Shandong Provincial Hospital Group), No. 317, Dongcheng South 1 Road, Dongying, 257000, China.
Kaiwei WuTraditional Chinese Medicine Department, Dongying People's Hospital (Dongying Hospital of Shandong Provincial Hospital Group), No. 317, Dongcheng South 1 Road, Dongying, 257000, China. Kaiwei-Wu7@hotmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In order to treat chronic atrophic gastritis (CAG) caused by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), the present study successfully fabricated a carboxymethyl chitosan (CMC)-silk fibroin (SF) hydrogel encapsulating cycloastragenol (Cyl) and sucralfate (SC) (Cyl-SC@SF/CMC). This represents a substantial improvement in drug delivery and therapeutic efficacy. The SEM analysis shows the porosity of fabricated Cyl-SC@SF/CMC revealed a network of pores inside the hydrogel. Thermogravimetric and rheological investigations confirmed that the hydrogel was the structure of SF and CFC forming intermolecular hydrogen bonds. A model was developed to stimulate the impact of MNNG on gastric epithelial cells. Furthermore, cell counting kit-8 (CCK-8) assay was employed to evaluate the viability and proliferation of MNNG induced CAG in GES-1 after exposed to fabricated Cyl-SC@SF/CMC hydrogels. The results displayed that Cyl-SC@SF/CMC is superior than SC@SF/CMC in promoting the growth of GES-1 cells while simultaneously reducing MNNG-triggered damage to GES-1 cells and mitochondrial dysfunction. Moreover, cell migration and invasion analysis revealed that Cyl-SC@SF/CMC significantly enhanced migration and suggesting its role in tissue repair and regeneration. Moreover, in CAG rats, Cyl and SC in the hydrogel exerted therapeutic effects by considerably reducing histological damage in gastric tissues as evidenced by histopathological examinations. Furthermore, the pharmacokinetics analysis showed that Cyl-SC@SF/CMC formulation exhibited a higher area under the curve (AUC

Indexed as

ChitosanFibroinsGastritis, AtrophicSucralfateAnimalsAnti-Ulcer AgentsCell LineHumansHydrogelsHypoxia-Inducible Factor 1, alpha SubunitMaleRatsRats, Sprague-DawleySignal TransductionVascular Endothelial Growth Factor AAnti-Ulcer Agentscarboxymethyl-chitosanChitosanFibroinsHydrogelsHypoxia-Inducible Factor 1, alpha SubunitSucralfateVascular Endothelial Growth Factor Avascular endothelial growth factor A, ratAngiogenesisCycloastragenolGastritisInflammationSilk fibroin

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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.