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Special Issue Editor

Dr. Dingpei Long

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Guest Editor

1. Digestive Disease Research Group, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303, USA
2. State Key Laboratory of Silkworm Genome Biology, Key Laboratory for Sericulture Functional Genomics & Biotechnology of Agricultural Ministry, Southwest University, Beibei, Chongqing 400716, China
Interests: inflammatory bowel disease (IBD); ulcerative colitis (UC); colitis-associated cancer (CAC); drug delivery systems (DDSs); natural lipid nanoparticles; natural/genetically modified silk fibroin nanoparticles
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammatory bowel disease (IBD) is a group of chronic conditions affecting the digestive tract, with Crohn's disease (CD) and ulcerative colitis (UC) as the two main forms. The exact cause of IBD is unknown, but a combination of genetic and environmental factors is believed to be involved. The disease is characterized by a range of symptoms, including abdominal pain, diarrhea, rectal bleeding, weight loss, and malnutrition. The pathophysiology of IBD involves an abnormal immune response in the gut, leading to chronic inflammation and damage to the intestinal lining. Treating IBD has been a challenge for the medical community due to the complexity of the disease and limited understanding of its pathophysiology. Current therapies include medications reducing inflammation, such as corticosteroids, immunosuppressants, and biologic therapies, but these can have significant side effects and may not be effective for all patients. Innovative therapeutic approaches for IBD, including stem cell transplantation, fecal microbiota transplantation, and modulation of the gut microbiome, are currently under investigation. Researchers are also exploring targeted therapies targeting the underlying causes of IBD, such as novel drug delivery platforms based on micro- and nanotechnology. Significant advances have been made in understanding the mechanisms of IBD and developing new therapeutic approaches in recent years. This Special Issue aims to publish the latest research advances in IBD and bring together researchers and clinical doctors participating in IBD research. Global experts will discuss topics such as the mechanisms of IBD, and research advances in prevention, diagnosis, and treatment of IBD.

Dr. Dingpei Long
Guest Editor

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Related Special Issue

Published Papers (1 paper)

Research

21 pages, 5581 KiB

Open AccessArticle

Ruscogenin Attenuates Ulcerative Colitis in Mice by Inhibiting Caspase-1-Dependent Pyroptosis via the TLR4/NF-κB Signaling Pathway

by Jingwei Li, Huihuan Wu, Jialiang Zhou, Rui Jiang, Zewei Zhuo, Qi Yang, Hao Chen and Weihong Sha

Biomedicines 2024, 12(5), 989; https://doi.org/10.3390/biomedicines12050989 - 30 Apr 2024

Viewed by 270

Abstract

Inflammatory bowel diseases (IBD) are chronic inflammatory disorders affecting the digestive tract, including ulcerative colitis and Crohn’s disease. Ruscogenin, a prominent steroidal sapogenin present in radix ophiopogon japonicus, has shown a protective effect on attenuating the inflammatory response associated with inflammatory diseases, but the efficacy of ruscogenin in IBD remains unclear. The aim of this study is to explore the effect of ruscogenin on intestinal barrier dysfunction and inflammatory responses as well as the underlying mechanism in ulcerative colitis. A dextran sulfate sodium salt (DSS)-induced C57BL/6 mouse colitis model was employed for the in vivo studies, while in vitro experiments were performed in THP-1 cells and human intestinal epithelial cells involved in inducing inflammatory responses and pyroptosis using LPS/nigericin. The results indicated that ruscogenin treatment attenuated the symptoms of ulcerative colitis, reduced the release of inflammatory cytokines and the expression of pyroptosis-associated proteins, and restored the integrity of the intestinal epithelial barrier in colon tissue in mice. Moreover, ruscogenin inhibited LPS/nigericin-induced pyroptosis in THP-1 cells. Mechanically, ruscogenin inhibited NLRP3 inflammasome activation and canonical pyroptosis, at least in part, through the suppression of the TLR4/NF-κB signaling pathway. These findings might provide new insights and a solid foundation for further exploration into the therapeutic potential of ruscogenin in the treatment of IBD. Full article

(This article belongs to the Special Issue Crohn's Disease and Ulcerative Colitis: From Pathophysiology to Novel Therapeutic Approaches (2nd Edition))

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