ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Ethnopharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1563275
This article is part of the Research TopicMetabolic dysfunction-associated fatty liver disease (MAFLD): Innovative Management strategies using Herbal MedicinesView all 6 articles
Bletilla striata polysaccharides ameliorate metabolic-associated fatty liver disease by decreasing the NLRP3 inflammasome and pyroptosis
Provisionally accepted- 1Hubei University of Chinese Medicine, Wuhan, Hubei Province, China
- 2Hubei Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Wuhan, Hubei Province, China
- 3Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, Hubei Province, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
The role of nucleotide-binding oligomerization domain-like receptors containing pyrin domain 3 (NLRP3) inflammasome and pyroptosis in the inflammatory microenvironment of metabolic-associated fatty liver disease (MASLD) has been posited as crucial. Bletilla striata polysaccharides (BSPs), extracted from the tubers of Bletilla striata (Thunb.) Rchb.f., exhibit significant anti-inflammatory properties.However, their potential protective effects on MASLD and their role in regulating pyroptosis remain unclear. This study investigates the efficacy of BSP-1, a purified metabolite isolated from crude BSPs, on MASLD by evaluating its ability to modulate the NLRP3/caspase-1/GSDMD signaling pathway. To simulate MASLD in vivo and in vitro, high-fat diet (HFD)-induced rat models and free fatty acid (FFA)-stimulated HepG2 cells were used. Serum indicators and histopathological staining were employed to assess liver injury and lipid deposition. Additionally, enzyme-linked immunosorbent assay (ELISA), immunohistochemistry (IHC), immunofluorescence, real-time quantitative polymerase chain reaction (RT-qPCR), and western blotting (WB) analysis were conducted to examine the NLRP3/caspase-1/GSDMD pathway and related cytokine levels. The results demonstrate that BSP-1 significantly ameliorates alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), and triglyceride (TG) levels in both rat serum and HepG2 cells. Furthermore, BSP-1 reduces inflammatory factors interleukin (IL)-1β and IL-18, while improving pathological changes in rat liver tissue. Mechanistically, BSP-1 regulates the expression of pyroptosis-related proteins and mRNAs in the NLRP3/caspase-1/GSDMD pathway, thereby protecting against MASLD. In conclusion, BSP-1 may represent a promising therapeutic agent for MASLD treatment by inhibiting the NLRP3/caspase-1/GSDMD signaling pathway.
Keywords: Bletilla striata polysaccharide, metabolic-associated fatty liver disease, nod-like receptor protein 3, pyroptosis, Inflammasome
Received: 21 Jan 2025; Accepted: 11 Jun 2025.
Copyright: © 2025 Yu, Xue, Tang, Wu, Li, Yang and Luo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Fan Yang, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, 430061, Hubei Province, China
Lei Luo, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, 430061, Hubei Province, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.