Puerarin attenuates LPS-induced inflammatory injury in gastric epithelial cells by repressing NLRP3 inflammasome-mediated apoptosis.

Toxicol In Vitro

Department of Clinical Laboratory, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Edong Healthcare Group, Hubei, People's Republic of China; Hubei Key Laboratory of Kidney Disease Pathogenesis and InterventionHubei, Huangshi, Hubei, People's Republic of China. Electronic address:

Published: June 2022

AI Article Synopsis

Article Abstract

The NLRP3 inflammasome plays a crucial role in microbially induced gastric epithelial injury, but the underlying mechanisms remain unclear. Here, we aimed to assess the impacts of puerarin on LPS-induced inflammatory damage and the involvement of the AMPK/SIRT1/NLRP3 signaling pathways in this process in GES-1 cells. Cell viability and cytotoxicity were determined using CCK-8 and lactate dehydrogenase assay kits. Apoptosis was measured using annexin staining followed by flow cytometry. Cytokine levels were detected by ELISA, and protein expression was analyzed using western blotting. Protein overexpression was achieved by transfection with relevant pcDNA3.1 vectors, and protein knockdown was achieved by transfection with relevant siRNAs. Puerarin ameliorated LPS-induced cytotoxicity and apoptosis, while repressing LPS-stimulated NLRP3 inflammasome-mediated pyroptosis in GES-1 cells, as evidenced by significantly decreased expression of NLRP3, ASC, cleaved caspase-1, IL-1β and IL-18. NLRP3 knockdown efficiently repressed LPS-induced inflammatory injury in GES-1 cells. Puerarin activated the AMPK/SIRT1 pathway in LPS-treated GES-1 cells, and knockdown of both AMPK and SIRT1 reversed the protective effects of puerarin against LPS-induced inflammatory damage. AMPK overexpression strengthened, while AMPK knockdown weakened, the ability of puerarin to inhibit NLRP3-mediated inflammatory injury in LPS-treated GES-1 cells. Our findings suggest that puerarin may ameliorate LPS-induced inflammatory injury in GES-1 cells by activating the AMPK/SIRT1 signaling pathway and thereby repressing NLRP3 inflammasome-mediated apoptosis.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.tiv.2022.105350DOI Listing

Publication Analysis

Top Keywords

ges-1 cells
24
lps-induced inflammatory
20
inflammatory injury
16
nlrp3 inflammasome-mediated
12
gastric epithelial
8
repressing nlrp3
8
inflammasome-mediated apoptosis
8
puerarin lps-induced
8
inflammatory damage
8
achieved transfection
8

Similar Publications

Objective: To investigate the role of heparan sulfate 6-O-sulfotransferase 2 (HS6ST2) in gastric cancer (GC).

Methods: HS6ST2 expression in GC and adjacent normal gastric mucosa was first detected via immunohistochemical (IHC) staining. The correlation between the expression level of HS6ST2 and clinicopathological parameters were observed.

View Article and Find Full Text PDF

Multidrug resistant bacteria are causing health problems and economic burden worldwide; alternative treatment options such as natural products and nanoparticles have attained great attention recently. Therefore, we aimed to determine the phytochemicals, antibacterial potential, and anticancer activity of W. unigemmata.

View Article and Find Full Text PDF
Article Synopsis
  • The study highlights the rising importance of assessing the cytotoxicity of gold nanoparticles (GNPs) in biomedical applications.
  • Researchers synthesized three types of GNPs—gold nanorods (GNRs), gold nanobipyramids (GNBPs), and gold nanocups (GNCs)—using a specific method and measured their sizes.
  • The experiments showed that the cytotoxic effects of GNPs varied based on their shape and surface coating, with CTAB-coated GNPs being more harmful than PEG-coated ones, indicating that these factors significantly influence GNP behavior in cells.
View Article and Find Full Text PDF

Yiqi Huayu Jiedu formula inhibits JAK2/STAT3-mediated partial EMT in treating chronic atrophic gastritis.

Phytomedicine

December 2024

State Key Laboratory of Traditional Chinese Medicine Syndrome/Department of Gastroenterology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Provincial Hospital of Chinese Medicine, Guangdong Provincial Academy of Chinese Medical Sciences/State Key Laboratory of Dampness Syndrome of Chinese Medicine, Guangzhou, China; Guangdong Provincial Key laboratory of Chinese Medicine for Prevention and Treatment of Refractory Chronic Diseases, Guangzhou, China. Electronic address:

Background: Chronic atrophic gastritis (CAG) is a precursor to gastric cancer, a leading cause of cancer-related deaths worldwide. Despite current therapeutic strategies, preventing the transition from gastritis to cancer remains a challenge. Traditional Chinese Medicine (TCM), particularly the Yiqi-Huayu-Jiedu (YQHYJD) formula, have exhibited promising results in CAG management.

View Article and Find Full Text PDF

Background: Adherence of Helicobacter pylori to the surface of the gastric mucosa is the initial and crucial step for its survival and colonization in the harsh conditions of the stomach. We had previously demonstrated that daphnetin has anti-adhesion effect.

Purpose: This study aims to explore the mechanisms of daphnetin to reduce H.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!