- Genomics, phytochemicals, and oxidative stress
- Plant Toxicity and Pharmacological Properties
- Nitric Oxide and Endothelin Effects
- Infant Nutrition and Health
- Selenium in Biological Systems
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cancer-related molecular mechanisms research
- Cerebrovascular and Carotid Artery Diseases
- Lipid metabolism and disorders
- Mycotoxins in Agriculture and Food
- Biomarkers in Disease Mechanisms
Yangzhou University
2023-2025
Guangzhou Medical University
2021
Dongguan People’s Hospital
2016
Deoxynivalenol (DON), one of the most common mycotoxins contaminating food and feed, has been shown to induce hepatotoxicity. Lactoferrin (LF) enriched in human milk is a critical functional component performs hepatoprotection function. Here, we aimed explore whether dietary LF supplementation can protect from DON-induced hepatotoxicity uncover underlying mechanism mice alpha mouse liver 12 (AML12) hepatocytes. In vivo results revealed that alleviated injury, reflected by repairing hepatic...
Inflammatory bowel disease (IBD), a chronic inflammatory disorder of the gastrointestinal tract, is frequently complicated by extraintestinal manifestations such as functional hyposplenism. Increasing evidence highlights its pathogenesis multifactorial interplay gut dysbiosis, intestinal barrier dysfunction, and dysregulated immune responses. While probiotics, particularly Lactobacillus spp., have emerged potential therapeutics for IBD, restoring homeostasis, their systemic immunomodulatory...
Deoxynivalenol (DON) is a common mycotoxin that induces intestinal inflammation and oxidative damage in humans animals. Given lithocholic acid (LCA) has been suggested to inhibit inflammation, we aimed investigate the protective effects of LCA on DON-exposed porcine epithelial IPI-2I cells underlying mechanisms. Indeed, rescued DON-induced cell death reduced DON-stimulated inflammatory cytokine levels stress. Importantly, nuclear receptor PPARγ was identified as key transcriptional factor...
To evaluate the influence of atractylenolide (Atr) III on sepsis-induced lung damage.