Aflatoxin B1 (AFB1), a potent carcinogen, is widely present in various crops, with limited prevention and treatment methods, continuously threatening food safety and public health. Moringa oleifera leaf extract (MOLE) is rich in bioactive compounds such as flavonoids, polysaccharides, triterpenes, and volatile oils, exhibiting antioxidant and anti-inflammatory potential. However, its specific effects and underlying mechanisms against AFB1-induced hepatotoxicity remain unclear. This study aimed to elucidate the alleviative effect of MOLE on AFB1 hepatotoxicity and its molecular mechanisms. In AFB1-induced mouse-liver tissue and hepatocyte models, MOLE significantly reduced the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Data indicated that MOLE treatment markedly suppressed AFB1-induced accumulation of reactive oxygen species (ROS) and malondialdehyde (MDA), while enhancing antioxidant indicators such as total antioxidant capacity (T-AOC) and glutathione (GSH). Network pharmacology identified 50 bioactive components in MOLE and revealed 78 common targets with AFB1-induced hepatotoxicity. Protein–protein interaction analysis identified 10 core targets. Key active compounds included naringenin, quercetin, and luteolin. GO and KEGG enrichment results were closely associated with ROS-related pathways. Molecular docking demonstrated strong binding affinity between MOLE components and core targets, particularly with PPARG. Mechanistically, MOLE significantly increased PPARγ protein levels and upregulated Nrf2 protein expression. It also enhanced the mRNA expression of HO-1, SOD, NQO1, CAT, and GPX1 and improved cellular total antioxidant capacity. Crucially, inhibiting PPARγ abolished the protective effects of MOLE and reversed its promotion of Nrf2. In conclusion, MOLE alleviates liver injury by binding to PPARγ to activate the Nrf2 pathway, thereby inhibiting AFB1-induced ROS accumulation.

The movements of mitochondrial are especially critical for neuronal growth and function. However, to analyze and quantify this process is technically challenging. Different from traditional hand-drawn method which lacks efficiency, we focus on automatic methods, which consist three key aspects (image enhancement, trajectories tracking and quantitative analyzing) and provide a discussion about different issues in these steps.

Background Aflatoxin B1 (AFB1) is a potent hepatotoxic mycotoxin that induces severe oxidative liver damage. Kaempferol (Kae), a natural flavonoid with known antioxidant properties, has unclear protective effects against AFB1-induced hepatotoxicity. This study aimed to evaluate the hepatoprotective role of Kae and elucidate its underlying mechanism using integrated in vivo, in silico, and in vitro approaches. Methods: In vivo (AFB1-challenged mice) and in vitro (hepatocyte) models were employed, combined with network pharmacology, molecular docking, and molecular dynamics simulations. Liver injury indices, oxidative stress markers, antioxidant enzyme activities, and Keap1/Nrf2 pathway expression were assessed. Results: Kae co-treatment reversed AFB1-induced increases in liver index, serum ALT/AST, histological lesions, and reduced antioxidant capacity in mice. Network pharmacology revealed 59 common targets, with NFE2L2 (Nrf2) as a key node. In vitro, Kae pretreatment significantly lowered AFB1-elevated ROS, MDA, ALT, and AST, while restoring GSH and total antioxidant capacity. Kae reversed AFB1-induced Keap1 upregulation and Nrf2 downregulation, and increased mRNA levels of HO-1, NQO1, SOD, GPX1, and CAT. Molecular docking and simulation showed stable Kae–Keap1 binding (−9.6 kcal/mol) with critical hydrogen bonds (VAL-606) and van der Waals contacts. Conclusions: Kae directly binds Keap1, activates Nrf2 signaling, upregulates antioxidant gene expression, and mitigates AFB1-induced oxidative liver injury. These findings support Kae as a promising candidate for preventing AFB1 hepatotoxicity.