Tuo Cai

Arsenic-induced myocardial injury (AIMI) is a cardiovascular consequence of arsenic exposure. Astragaloside IV (AS-IV), a primary bioactive compound from Astragalus membranaceus, is known for its cardioprotective properties, yet its efficacy against AIMI remains unexplored. This study combined network toxicology, molecular docking, molecular dynamics simulations, and in vivo experiments to assess AS-IV’s protective effects and potential mechanisms in AIMI. We identified 101 overlapping targets between AS-IV and AIMI. Functional enrichment implicated apoptosis-related processes and inflammatory pathways in AS-IV’s actions. Five hub genes—LGALS3, MMP9, IL2, AR, and BCL2L1—were identified. Docking and simulations predicted potential interactions of AS-IV with MMP-9 and galectin-3 (encoded by MMP9 and LGALS3). In vivo, AS-IV ameliorated arsenic-induced histopathological damage and reduced cTnI levels. Arsenic exposure decreased myocardial GSH-Px activity but increased T-SOD activity, whereas MDA levels showed no statistically significant changes across groups. AS-IV restored GSH-Px activity and further increased T-SOD activity without significantly altering MDA levels. In addition, AS-IV attenuated cardiomyocyte apoptosis, as evidenced by reduced TUNEL positivity and cleaved caspase-3 expression. Notably, arsenic upregulated galectin-3, which AS-IV dose-dependently reduced, while MMP-9 remained unchanged in this early-stage model, consistent with minimal fibrosis. Further bioinformatic analyses linked galectin-3 to early immune-inflammatory and extracellular matrix remodeling signals. In conclusion, AS-IV attenuated arsenic-induced myocardial injury and cardiomyocyte apoptosis in mice. The protective effects were accompanied by changes in oxidative stress-related enzyme activities and reduced myocardial Galectin-3 expression. These findings suggest that galectin-3 may represent a candidate target associated with AS-IV treatment, although its causal involvement in the cardioprotective effects of AS-IV requires further investigation.

Pneumoconiosis is a common occupational disease that can worsen with accompanying infection. Torque teno virus (TTV) is a prevalent human virus with multiple genotypes that can chronically and persistently infect individuals. However, the prevalence of TTV in pneumoconiosis patients is still unclear. This research aims to detect the presence and prevalence of TTV in the alveolar lavage fluid of pneumoconiosis patients in the Hunan Province of China using PCR. As a result, a 65.5% positive rate (19 out of 29) of TTV was detected. The TTV detection rate varies among different stages of silicosis and different pneumoconiosis patient ages. Nine novel TTV genomes ranging in size from 3719 to 3908 nt, named TTV HNPP1, HNPP2, HNPP3, HNPP4, HNPP5, HNPP6-1, HNPP6-2, HNPP7-1 and HNPP7-2, were identified. A genomic comparison and phylogenetic analysis indicated that these nine TTVs represent five different species with high genetic diversity which belong to the genus Alphatorquevirus. HNPP6-1 and HNPP6-2 belong to TTV3, HNPP5 belongs to TTV13, HNPP1 belongs to TTV24, HNPP4 belongs to TTV20, and the others belong to TTV19. The genomes of TTV HNPP1, HNPP6-1, and HNPP6-2 contain three putative open reading frames (ORFs) coding for proteins, ORF1, ORF2, and ORF3, while the other six TTV genomes contain two ORFs coding for proteins, ORF1 and ORF2. These results provide the first description of TTV epidemiology in pneumoconiosis patients in China. The newly identified TTV genome sequences reveal the high genetic diversity of TTV in pneumoconiosis patients and could contribute to a deeper understanding of TTV retention and infection in humans.