Syringin alleviates bisphenol A-induced spermatogenic defects and testicular injury by suppressing oxidative stress and inflammation in male zebrafish.

Syringin (SRG) is a bioactive principle possessing extensive activities including scavenging of free radicals, inhibition of apoptosis, and anti-inflammatory properties. However, its effects on spermatogenic defects and testicular injury as well as the underlying mechanisms are still unclear. This study aims to investigate the protective effect of SRG on testis damage in zebrafish and explore its potential molecular events. Zebrafish testicular injury was induced by exposure to bisphenol A (BPA) (3000 µg/L) for two weeks. Fish were treated with intraperitoneal injection of SRG at different doses (5 and 50 mg/kg bodyweight) for two more weeks under BPA induction. Subsequently, the testis and sperm were collected for morphological, histological, biochemical and gene expression examination. It was found that the administration of SRG resulted in a significant protection from BPA-caused impact on sperm concentration, morphology, motility, fertility rate, testosterone level, spermatogenic dysfunction and resulted in increased apoptotic and reactive oxygen species' levels. Furthermore, testicular transcriptional profiling alterations revealed that the regulation of inflammatory response and oxidative stress were generally enriched in differentially expressed genes (DEGs) after SRG treatment. Additionally, it was identified that SRG prevented BPA-induced zebrafish testis injury through upregulation of fn1a, krt17, fabp10a, serpina1l and ctss2. These results indicate that SRG alleviated spermatogenic defects and testicular injury by suppressing oxidative stress and inflammation in male zebrafish.

Multi- and transcriptomic changes of chronic exposure to bisphenol A reveals reproductive toxicity in male zebrafish.

Bisphenol A (BPA) is considered to be a threat to marine organisms owning to its widespread usage and potential aquatic toxicity. However, the reproductive toxicity of BPA to transgenerational inheritance in aquatic organisms is still unclarified. In this study, the morphological, histological, and transgenerational changes by BPA in zebrafish testis were investigated. Results showed that BPA caused abnormities in sperm number, activity, and fertility rate. Testicular transcriptional alterations detected by RNA-seq identified 1940 differentially expressed genes (DEGs) after BPA exposure, of which 392 were upregulated and 1548 were downregulated. Gene Ontology analysis showed that acrosin binding, binding of sperm to zona pellucida, and positive regulation of acrosome reaction were significantly enriched in BPA-induced DEGs. Pathway analysis indicated that cell adhesion molecules, steroid hormone biosynthesis and fatty acid biosynthesis, elongation, and metabolism were remarkably changed after BPA treatment. Thus, we deduce here that multi- and transcriptomic changes of chronic exposure to BPA reveals reproductive toxicity in male zebrafish.

Protective Effects of Lactobacillus gasseri against High-Cholesterol Diet-Induced Fatty Liver and Regulation of Host Gene Expression Profiles.

Fatty liver is one of the most pervasive liver diseases worldwide. Probiotics play an important role in the progression of liver disease, but their effects on host regulation are poorly understood. This study investigated the protective effects of lactobacillus gasseri (L. gasseri) against high-cholesterol diet (HCD)-induced fatty liver injury using a zebrafish larvae model. Liver pathology, lipid accumulation, oxidative stress and hepatic inflammation were evaluated to demonstrate the changes in a spectrum of hepatic injury. Moreover, multiple indexes on host gene expression profiles were comprehensively characterized by RNA screening. The results showed that treatment with L. gasseri ameliorated HCD-induced morphological and histological alterations, lipid regulations, oxidative stress and macrophage aggregation in the liver of zebrafish larvae. Furthermore, the enrichment of the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway revealed that the core pathways of L. gasseri regulation were interleukin-17 (IL-17) signaling, phosphoinositide 3-kinase (PI3K)-AKT signaling pathway, the regulation of lipolysis and adipocytes and fatty acid elongation and estrogen signaling. The genes at key junction nodes, hsp90aa1.1, kyat3, hsd17b7, irs2a, myl9b, ptgs2b, cdk21 and papss2a were significantly regulated by L. gasseri administration. To conclude, the current research extends our understanding of the protective effects of L. gasseri against fatty liver and provides potential therapeutic options for fatty liver treatment.