With the increase in fishing intensity and the intensification of marine pollution, the fishery resources in the Zhoushan Sea are seriously degraded, and the difficulty of censusing fish diversity hampers effective management in marine fishes. Environmental DNA metabarcoding and bottom trawl methods were used to determine the ability of the methods to distinguish fish assemblages in the Zhoushan Sea. The species composition and diversity of the Zhoushan Sea were assessed via high-throughput sequencing analysis of eDNA coupled with bottom trawl fishery survey data, after which the two methods were compared. eDNA screening identified 38.2% more fish species than bottom trawls. Combining these two methods, 33 orders, 65 families, and 130 species of fishes were identified. Perciformes and Clupeiformes, the most abundant orders in the catch, represented 31.5 and 10.0% of the total fish abundance, respectively. The results of ANOSIM and redundancy analyses indicated that the fish community structure varied significantly between summer and winter, however depth and temperature being the main environmental factors influencing fish distribution. The biodiversity index was higher in summer than in winter. Thus, our work provides more detailed seasonal data on biodiversity in the Zhoushan Sea, which is essential for the long-term management and conservation of coastal biodiversity. Compared with traditional survey methods, eDNA determination is highly sensitive, accurate, cost-efficient, and suitable for fish diversity studies in relevant sea areas. Although this approach cannot completely replace traditional methods, our findings demonstrate that it provides a reliable complementary method for assessing fish diversity in marine ecosystems.

To investigate the effect of piperazine ferulate (PF) on hypertension and endothelial function, and to assess the possible underlying mechanism.Human umbilical vein endothelial cells (HUVEC), adult male Wistar Kyoto (WKY) rats aged 12 to 14 weeks, and spontaneously hypertensive (SH) and Sprague Dawley (SD) rats were used for this study. Cell viability, activities of angiotensin-converting enzyme (ACE) and heme oxygenase-1 (HO-1), in vivo NO synthesis, arterial systolic blood pressure, vascular function, expressions of endothelial NO synthase (eNOS) and phosphorylated-eNOS (p-eNOS) were determined or assessed as appropriate. The results of MTT assay showed the number of viable cells were significantly increased with increase in PF concentration (p < 0.05). The level of expression of ACE was significantly reduced with increase in PF concentration (p < 0.05), while the level of HO-1 expression significantly increased (p < 0.05). Results of DAF-FM fluorescent staining showed that the amounts of NO synthesized in vivo was significantly higher in aortic rings of SH and SD rats treated with PF than in the corresponding control groups (p < 0.05). Treatment with PF in vivo significantly improved impaired acetylcholine-induced aortic relaxation in SH rats. Total eNOS expression was significantly increased after treatment with PF (p < 0.05). The expressions of total eNOS and p-eNOS in both groups were not affected by PF when compared to the control group. These results indicate that PF exerts antihypertensive effect and improves endothelial function in vitro and in vivo via the activation of eNOS.

Accumulating evidence suggests that cardiomyocyte autophagy is relevant to the onset of cardiac hypertrophy (CH). Several miRNAs are involved in the occurrence of heart failure, and relevant therapeutic treatments are currently being developed. MicroRNA-377 (miR-377) is known to correlate with the progression of various cancers, however, its function in CH has not been determined. Therefore, this study aimed to evaluate miR-377 expression in H2C9 hypertrophic cardiomyocytes in vitro and in a murine model of CH. Gene expression changes were verified via qRT-PCR. Western blotting was used for evaluation of alterations in the expression of signaling pathway-related proteins. Our results indicated that miR-377 expression was markedly upregulated in mice with hypertrophic cardiomyopathy. Autophagy markers were downregulated in these mice and in hypertrophic cardiomyocytes following miR-377 transfection. In addition, we demonstrated that miR-377 acts by targeting peroxisome proliferator-activated receptor γ (PPARγ ). PPARγ overexpression promoted autophagy and suppressed cyclosporine A-induced CH. In contrast, PPARγ knockdown further suppressed CH and autophagy. In conclusion, our findings indicated that miR-377 accelerates CH by inhibiting autophagy via targeting PPARγ . This newly identified miR-377/PPARγ axis improves our understanding of the molecular mechanisms underlying CH, and provides a potential new therapeutic target for its treatment.

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