Background: The dibutyl phthalate (DBP) is a member of the phthalate family and is widely used as a plasticizer in daily life and production. However, the influence of DBP on the vascular developmental remains unclear. Methods: In this study, we used zebrafish as a model organism to investigate the effects of DBP on vascular development in vivo. Death curves of zebrafish at different concentrations of DBP exposure and different times incubation were made firstly. Zebrafish embryos after fertilization for 5.5 h were exposed to different concentrations of DBP solution (0, 0.4, 0.8, 1.2 mg/L), the body length, yolk sac absorption area, mortality and heart rate of zebrafish were measured, and the number and area of sprouting of ventral vessels were quantified by transgenic fish system. Reactive oxygen species (ROS) in zebrafish embryos were observed by DCFH-DA staining. Super oxide dimutese (SOD) and catalase (CAT) were determined with ELISA kits. Results: We found that DBP increased the oxidative stress level of zebrafish exposed to DBP, and the genes related to vascular development also increased. Meanwhile, the activities of SOD and CAT were greatly decreased after DBP exposure. In the rescue experiment, we found that the antioxidant astaxanthin and the small molecule VEGF inhibitor ZM-306,416 can reverse the vascular dysplasia caused by DBP. Conclusions: DBP induced vascular developmental toxicity by enhancing oxidative stress levels, activating HIF pathway, and interfering with the expression of vascular development-related pathways in zebrafish, results in the abnormal development of the subintestinal vessels in zebrafish.
Abstract In this work, the thiadiazolopyridine (PT) unit was introduced as the core structure, with N 3 , N 3 , N 6 , N 6 ‐tetrakis(4‐methoxyphenyl)‐9‐phenyl‐9 H ‐carbazole‐3,6‐diamine as the peripheral group, to obtain a new compound, JY8, for use as a hole‐transport material (HTM) in planar perovskite solar cells (PSCs). Compared with the previously reported JY5 with benzothiadiazole as the core structure, the PT unit with stronger electron‐withdrawing ability enhanced the intermolecular dipole–dipole interaction. Moreover, the introduction of the PT unit made the central part in JY8 more planar than its analogue JY5, which is conducive to charge transport. Field‐emission (FE)‐SEM images suggested a smooth and condense morphology of the JY8 film, which could improve the contact between the perovskite layer and the metal electrode. Space‐charge limitation of current results, steady‐state, and time‐resolved photoluminescence decay curves indicated that JY8 as HTM facilitated hole extraction and hole transport. Consequently, planar PSCs fabricated with JY8 as the HTM exhibited a decent efficiency of 19.14 % with a high fill factor of 81 %.
Thrombosis is a key pathological event in cardiovascular diseases and is also the most important targeting process for their clinical management. In this study, arachidonic acid (AA) was used to induce thrombus formation in zebrafish larvae. Blood flow, red blood cell (RBCs) aggregation and cellular oxidative stress were measured to evaluate the antithrombotic effect of Tibetan tea (TT). Meanwhile, the potential molecular mechanism was further explored by transcriptome sequencing (RNA-seq). The results indicated that TT could significantly restore heart RBCs intensity of thrombotic zebrafish, whilst decreasing RBCs accumulation in the caudal vein. The transcriptome analysis revealed that the preventive effect of TT on thrombosis could be mostly attributed to changes in lipid metabolism related signaling pathways, such as fatty acid metabolism, glycerollipid metabolism, ECM-receptor interaction and steroid biosynthesis signaling pathway. This study demonstrated that Tibetan tea could alleviate thrombosis by reducing oxidative stress levels and regulating lipid metabolism.
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