Résumé
Objective@#To investigate the developmental toxicity of 2,4-dinitrochlorobenzene in zebrafish embryos.@*Methods@#AB wild-type male and female zebrafish were selected to mate and spawn, then the eggs were cultured with Holt buffer solution. Six dose groups ( 0.4, 0.8, 1.0, 1.2, 1.6, 2.0 μg/mL ), a solvent control group and a cosolvent control group, were set up with 20 embryos each. Malformations and death of embryos were observed at 48, 72 and 96 hpf ( hours post fertilization ), the mortality and 50% lethal concentration ( LC50 ) were also calculated. @*Results@#At 48, 72 and 96 hpf, the LC50 of 2,4-dinitrochlorobenzene on zebrafish embryos were 1.668, 1.043 and 0.895 μg/mL, respectively, with a downward trend. After 72 hpf, when the concentration reached 2.0 μg/mL, all the zebrafish died. In the range of 0.4-2.0 μg/mL, the mortality of zebrafish at 48, 72 and 96 hpf increased with the increase of 2,4-dinitrochlorobenzene concentration ( all P<0.05 ); the malformation rate of zebrafish embryos at 48 hpf increased with the increase of 2,4-dinitrochlorobenzene concentration ( P<0.05 ). Zebrafish embryos exposed to 2,4-dinitrochlorobenzene led to yolk sac edema, pericardial edema and spinal curvature. @*Conclusion@#2,4-dinitrochlorobenzene can affect the development of zebrafish embryos, which will lead to lethal and teratogenic effects.
Résumé
Wound scarring remains a major challenge for plastic surgeons. Transforming growth factor (TGF)-β plays a key role in the process of scar formation. Previous studies have demonstrated that truncated TGF-β type II receptor (t-TGF-βRII) is unable to continue signal transduction but is still capable of binding to TGF-β, thereby blocking the TGF-β signaling pathway. Hepatocyte growth factor (HGF) is a multifunctional growth factor that promotes tissue regeneration and wound healing. Theoretically, the combination of HGF and t-TGF-βRII would be expected to exert a synergistic effect on promoting wound healing and reducing collagen formation. In the present study, lentivirus-mediated transfection of the two genes (t-TGF-βRII/HGF) into fibroblasts in vitro and in a rat model in vivo was used. The results demonstrated that the expression of t-TGF-βRII and HGF in NIH-3T3 cells was successfully induced. The expression of both molecules significantly reduced collagen I and III expression, and also inhibited fibroblast proliferation. Furthermore, histological examination and scar quantification revealed less scarring in the experimental wound in a rat model. Moreover, on macroscopic inspection, the experimental wound exhibited less visible scarring compared with the control. Therefore, the present study demonstrated that the combination gene therapy of t-TGF-βRII and HGF promoted wound healing, with less scarring and more epithelial tissue formation, not only by suppressing the overgrowth of collagen due to its antifibrotic effect, but also by promoting tissue regeneration.