Mechanistic action of the acute toxicity of Bajitian(Morinda officinalis)in zebrafish embryos

Objectives:To investigate acute toxicity of Bajitian(Morinda officinalis)in zebrafish embryos.Methods:Zebrafish embryos at 48-h post fertilization(hpf)were exposed to Bajitian ethanol extract for72 h.The causative action of a delay in yolk sac absorption by Bajitian was investigated by RT-PCR analysis of lipid metabolism-related microsomal triglyceride transfer protein(MTP),apolipoprotein CII(ApoC2)and lipogenesis-related liver x receptor(LXR)genes.The effect of Bajitian eliciting an inflammatory response was studied by exposing 72 hpf myeloperoxidase(MPO):GFP transgenic zebrafish embryos to Bajitian extract for 4 h.Assessment was done by TUNEL,caspase-3/7,and RT-PCR analysis of the apoptosis related pathway B-cell lymphoma 2 associated X protein(Bax),Nuclear factor kappa-lightchain-enhancer of activated B cells(NF-k B)genes,neutrophil development-related stem cell leukaemia(SCL)and transcription factor PU.1 genes,to reveal the causative action of Bajitian reducing neutrophils.Results:RT-PCR analysis found that Bajitian extract had no effect on the expression of MTP or ApoC2 genes,but upregulated LXR gene,which might explain the delay in yolk sac absorption.Analysis of the inflammatory response showed that compared with negative controls,Bajitian extract significantly(P<.05)reduced the number of neutrophils in MPO:GFP embryos.TUNEL,caspase-3/7,and RT-PCR analysis of Bax and NF-k B genes found that Bajitian extract did not trigger the cell apoptosis.Further RT-PCR analysis found that Bajitian extract did not affect SCL expression,but did lead to down-regulation of PU.1.The inhibition of neutrophil development/differentiation may explain the decline in the total number of neutrophils following Bajitian treatment,which could be attributed to the anti-inflammatory effects found clinically for this drug.Conclusions:This study demonstrated that Bajitian caused a delay in yolk sac absorption and a decrease neutrophil in zebrafish embryos,which may be related to the inhibition of neutrophil development.

Insights into Triclosan-Induced Endocrine Disruption:Evidence from the National Health and Nutrition Examination Survey and Zebrafish Models

Triclosan(TCS)has garnered significant attention due to its widespread use and associated endocrine-disrupting effects.However,its impact on the neuroendocrine system and underlying mechanisms remain poorly understood.Here,we established correlations between TCS exposure and serum sex hormone levels in participants of the National Health and Nutrition Examination Survey(NHANES).Additionally,we investigated TCS’s influence on the neuroendocrine system using adult zebrafish exposed to environmentally relevant concentrations of TCS(0.361–48.2μg/L)for 21 days.Assessment of reproductive and neurotoxicity included histopathological examination and behavioral tests.Transcriptomics,proteomics analyses,and biochemical detection were employed to elucidate mechanisms underlying TCS-induced neuroendocrine disruption.Significant correlations were found between TCS exposure and estradiol,testosterone,and sex hormone-binding globulin levels in NHANES participants.In addition,TCS exposure inhibited ovary development and spermatogenesis in zebrafish.Transcriptomics and proteomics analysis revealed gender-specific key signaling and metabolism-related pathways implicated in TCS-induced reproductive toxicity.Moreover,TCS exposure induced nervous system impairment,as evidenced by histological changes and altered motor behavior,possibly associated with oxidative damage.Correlation analysis further highlighted the potential connection between endocrine system disruption and nervous system impairment following TCS exposure.Overall,this study provided evidence supporting TCS-induced endocrine disruption and offered insights into its underlying mechanisms.