As a promising novel marine fish model for future research on marine ecotoxicology as well as an animal model of human disease, the genome information of yellowstripe goby (Mugilogobius chulae) remains unknown. Here we report the first annotated chromosome-level reference genome assembly for yellowstripe goby. A 20.67-cM sex determination region was discovered on chromosome 5 and seven potential sex-determining genes were identified. Based on combined genome and transcriptome data, we identified three key lipid metabolic pathways for high-fat accumulation in the liver of yellowstripe goby. The changes in the expression patterns of MGLL and CPT1 at different development stage of the liver, and the expansion of the ABCA1 gene, innate immune gene TLR23, and TRIM family genes may help in balancing high-fat storage in hepatocytes and steatohepatitis. These results may provide insights into understanding the molecular mechanisms of sex determination and high-fat storage in the liver of marine fishes.

The effect of caffeine on the behavior and sleep patterns of zebrafish larvae, as well as its underlying mechanisms, has been a topic of great interest. This study aimed to investigate the impact of caffeine on zebrafish larval sleep/wake behavior and the expression of key regulatory genes such as cAMP-response element binding protein (CREB) and adenosine (ADA) in the sleep pathway. To begin, the study determined the optimal dose and duration of caffeine exposure, with the optimal doses found to be 31.25 μM, 62.5 μM, and 120 μM. Similarly, the optimal exposure time was established as no more than 120 h, ensuring a mortality rate of less than 10%. The confirmation of these conditions was achieved through the assessment of angiogenesis and the inflammatory reaction. As a result, the treatment time point of 24 h post-fertilization (hpf) was selected to examine the effects of caffeine on zebrafish larval sleep rhythm (48 h, with a light cycle of 14:10). Furthermore, the study analyzed the expression of clock genes (bmal1a, per1b, per2, per3, cry2), adenosine receptor genes (adora1a, adora1b, adora2aa, adora2ab, adora2b), and key regulatory factors (CREB and ADA). The research confirmed that caffeine could induce sleep pattern disorders, significantly upregulate adenosine receptor genes (adora1a, adora1b, adora2a, adora2ab, adora2b) (p < 0.05), and markedly decrease the total sleep time and sleep efficiency of the larvae. Additionally, the activity of ADA significantly increased during the exposure (p < 0.001), and the tissue-specific expression of CREB was also significantly increased, as assessed by immunofluorescence. Caffeine may regulate circadian clock genes through the ADA/ADORA/CREB pathway. These findings not only enhance our understanding of the effects of caffeine on zebrafish larvae but also provide valuable insights into the potential impact of caffeine on human behavior and sleep.

Kaempferia galanga L. is well known for its use in medicinal and edible homologous application. Various diseases, including those related to oxidation, are commonly treated with it. However, its antioxidant effect is still lacking systematical study. We aimed to screen the most potential antioxidant fraction of the crude ethanolic extract from K. galanga (KG) and evaluate its antioxidant activity and potential mechanism. The ethyl acetate fraction of ethanolic extract from K. galanga (KGEA) was chosen as the most potent antioxidant activity from all the fractions tested. UPLC-Q-TOF-MS/MS was used to determine 43 compounds in KGEA, and 25 potential bioactive compounds were identified by pharmacokinetic analysis. Network pharmacology revealed 174 overlapping targets of chemical and antioxidant targets, and the key targets were identified. Molecular docking and MD simulation revealed a strong binding affinity between the core compounds and their targets. In tests against DPPH and ABTS, KGEA exhibited potent radical scavenging activity. In H₂O₂-induced cells, KGEA could decrease reactive oxygen species (ROS) production; alleviate mitochondrial damage; promote the increase in antioxidant enzymes SOD, CAT, GSH-Px; and reduce the levels of MDA. Mechanistically, KGEA regulated PI3K/Akt and MAPK signaling pathways against oxidative damage. Moreover, in H₂O₂-induced zebrafish, KGEA attenuated ROS generation, cell death, lipid peroxidation, and increased SOD, CAT, GSH-Px activities; it also decreased MDA levels. The antioxidant properties of KGEA were demonstrated in vitro and in vivo, and it should be considered as an antioxidant agent for further profound study.

Introduction: Stytontriterpene D ( STD ) is a compound isolated from dried resin of Styrax tonkinensis (Pierre) Craib ex Hartw. In this study, we explored the anti-inflammatory effect of STD in vitro and in vivo and examined its potential anti-inflammatory mechanism for the first time.Methods: In vitro, we evaluated the toxicity of STD to RAW 264.7 cells using the CCK8 method and detected the reactive oxygen species (ROS) and nitric oxide (NO) contents in cells using diacetyldichlorofluorescein (DCFH-DA) and the Griess method. We detected the levels of interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), interleukin-10 (IL-10), and arginase-1 (ARG1) via enzyme-linked immunosorbent assay and measured the expression of related proteins in the NF-κB pathway via western blotting. The toxicity of STD to AB zebrafish was detected in vivo, and the recruitment of neutrophils and macrophages was evaluated in tail cut-induced and copper sulfate-induced zebrafish inflammation models. We used quantitative real-time polymerase chain reaction to study the expression of inflammation-related genes in zebrafish with inflammation induced by copper sulfate.Results: In lipopolysaccharide (LPS)-induced RAW 264.7 cells, STD decreased IL-6, IL-1β, NO, ROS, and TNF-α production, and increased the expression of IL-10 and ARG1 while also blocking inhibitory κBα (IκBα) phosphorylation and suppressing P65 nuclear translocation. STD also reduced the recruitment of inflammatory cells in zebrafish with inflammation induced by tail cutting and copper sulfate. STD not only reduced the copper sulfate–induced gene expression of zebrafish inflammatory factors, but it also inhibited the mRNA levels of NF-κB p65 and IκBα.Conclusion: These results demonstrated that STD has an obvious anti-inflammatory effect, and its intrinsic molecular mechanism is possibly caused by inhibiting the NF-κB signaling pathway and regulating the phenotypic changes of M1 and M2 macrophages. Thus, STD may play a potential role in the treatment of inflammatory diseases.

Corrigendum: Anti-inflammatory effect and mechanism of stytontriterpene D on RAW264.7 cells and zebrafish* Correspondence: Feng Wang,wfeng1230@163.com. Lei Cai,cailei17@163.comKeywords: stytontriterpene D, anti-inflammatory, mechanism, RAW 264.7 cell, zebrafishA Corrigendum on full citation of the original version of the articleText Correction 1In the published article, there was an error. [In the methods section of the abstract on the first page of the article, (TNF - α) was mistakenly written as (TNF - κ), and the correct expression should be (TNF - α).(NF - κB) was mistakenly written as (NF - αB), and the correct expression should be (NF - κB)].A correction has been made to [Methods]. This sentence previously stated:“[TNF - κ]”“(NF - αB)”The corrected sentence appears below:“[TNF - α]”“(NF - κB)”The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.Text Correction 2In the published article, there was an error. [In sections 2.12.1, 2.12.2, 2.13.1, and 2.13.2 on page 5 of the text, the concentration of DEX was mistakenly written as 61.2 μ M, while the correct one is DEX (51.0 μ M). Therefore, the DEX concentration of the above four sections should be changed to 51.0 μ M].A correction has been made to [2.12 and 2.13][In sections 2.12.1, 2.12.2, 2.13.1, and 2.13.2] . This sentence previously stated:“[DEX(61.2 μ M)]”The corrected sentence appears below:“[DEX(51.0 μ M)]”The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.Text Correction 3In the published article, there was an error. [In sections 2.13.1 and 2.13.2 on page 5 of the text, it was mistakenly written as 1.6 μ M copper sulfate, while the correct one is 10.0 μ M copper sulfate.Therefore, the concentration of copper sulfate in both sections should be changed to 10.0 μ M].A correction has been made to [2.13][In sections 2.13.1, and 2.13.2] . This sentence previously stated:“[all of which contained 1.6 μ M copper sulfate]”The corrected sentence appears below:“[all of which contained 10.0 μ M copper sulfate]”The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.Text Correction 4In the published article, there was an error. [In the last sentence of the second paragraph of the discussion section, we mistakenly wrote 'STD' as' DE '].A correction has been made to [discussion],[Paragraph 2]. This sentence previously stated:“[while DE significantly increased the expression of M2 phenotype (ARG1 and IL-10) mRNA, exerting anti-inflammatory effects by modulating macrophage polarization. ]”The corrected sentence appears below:“[while STD significantly increased the expression of M2 phenotype (ARG1 and IL-10) mRNA, exerting anti-inflammatory effects by modulating macrophage polarization.]”The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.Error in Figure/Table LegendIn the published article, there was an error in the legend for [Figure 8] as published. [On page 12 of the article, We wrote DEX and copper sulfate in reverse]. The corrected legend appears below. [Groups other than the control were treated with a copper sulfate solution that had 5.1 μM DEX and various amounts of STD (13.2, 26.5,and 53.0 μM).]The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.Error in Figure/TableIn the published article, there was an error in [Figure 6,Figure 7, and Figure 8] as published. [Due to a concentration writing error, the concentrations in Figures 6, 7, and 8 should also be modified accordingly. We have attached Figures 6, 7, and 8 as attachments ]. The corrected [Figure 6,Figure 7, and Figure 8] and its caption **[Figure 6,Figure 7, and Figure 8] appear below.