# Suppressive Effects of an Inhibitor Composition on Skin Ulceration and Transcriptomic Analysis in the Sea Cucumber Apostichopus japonicus Exposed to No. 0 Diesel Oil

**Authors:** Xiaonan Li, Yajie Deng, Shufeng Li, Haoran Xiao, Fenglin Tian, Qi Ye, Lingshu Han, Chong Zhao, Jun Ding

PMC · DOI: 10.3390/biology15060482 · Biology · 2026-03-18

## TL;DR

This study shows that an inhibitor composition can protect sea cucumbers from diesel oil-induced skin ulcers by reducing damage and supporting repair and detoxification processes.

## Contribution

The study introduces a novel inhibitor composition that mitigates diesel-induced skin ulceration in sea cucumbers through multi-level protective mechanisms.

## Key findings

- The inhibitor reduced ulceration area by over 50% in sea cucumbers exposed to diesel oil.
- Transcriptomic analysis identified key genes and pathways involved in tissue repair and detoxification.
- The composition enhanced antioxidant and neural function-related enzyme activities.

## Abstract

Marine diesel oil pollution poses a serious threat to sea cucumber aquaculture by causing skin ulceration and physical damage. This study investigated the protective effects and mechanisms of an inhibitor composition under diesel stress. The results showed that the inhibitor significantly reduced ulceration area, suppressed the overactivation of autolytic enzymes (cathepsin L and B), and enhanced antioxidant and neural function-related enzymes. Transcriptomic analysis revealed that the protective mechanism involves coordinated regulation of tissue repair, detoxification, and antioxidant pathways. This research offers a potential strategy to mitigate diesel pollution impacts in aquaculture, supporting marine environmental protection and sustainable fishery development.

No. 0 diesel oil may pose a serious threat to sea cucumber (Apostichopus japonicus) aquaculture by inducing skin ulceration. This study aimed to evaluate the protective efficacy and mechanism of a previously developed inhibitor composition against diesel-induced injury. The inhibitor composition significantly alleviated skin ulceration in the experimental group (Eg), reducing the lesion area to 14.44 ± 1.79% after 96 h, compared to 33.19 ± 2.94% in the diesel-exposed control group (Cg) (p < 0.05). It effectively suppressed the overactivation of autolytic enzymes (cathepsin L and B) while enhancing the activities of acetylcholinesterase, superoxide dismutase, and catalase. Transcriptomic profiling revealed 3137 differentially expressed genes, with functional enrichment in pathways related to Notch signaling, ECM–receptor interaction, glycosaminoglycan biosynthesis, and detoxification. The upregulation of genes such as HES-C, CYP1A1, GST, and UGT may be linked to the regulation of apoptosis inhibition, xenobiotic metabolism, and antioxidant defense. Furthermore, enhanced expression of NAD kinase and PNLIPRP may indicate a potential strengthening of energy metabolism and lipid utilization during stress adaptation. This study suggests that the inhibitor composition may exert a multi-level protective effect against diesel-induced injury by coordinating tissue repair, oxidative balance, and detoxification processes, offering a potential strategy to mitigate pollution impacts in sea cucumber aquaculture.

## Linked entities

- **Genes:** HESC (hes family bHLH transcription factor 5C) [NCBI Gene 107057363], CYP1A1 (cytochrome P450 family 1 subfamily A member 1) [NCBI Gene 1543], SLCO6A1 (solute carrier organic anion transporter family member 6A1) [NCBI Gene 133482], SLC35A2 (solute carrier family 35 member A2) [NCBI Gene 7355], NAD_kinase (NAD kinase) [NCBI Gene 19017336]
- **Proteins:** Cat (Catalase)
- **Species:** Apostichopus japonicus (taxon 307972)

## Full-text entities

- **Genes:** catalase [NCBI Gene 101216662], superoxide dismutase [NCBI Gene 101207896]
- **Diseases:** cytotoxic (MESH:D064420), neurotoxicity (MESH:D020258), injury to (MESH:D014947), SUS (MESH:D012883)
- **Chemicals:** FUT-175 (MESH:C032855), chondroitin sulfate (MESH:D002809), Nicotinate (MESH:D009525), ascorbic acid (MESH:D001205), PAH (MESH:D011084), Emricasan (MESH:C487112), Trizol (MESH:C411644), ammonium sulphate (MESH:D000645), Ilomastat (MESH:C119203), FucCSs (MESH:C517150), glycans (MESH:D011134), dermatan sulfate (MESH:D003871), NADP+ (MESH:D009249), nicotinamide (MESH:D009536), lipid (MESH:D008055), nitrogen (MESH:D009584), sulfated fucans (MESH:C007789), magnesium (MESH:D008274), aromatic hydrocarbons (MESH:D006841), Diesel (-), ROS (MESH:D017382), glucuronic acid (MESH:D020723), NAD+ (MESH:D009243), GM6001 (MESH:C078131), H2O2 (MESH:D006861), dUTP (MESH:C027078), Oil (MESH:D009821), Glycosaminoglycan (MESH:D006025), Glutathione (MESH:D005978), acetylcholine (MESH:D000109), Sephadex G-100 (MESH:C025614)
- **Species:** Homo sapiens (human, species) [taxon 9606], Cucumis sativus (cucumber, species) [taxon 3659], Escherichia coli (E. coli, species) [taxon 562], Holothuroidea (holothurians, class) [taxon 7705], Vibrio splendidus (species) [taxon 29497], Apostichopus japonicus (Japanese sea cucumber, species) [taxon 307972], Vibrio (genus) [taxon 662]
- **Mutations:** H1750R
- **Cell lines:** H635 — Homo sapiens (Human), Maturity-onset diabetes of the young, Induced pluripotent stem cell (CVCL_LL30), H440- — Homo sapiens (Human), Galactosemia, Finite cell line (CVCL_V430)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13024229/full.md

## Figures

22 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13024229/full.md

## References

65 references — full list in the complete paper: https://tomesphere.com/paper/PMC13024229/full.md

---
Source: https://tomesphere.com/paper/PMC13024229