Fucoidan may treat jellyfish dermatitis by inhibiting the inflammatory effect of jellyfish venom

Li, Aoyu; Yue, Yang; Li, Rongfeng; Yu, Chunlin; Wang, Xueqin; Liu, Song; Xing, Ronge; Li, Pengcheng; Zhang, Quanbin; Yu, Huahua

doi:10.1016/j.ijbiomac.2023.127449

Cited by 3 publications

(4 citation statements)

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“…HaCaT cells, with different concentrations of TE, can trigger inflammatory factors (IL-1β, IL-6, IL-8, and TNF-α) that rapidly reach their highest level in 2 h. Mice blood cytokine protein expression exhibits a dose-dependent trend of increase. Consistent with these results, TE rapidly and strongly triggered an acute inflammatory response ( 6 , 18 , 32 ). In addition, the accumulation and excessive production of ROS in cells results in oxidative stress, which is one of the primary factors reason for inflammatory diseases.…”

Section: Discussionsupporting

confidence: 84%

“…Under homeostatic conditions, a dynamic equilibrium of mechanisms that generate and remove ROS maintains the redox state of cells ( 33 ). When mice received Nemopilema nomurai, the levels of MDA and glutathione (GSH) significantly increased ( 18 ). Our fluorescence microscopy analysis further indicated that TE dose-dependently induced a significant increase in intercellular ROS and MDA accumulation, which aggravated the lipid peroxidation response.…”

Section: Discussionmentioning

confidence: 99%

“…ROS overproduction-induced cytotoxicity is regulated by the release of cytokines as a result of the translocation of nuclear factor NF-kappaB p65 ( 38 ). According to recent studies, TE dramatically enhances oxidative stress in mouse skin tissues by regulating the production of proteins linked to the NF-κB and MAPK pathways ( 18 ). This result was further supported by our transcriptome data involving TE-stimulated HaCaT cells, revealing the underlying molecular mechanisms of jellyfish dermatitis.…”

Section: Discussionmentioning

confidence: 99%

“…Oxidative stress from major indicators of mouse serum lipid peroxidation and the accumulation of intercellular ROS may be additional pathways for the effects of jellyfish venom ( 16 , 17 ). According to recent findings, skin oxidative damage and inflammation induced by Nemopilema nomurai can be mitigated through a class of natural antioxidant algal-derived polysaccharides by inhibiting mitogen-activated protein kinases (MAPK) and nuclear factor-kappa B (NF-κB) pathways ( 18 ). ROS accumulation between cells leads to activate the MAPK signaling pathway, which further aggravated inflammation response ( 19 )..…”

Section: Introductionmentioning

confidence: 99%

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Troxerutin suppress inflammation response and oxidative stress in jellyfish dermatitis by activating Nrf2/HO-1 signaling pathway

Liu,

Wang,

Kuai

et al. 2024

Front. Immunol.

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BackgroundStomolophus meleagris envenomation causes severe cutaneous symptoms known as jellyfish dermatitis. The potential molecule mechanisms and treatment efficiency of dermatitis remain elusive because of the complicated venom components. The biological activity and molecular regulation mechanism of Troxerutin (TRX) was firstly examined as a potential treatment for jellyfish dermatitis. MethodsWe examined the inhibit effects of the TRX on tentacle extract (TE) obtained from S. meleagris in vivo and in vitro using the mice paw swelling models and corresponding assays for Enzyme-Linked Immunosorbent Assay (ELISA) Analysis, cell counting kit-8 assay, flow cytometry, respectively. The mechanism of TRX on HaCaT cells probed the altered activity of relevant signaling pathways by RNA sequencing and verified by RT-qPCR, Western blot to further confirm protective effects of TRX against the inflammation and oxidative damage caused by TE. ResultsTE significantly induced the mice paw skin toxicity and accumulation of inflammatory cytokines and reactive oxygen species in vivo and vitro. Moreover, a robust increase in the phosphorylation of mitogen-activated protein kinase (MAPKs) and nuclear factor-kappa B (NF-κB) signaling pathways was observed. While, the acute cutaneous inflammation and oxidative stress induced by TE were significantly ameliorated by TRX treatment. Notablly, TRX suppressed the phosphorylation of MAPK and NF-κB by initiating the nuclear factor erythroid 2-related factor 2 signaling pathway, which result in decreasing inflammatory cytokine release. ConclusionTRX inhibits the major signaling pathway responsible for inducing inflammatory and oxidative damage of jellyfish dermatitis, offering a novel therapy in clinical applications.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%