PDF(Pubmed)
Abstract：
UNASSIGNED: Stomolophus 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.
UNASSIGNED: We 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.
UNASSIGNED: TE 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.
UNASSIGNED: TRX inhibits the major signaling pathway responsible for inducing inflammatory and oxidative damage of jellyfish dermatitis, offering a novel therapy in clinical applications.
UNASSIGNED: We 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.
UNASSIGNED: TE 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.
UNASSIGNED: TRX inhibits the major signaling pathway responsible for inducing inflammatory and oxidative damage of jellyfish dermatitis, offering a novel therapy in clinical applications.
摘要：
■Stomolophusmeleagris毒素引起严重的皮肤症状，称为水母皮炎。由于复杂的毒液成分，皮炎的潜在分子机制和治疗效率仍然难以捉摸。首先研究了Troxerutin（TRX）的生物学活性和分子调节机制，可作为水母皮炎的潜在治疗方法。
■我们使用小鼠爪肿胀模型和相应的酶联免疫吸附测定（ELISA）分析，在体内和体外检查了TRX对从S.meleagris获得的触手提取物（TE）的抑制作用。细胞计数试剂盒-8测定，流式细胞术,分别。TRX对HaCaT细胞的作用机制通过RNA测序探索相关信号通路活性的改变，并通过RT-qPCR验证，Westernblot进一步证实TRX对TE引起的炎症和氧化损伤的保护作用。
■TE在体内和体外显着诱导了小鼠爪皮肤毒性和炎性细胞因子和活性氧的积累。此外，丝裂原活化蛋白激酶(MAPKs)和核因子-κB(NF-κB)信号通路的磷酸化显著增加.同时,TRX治疗可显着改善TE引起的急性皮肤炎症和氧化应激。值得注意的是，TRX通过启动核因子红系2相关因子2信号通路抑制MAPK和NF-κB的磷酸化,这导致炎性细胞因子释放减少。
■TRX抑制了引起水母皮炎炎症和氧化损伤的主要信号通路，在临床应用中提供了一种新的疗法。
■我们使用小鼠爪肿胀模型和相应的酶联免疫吸附测定（ELISA）分析，在体内和体外检查了TRX对从S.meleagris获得的触手提取物（TE）的抑制作用。细胞计数试剂盒-8测定，流式细胞术,分别。TRX对HaCaT细胞的作用机制通过RNA测序探索相关信号通路活性的改变，并通过RT-qPCR验证，Westernblot进一步证实TRX对TE引起的炎症和氧化损伤的保护作用。
■TE在体内和体外显着诱导了小鼠爪皮肤毒性和炎性细胞因子和活性氧的积累。此外，丝裂原活化蛋白激酶(MAPKs)和核因子-κB(NF-κB)信号通路的磷酸化显著增加.同时,TRX治疗可显着改善TE引起的急性皮肤炎症和氧化应激。值得注意的是，TRX通过启动核因子红系2相关因子2信号通路抑制MAPK和NF-κB的磷酸化,这导致炎性细胞因子释放减少。
■TRX抑制了引起水母皮炎炎症和氧化损伤的主要信号通路，在临床应用中提供了一种新的疗法。
