Daboia siamensis 毒液和分馏物诱发的急性肾损伤中的急性期反应:体内兔肾模型和体外兔肾模型中氧化应激和炎症途径的作用。

IF 1.8 3区 医学 Q4 TOXICOLOGY Journal of Venomous Animals and Toxins Including Tropical Diseases Pub Date : 2024-05-20 eCollection Date: 2024-01-01 DOI:10.1590/1678-9199-JVATITD-2023-0070
Narongsak Chaiyabutr, Jureeporn Noiprom, Kanyanat Promruangreang, Taksa Vasaruchapong, Panithi Laoungbua, Orawan Khow, Lawan Chanhome, Visith Sitprija
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引用次数: 0

摘要

背景:本研究探讨了暹罗鲎(Daboia siamensis)毒液(RVV)和毒液馏分在体内和离体灌注肾(IPK)中的直接肾毒性作用,以了解炎症通路和氧化应激易感性在毒液或馏分诱导的急性肾衰竭中的作用:我们在体内和 IPK 模型中给兔子注射了 RVV 及其毒液组分(PLA2、MP、LAAO 和 PDE)。我们测量了肾组织中的氧化应激生物标志物(SOD、CAT、GSH 和 MDA),以及血浆和尿液中的炎症细胞因子(TNF-α、IL-1β、IFN-γ、IL-4、IL-5 和 IL-10)、MDA 和 GSH 水平。我们还计算了促/抗炎细胞因子和氧化应激生物标志物的排泄分数(FE),包括毒液中毒后尿液中促/抗炎细胞因子的比率:结果:在两种肾脏模型中,注射 RVV 和毒液馏分后,肾脏组织中的 MDA、SOD、CAT 和 GSH 水平明显升高,血浆和尿液中的 MDA 和 GSH 浓度也升高。此外,注射 RVV 会导致 FEMDA 逐渐增加,FEGSH 逐渐减少。注射 RVV 后,血浆中的 IL-4、IL-5、IL-10、IFN-γ 和 TNF-α 浓度增加,IPK 模型尿液中的浓度也增加,但血浆和尿液中的 IL-1β 浓度没有增加。尿液中TNF-α、IL-1β、IFN-γ、IL-4、IL-5和IL-10的部分排泄量在体内呈下降趋势,但在IPK模型中则呈上升趋势。体内注射一次 RVV 会破坏尿液细胞因子的平衡,显著降低 TNF-α/IL-10 比率或 IFN-γ/IL-10 比率:结论:RVV 通过增加氧化应激的产生和升高尿液中的炎症细胞因子诱导肾小管毒性。在急性肾损伤的急性期,尿液细胞因子的平衡在 RVV 和毒液分馏后的头两个小时内转向抗炎主导。
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Acute phase reactions in Daboia siamensis venom and fraction-induced acute kidney injury: the role of oxidative stress and inflammatory pathways in in vivo rabbit and ex vivo rabbit kidney models.

Background: This study examines the direct nephrotoxic effects of Daboia siamensis venom (RVV) and venom fractions in in vivo and isolated perfused kidneys (IPK) to understand the role of inflammation pathways and susceptibility to oxidative stress in venom or fraction-induced acute renal failure.

Methods: We administered RVV and its venom fractions (PLA2, MP, LAAO, and PDE) to rabbits in vivo and in the IPK model. We measured oxidative stress biomarkers (SOD, CAT, GSH, and MDA) in kidney tissue, as well as inflammatory cytokines (TNF-α, IL-1β, IFN-γ, IL-4, IL-5, and IL-10), MDA and GSH levels in plasma and urine. We also calculated fractional excretion (FE) for pro-/anti-inflammatory cytokines and oxidative stress biomarkers, including the ratios of pro-/anti-inflammatory cytokines in urine after envenomation.

Results: In both kidney models, significant increases in MDA, SOD, CAT, and GSH levels were observed in kidney tissues, along with elevated concentrations of MDA and GSH in plasma and urine after injecting RVV and venom fractions. Moreover, RVV injections led to progressive increases in FEMDA and decreases in FEGSH. The concentrations of IL-4, IL-5, IL-10, IFN-γ, and TNF-α in plasma increased in vivo, as well as in the urine of the IPK model, but not for IL-1β in both plasma and urine after RVV administrations. Urinary fractional excretion of TNF-α, IL-1β, IFN-γ, IL-4, IL-5, and IL-10 tended to decrease in vivo but showed elevated levels in the IPK model. A single RVV injection in vivo disrupted the balance of urinary cytokines, significantly reducing either the TNF-α/IL-10 ratio or the IFN-γ/IL-10 ratio.

Conclusion: RVV induces renal tubular toxicity by increasing oxidative stress production and elevating inflammatory cytokines in urine. During the acute phase of acute kidney injury, the balance of urine cytokines shifts toward anti-inflammatory dominance within the first two hours post-RVV and venom fractions.

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来源期刊
CiteScore
4.80
自引率
8.30%
发文量
39
审稿时长
6-12 weeks
期刊介绍: Journal of Venomous Animals and Toxins including Tropical Diseases (JVATiTD) is a non-commercial academic open access publication dedicated to research on all aspects of toxinology, venomous animals and tropical diseases. Its interdisciplinary content includes original scientific articles covering research on toxins derived from animals, plants and microorganisms. Topics of interest include, but are not limited to:systematics and morphology of venomous animals;physiology, biochemistry, pharmacology and immunology of toxins;epidemiology, clinical aspects and treatment of envenoming by different animals, plants and microorganisms;development and evaluation of antivenoms and toxin-derivative products;epidemiology, clinical aspects and treatment of tropical diseases (caused by virus, bacteria, algae, fungi and parasites) including the neglected tropical diseases (NTDs) defined by the World Health Organization.
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