2,5-Dihydroxyacetophenone attenuates acute kidney injury induced by intra-abdominal infection in rats.

IF 2.4 4区 医学 Q2 UROLOGY & NEPHROLOGY Nephrology Pub Date : 2024-10-01 Epub Date: 2024-07-25 DOI:10.1111/nep.14335
Tao Han, Ye Jiang, Weixing Ge, Yuyu Lu, Rongming Liu, Zunpeng Sun
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Abstract

Aims: As one of the most serious complications of sepsis, acute kidney injury (AKI) is pathologically associated with excessive inflammation. 2,5-Dihydroxyacetophenone (DHAP) is isolated from Radix rehmanniae praeparata and exhibit potent anti-inflammatory property. This research aimed at determining the role of DHAP in sepsis-associated AKI (SA-AKI) and the underlying mechanism.

Methods: Plasma creatinine (Cre), blood urea nitrogen (BUN), tumour necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels of SA-AKI patients were detected to evaluate their clinical characteristics. SA-AKI rat models were established by using caecum ligation puncture (CLP) surgery. CLP-induced rats were administered via oral gavage with 20 or 40 mg DHAP after 2 h of CLP surgery. Subsequently, survival rates, serum indexes, histopathological changes, inflammatory factors, renal function indexes and extracellular regulated protein kinases (ERK) and nuclear factor-κB (NF-κB) signalling pathways were detected.

Results: SA-AKI patients exhibited markedly higher levels of plasma Cre, BUN, TNF-α and IL-1β than healthy people. Compared with sham rats, CLP-induced septic rats showed significantly decreased survival rate, increased serum lactate dehydrogenase activity and serum lactate level, obvious renal histopathological injury, upregulated TNF-α, IL-1β and TGF-β1 levels, elevated serum creatinine, BUN and serum cystatin C concentrations, serum neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 levels and reduced renal artery blood flow. All the above CLP-induced changes in septic rats were mitigated after DHAP administration. Additionally, CLP-induced elevation in phosphorylated-ERK1/2 and nuclear NF-κB p65 protein levels was inhibited by DHAP treatment.

Conclusion: DHAP hinders SA-AKI progression in rat models by inhibiting ERK and NF-κB signalling pathways.

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2,5-二羟基苯乙酮可减轻大鼠腹腔内感染引起的急性肾损伤。
目的:作为败血症最严重的并发症之一,急性肾损伤(AKI)在病理学上与过度炎症有关。2,5-二羟基苯乙酮(DHAP)是从地黄中分离出来的,具有很强的抗炎作用。本研究旨在确定 DHAP 在败血症相关性 AKI(SA-AKI)中的作用及其内在机制:方法:检测 SA-AKI 患者的血浆肌酐(Cre)、血尿素氮(BUN)、肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)水平,以评估其临床特征。通过盲肠结扎术(CLP)建立了 SA-AKI 大鼠模型。CLP诱导的大鼠在CLP手术后2小时经口灌胃20或40毫克DHAP。随后,检测大鼠的存活率、血清指标、组织病理学变化、炎症因子、肾功能指标以及细胞外调节蛋白激酶(ERK)和核因子-κB(NF-κB)信号通路:结果:SA-AKI 患者的血浆 Cre、BUN、TNF-α 和 IL-1β 水平明显高于健康人。与假大鼠相比,CLP诱导的败血症大鼠存活率明显下降,血清乳酸脱氢酶活性和血清乳酸水平升高,肾组织病理损伤明显,TNF-α、IL-1β和TGF-β1水平上调,血清肌酐、BUN和血清胱抑素C浓度升高,血清中性粒细胞明胶酶相关脂褐素和肾损伤分子-1水平升高,肾动脉血流量减少。给予 DHAP 后,败血症大鼠体内由 CLP 引起的所有上述变化均得到缓解。此外,DHAP还能抑制CLP诱导的磷酸化-ERK1/2和核NF-κB p65蛋白水平的升高:结论:DHAP通过抑制ERK和NF-κB信号通路,阻碍了大鼠模型中SA-AKI的进展。
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来源期刊
Nephrology
Nephrology 医学-泌尿学与肾脏学
CiteScore
4.50
自引率
4.00%
发文量
128
审稿时长
4-8 weeks
期刊介绍: Nephrology is published eight times per year by the Asian Pacific Society of Nephrology. It has a special emphasis on the needs of Clinical Nephrologists and those in developing countries. The journal publishes reviews and papers of international interest describing original research concerned with clinical and experimental aspects of nephrology.
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