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姜黄素类似物FLLL32可改善坏死性小肠结肠炎中的肠道损伤。

FLLL32, a curcumin analog, ameliorates intestinal injury in necrotizing enterocolitis.

作者信息

Eckert Jeffrey, Scott Brian, Lawrence Shelley M, Ihnat Michael, Chaaban Hala

机构信息

Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City, OK.

Department of Pediatrics, University of Texas Health Science Center at San Antonio, San Antonio, TX.

出版信息

J Inflamm Res. 2017 Jun 14;10:75-81. doi: 10.2147/JIR.S131051. eCollection 2017.

Abstract

BACKGROUND

Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease that primarily affects premature infants. It is characterized by inflammation and leukocyte infiltration that can progress to intestinal necrosis, perforation, systemic inflammatory response, and death. In this study, we examined the effect of FLLL32, a curcumin analog, on an NEC-like neonatal intestinal injury model.

METHODS

NEC was induced in CD-1 mice pups using the Paneth cell ablation and infection model. Pups were divided into sham, NEC, and NEC + FLLL32 groups. At the end of the experiment, pups were euthanized; whole blood and small intestines were harvested. Intestinal inflammatory cytokine profile, in vivo intestinal permeability using serum fluorescein isothiocyanate-dextran, and histological injury scores were compared between the groups.

RESULTS AND CONCLUSION

FLLL32-treated pups had lower intestinal injury, improved intestinal permeability, and lower proinflammatory cytokine profiles compared to those in untreated pups with NEC. These results suggest that FLLL32 plays a protective role in NEC.

摘要

背景

坏死性小肠结肠炎(NEC)是一种主要影响早产儿的毁灭性胃肠道疾病。其特征为炎症和白细胞浸润,可进展为肠坏死、穿孔、全身炎症反应及死亡。在本研究中,我们检测了姜黄素类似物FLLL32对类NEC新生儿肠道损伤模型的影响。

方法

使用潘氏细胞消融和感染模型在CD-1小鼠幼崽中诱导NEC。幼崽被分为假手术组、NEC组和NEC + FLLL32组。实验结束时,对幼崽实施安乐死;采集全血和小肠。比较各组之间的肠道炎性细胞因子谱、使用血清异硫氰酸荧光素-葡聚糖检测的体内肠道通透性以及组织学损伤评分。

结果与结论

与未治疗的NEC幼崽相比,接受FLLL32治疗的幼崽肠道损伤较轻,肠道通透性改善,促炎细胞因子水平较低。这些结果表明FLLL32在NEC中发挥保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2122/5476581/07d34cb32749/jir-10-075Fig1.jpg

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