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阿托伐他汀减轻实验性对比剂诱导的急性肾损伤：Toll样受体4/髓样分化因子88信号通路的作用

Atorvastatin attenuates experimental contrast-induced acute kidney injury: a role for TLR4/MyD88 signaling pathway.

作者信息

Yue Rongzheng, Zuo Chuan, Zeng Jing, Su Baihai, Tao Ye, Huang Songmin, Zeng Rui

机构信息

a Department of Nephrology , West China Hospital, School of Clinic Medicine, Sichuan University , Chengdu , PR China.

b Department of Rheumatology and Immunology , West China Hospital, School of Clinic Medicine, Sichuan University , Chengdu , PR China.

出版信息

Ren Fail. 2017 Nov;39(1):643-651. doi: 10.1080/0886022X.2017.1361838.

DOI:10.1080/0886022X.2017.1361838
PMID:28805489
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6447912/
Abstract

OBJECTIVES

To investigate the protective effect of different atorvastatin doses on contrast-induced acute kidney injury and the related mechanism.

METHODS

Healthy male Sprague-Dawley (SD) rats were randomly divided into the blank control group, experimental control group and different-dose atorvastatin groups. A rat model of contrast-induced acute kidney injury was established. We detected changes in serum creatinine (Scr) and blood urea nitrogen (BUN) before and after model establishment, observed and scored renal tubular injury, analyzed rat renal cell apoptosis, and measure the expression of signal pathway proteins and downstream inflammatory factors.

RESULTS

After contrast agent injection, the Scr and BUN levels of the experimental control group were significantly increased, the different doses applied in the atorvastatin group significantly reduced the Scr and BUN levels (p < .05) and ameliorated the contrast-induced acute kidney injury (p < .05) and significantly reduced Toll-like receptor 4 (TLR4), Myeloid differentiation factor 88 (Myd88), and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) protein expression and relative mRNA expression levels (p < .05) and significantly decreased expression levels of downstream inflammatory factors (p < .05).

CONCLUSION

Different atorvastatin doses have protective effects on contrast-induced acute renal tubular injury in rats, possibly by targeting TLR4, suppressing TLR4 expression, regulating the TLR4/Myd88 signaling pathway, and inhibiting the expression of downstream inflammatory factors.

摘要

目的

探讨不同剂量阿托伐他汀对造影剂诱导的急性肾损伤的保护作用及其相关机制。

方法

将健康雄性Sprague-Dawley（SD）大鼠随机分为空白对照组、实验对照组和不同剂量阿托伐他汀组。建立造影剂诱导的急性肾损伤大鼠模型。检测造模前后血清肌酐（Scr）和血尿素氮（BUN）的变化，观察并对肾小管损伤进行评分，分析大鼠肾细胞凋亡情况，并检测信号通路蛋白及下游炎症因子的表达。

结果

注射造影剂后，实验对照组的Scr和BUN水平显著升高，阿托伐他汀组不同剂量均显著降低了Scr和BUN水平（p＜0.05），改善了造影剂诱导的急性肾损伤（p＜0.05），并显著降低了Toll样受体4（TLR4）、髓样分化因子88（Myd88）和核因子κB（NF-κB）蛋白表达及相关mRNA表达水平（p＜0.05），同时显著降低了下游炎症因子的表达水平（p＜0.05）。

结论

不同剂量阿托伐他汀对大鼠造影剂诱导的急性肾小管损伤具有保护作用，可能是通过靶向TLR4、抑制TLR4表达、调节TLR4/Myd88信号通路并抑制下游炎症因子的表达来实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8f5/6447912/0adf741eab91/IRNF_A_1361838_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8f5/6447912/f3ee8b63c58a/IRNF_A_1361838_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8f5/6447912/6b219518d342/IRNF_A_1361838_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8f5/6447912/ade5a1b1a98b/IRNF_A_1361838_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8f5/6447912/0adf741eab91/IRNF_A_1361838_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8f5/6447912/f3ee8b63c58a/IRNF_A_1361838_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8f5/6447912/6b219518d342/IRNF_A_1361838_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8f5/6447912/ade5a1b1a98b/IRNF_A_1361838_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8f5/6447912/0adf741eab91/IRNF_A_1361838_F0004_B.jpg

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