Effect of N-acety-L-cysteine on iopromide-induced injury in renal tubular epithelial HK-2 cells and its underlying mechanisms
10.16571/j.cnki.1008-8199.2019.08.002
- VernacularTitle: N⁃乙酰半胱氨酸对抗碘普罗胺诱导的肾小管上皮细胞损伤的机制研究
- Author:
Yan-ling CHEN
1
,
2
,
3
;
Ting LUO
1
,
2
,
3
;
Xin-yue GAO
1
,
2
,
3
;
Yang CHEN
1
,
2
,
3
;
Xiu-xiang WU
1
,
2
,
3
;
Dong FAN
1
,
2
,
3
;
Han AI
1
,
2
,
3
;
Jun-feng JIN
1
,
2
,
3
;
Xiao-dong ZHUANG
1
,
2
,
3
Author Information
1. Department of Pathophysiology, Zhuhai Campus of Zunyi Medical University, Zhuhai 519041, Guangdong, China
2. Zhuhai Key Laboratory of Fundamental and Applied Research in Traditional Chinese Medicine, Zhuhai Campus of Zunyi Medical University, Zhuhai 519041, Guangdong, China
3. Department of Cardiovasology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, Guangdong, China
- Publication Type:Journal Article
- Keywords:
N-acetylcysteine;
iopromide;
nuclear factor kappa⁃B;
Nod-like receptor protein 3
- From:
Journal of Medical Postgraduates
2019;32(8):791-796
- CountryChina
- Language:Chinese
-
Abstract:
Objective N-acety-L-cysteine (NAC) can attenuate the injury of podocytes and renal tubular epithelial HK-2 cells induced by contrast agents, but its specific action mechanisms needs to be further clarified. In this study, we investigated the effects of NAC on iopromide (IPM)-induced injury and the NF-κB/NLRP3 signaling pathway in HK-2 cells. Methods Renal tubular epithelial HK-2 cells were divided into seven groups, control, IPM, and IPM + NAC at 2, 4, 8, 16 and 32 mmol/L. After a 24-hour treatment of the HK-2 cells with NAC, CCK-8, DAPI staining, DCFH-DA and Western blot were employed for determination of the viability, apoptosis and morphology of the cells as well as the level of reactive oxygen species (ROS) and the expressions of Bax, Bcl-2, NLRP3, ASC, Caspase-1, IL-1β and NF-κB in the cells. Results Compared with the control, the cells of the IPM group showed a significantly reduced viability ([100 ± 4.749]% vs [48.819 ± 2.045]%, P < 0.05), increased apoptosis, elevated ROS level, and up-regulated expressions of Bax, Bcl-2, NLRP3, ASC, Caspase-1, IL-1β and NF-κB. In comparison with the IPM group, the HK-2 cells treated with NAC at 2, 4, 8, 16 and 32 mmol/L exhibited a remarkably increased viability ([55.398 ± 3.609]%, [58.953 ± 2.859]%, [61.531 ± 5.179]%, [59.845 ± 6.365]% and [59.094 ± 6.285]%) and decreased ROS level and expressions of Bax, Bcl-2, NLRP3, ASC, Caspase-1, IL-1β and NF-κB. The mean fluorescence intensity was significantly higher in the HK-2 cells of the IPM group than in the control cells (5050.85 ± 606.76 vs 1502.17 ± 55.91, P < 0.05), but remarkably decreased in those treated with NAC at 2, 4, 8, 16 and 32 mmol/L (4065.39 ± 106.59, 4162.05 ± 28.93, 3675.71 ± 50.38, 3133.79 ± 66.07 and 2675.80 ± 92.39) (P < 0.05). Conclusion NAC can effectively improve IPM-induced injury of renal tubular epithelial cells, which may be associated with its abilities of inhibiting ROS production and activating the NF-κB/NLRP3 signaling pathway.
