DataSheet_1_Low-Dose Aspirin Prevents Kidney Damage in LPS-Induced Preeclampsia by Inhibiting the WNT5A and NF-κB Signaling Pathways.pdf
Preeclampsia (PE) is a serious pregnancy-related disease, and patients usually present with a high inflammatory response. Previous studies have suggested that aspirin (ASP) may have a role in alleviating the pathogenesis of preeclampsia. However, whether ASP can improve kidney damage and the mechanism for improving it is currently unclear. Here we optimized a lipopolysaccharide (LPS)-induced PE mouse model to identify the role of ASP in renal protection. We found that ASP treatment ameliorated LPS-induced renal failure and pathological changes, the tubular injury was significantly attenuated by ASP. Administration of ASP decreased the renal expression of pro-inflammatory factors, resulting in reduced kidney inflammation. The number of GALECTIN-3-positive cells was reduced, and the up-regulation of IL-6 and TNF-α was decreased. In addition, ASP also suppressed renal cell apoptosis and oxidative stress. An in vitro study indicated that ASP relieved LPS-induced HK-2 cell damage by inhibiting WNT5A/NF-κB signaling. Collectively, our data suggest that ASP is a useful therapeutic option for PE-related kidney injury.
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References
- https://doi.org//10.1016/S0140-6736(15)00070-7
- https://doi.org//10.1007/s11906-017-0757-7
- https://doi.org//10.1016/S0140-6736(18)33212-4
- https://doi.org//10.1007/s12026-017-8921-3
- https://doi.org//10.1016/j.bpobgyn.2019.06.005
- https://doi.org//10.1016/j.annfar.2010.02.022
- https://doi.org//10.3389/fphar.2019.01244
- https://doi.org//10.1002/wsbm.1487
- https://doi.org//10.1097/AOG.0b013e3181e9322a
- https://doi.org//10.1055/s-0032-1310527
- https://doi.org//10.1007/s11906-016-0664-3
- https://doi.org//10.1016/j.ejogrb.2020.03.038
- https://doi.org//10.1159/000336662
- https://doi.org//10.1002/pd.5645
- https://doi.org//10.1093/biolre/ioy025
- https://doi.org//10.3390/ijms21144852
- https://doi.org//10.1242/dev.033910
- https://doi.org//10.1038/nri2360
- https://doi.org//10.1016/j.cell.2017.05.016
- https://doi.org//10.1124/pr.117.013896
- https://doi.org//10.1016/bs.pmbts.2017.11.019
- https://doi.org//10.3892/ijmm.2018.3689
- https://doi.org//10.2174/1389203720666190507094441
- https://doi.org//10.3389/fimmu.2016.00378
- https://doi.org//10.1002/jbt.22453
- https://doi.org//10.1007/s10753-019-00988-1
- https://doi.org//10.1007/s11010-020-03804-9
- https://doi.org//10.1038/ncomms13636
- https://doi.org//10.1590/1516-3180.2019.0304.r2.09122019
- https://doi.org//10.3109/14767058.2016.1138102
- https://doi.org//10.1016/j.preghy.2018.06.022
- https://doi.org//10.1016/j.ajog.2016.09.076
- https://doi.org//10.1007/s00018-014-1794-x
- https://doi.org//10.1152/physiolgenomics.00125.2015
- https://doi.org//10.1161/CIRCULATIONAHA.114.013740
- https://doi.org//10.1006/meth.2001.1262
- https://doi.org//10.1111/j.1600-0897.1998.tb00398.x
- https://doi.org//10.1159/000492407
- https://doi.org//10.1007/s00280-020-04164-3
- https://doi.org//10.1111/apha.12764
- https://doi.org//10.1038/35080570
- https://doi.org//10.3109/10641963.2013.783046
- https://doi.org//10.1016/S0140-6736(07)60712-0
- https://doi.org//10.1016/j.ajog.2016.10.016
- https://doi.org//10.1161/HYPERTENSIONAHA.118.11290
- https://doi.org//10.1016/j.preghy.2016.09.004
- https://doi.org//10.1038/bjc.2017.451
- https://doi.org//10.1002/cbin.10551
- https://doi.org//10.1007/s00018-015-2076-y
- https://doi.org//10.1161/HYPERTENSIONAHA.113.01115
- https://doi.org//10.1016/j.preghy.2011.09.004
- https://doi.org//10.1152/ajprenal.00442.2007
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