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. 2021 Feb 25;13(4):6182–6193. doi: 10.18632/aging.202626

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Copyright: © 2021 Chen et al.

This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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DEX alleviated MTX-induced cytotoxicity and inflammatory injury in HT22 cells via NCOA4 mediated ferritinophagy. (A) Representative bands of Western blot analysis for the expression of NCOA4 in HT22 cells treated with NCOA4-siRNA. (B) The cell viability of HT22 cells in MTX, DEX and NCOA4-siRNA group were measured by CCK-8 assay. (C) The activity of LDH in HT22 cells with MTX, DEX and NCOA4-siRNA were measured using LDH assay kit. (D) The levels of IL-1β and (E) TNF-α in HT22 cells with MTX, DEX and NCOA4-siRNA were measured using ELISA. (F) The representative results of apoptotic cells in control, MTX (G), MTX+50ng/mLDEX+NC-siRNA (H), and MTX+50ng/mLDEX+NCOA4-siRNA (J) group were tested by flow cytometry. (K) Flow cytometry analysis of HT22 cells in MTX, DEX and NCOA4-siRNA group. n=3; #p<0.05, vs Control; *p<0.05, vs MTX group; &p<0.05, vs MTX+DEX+NC-siRNA.