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. 2022 Oct 29;14(2):205–220. doi: 10.1111/jdi.13930

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© 2022 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Suramin treatment suppresses the upregulation of active caspase‐1 and mature IL‐18 in ATP‐stimulated MMCs. (a, b) Quantification of P2X4 (a) and P2X7 (b) mRNA expression in MMCs by real‐time RT‐PCR (n = 4). (c) Analysis of P2X4, (e) P2X7, (g) NLRP3, (i) caspase‐1, and (k) IL‐18 protein expression in MMCs by western blotting analysis. Quantified data for (d) P2X4, (f) P2X7, (h) NLRP3, (j) caspase‐1, and (l) IL‐18 expression (n = 4). Data are presented as mean ± SEM. *P < 0.05, **P < 0.001 vs control group. ^† P < 0.05 vs ATP group. Control, MMCs + vehicle alone; Control(S), MMCs +1 μM suramin; ATP, MMCs +5 mM ATP; ATP(LS), MMCs +5 mM ATP and 0.1 μM suramin; ATP(S), MMCs +5 mM ATP and 1 μM suramin. MMCs, mouse mesangial cells; NLRP3, nucleotide‐binding oligomerization domain‐like receptor family pyrin domain containing 3.