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. 2020 May 28;24:409–422. doi: 10.1016/j.jare.2020.05.021

Fig. 4.

Fig. 4

Effect of BK on inflammatory signals in podocytes (a) BK stimulated COX-2 protein expression in podocytes. Quiescent podocytes were stimulated with BK (10−7M) for 3, 6, and 24 h, and with PMA (10−6M) and DMSO was used as vehicle and did not exceed 0.1% (10−6 M). Bar graph represents the fold change in COX-2 protein levels (*p-value = 0.008 vs, control; +p-value = 0.05 vs DMSO) and correspond to the average of 3 or more separate experiments. (b) BK stimulated PGE2 release in podocytes. Quiescent podocytes were stimulated with BK (10−7 M) for 3, 6, and 24 h. Bar graph represents the fold change in measured PGE2 levels (*p < 0.001 BK 6 h vs Control, +p < 0.001 BK 24 h vs Control), and is the sum of 3 or more separate experiments. (c) Ibuprofen inhibits BK-stimulated PGE2 release in podocytes. Quiescent podocytes were stimulated with BK (10−7 M) for 6 h in the presence and absence of Ibuprofen (10−6 M). PGE2 levels were measured by EIA. Bar graph represents the fold change in measured PGE2 levels (*p < 0.016 BK 6 h vs Control, +p = 0.016 BK 6 h-IB vs BK 6 h) and is the average of at least 3 separate experiments.