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. 2015 Jun 12;65(8):1333–1346. doi: 10.1136/gutjnl-2014-308553

Figure 7.

Figure 7

Genetic or pharmacological mitochondrial permeability transition pore (MPTP) inhibition abolishes or markedly attenuates biochemical and histological responses of taurolithocholic acid sulfate acute pancreatitis (TLCS-AP), fatty acid ethyl ester (FAEE)-AP and choline-deficient ethionine-supplemented (CDE)-AP. (A) Characteristic elevations in TLCS-AP of serum amylase (U/L), interleukin-6 (pg/mL), pancreatic (P) myeloperoxidase activity (normalised to TLCS-AP in wild type (Wt) at 100) and histology scores (*p<0.05 for all elevations vs sham controls) were all significantly reduced in Ppif−/− or in Wt treated with DEB025 or TRO40303 (†p<0.05 vs TLCS-AP in Wt without treatment). (B) Characteristic elevations in lung (L) myeloperoxidase activity (normalised to TLCS-AP in Wt at 100; *p<0.05 vs sham controls) were significantly reduced in Wt treated with TRO40303 (†p<0.05 vs TLCS-AP in Wt without treatment). (E) Representative histology showing protective effects of Ppif−/− in TLCS-AP, of DEB025 on TLCS-AP in Wt and of Ppif−/− in FAEE-AP and CDE-AP.