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. Author manuscript; available in PMC: 2014 May 23.
Published in final edited form as: Biochem Biophys Res Commun. 2013 Mar 21;434(4):705–709. doi: 10.1016/j.bbrc.2013.03.032

Fig. 1.

Fig. 1

Heterozygosity of or long-term treatment with functional acid sphingomelinase inhibitors reduces the enzyme activity in the lung. Cftr-deficient mice (CF) were crossed with mice lacking acid sphingomyelinase (gene symbol Smpd1) to obtain mice lacking Cftr and heterozygous for acid sphingomyelinase (Cftr−/−/ Smpd1+/−) or treated for 6.5 months with amitriptyline (Ami) or fluoxetine (Fluo) applied via the drinking water. Untreated Cftr or wild-type (wt) mice served as controls. The activity of acid sphingomyelinase was determined in lung extracts by an in vitro enzyme assay. Both, genetic heterozygosity or treatment with functional acid sphingomyelinase inhibitors reduced the activity of acid sphingomyelinase. Data are the mean ± SD with n = 5 per group, ***p < 0.001 compared to wt.