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. 2013 Feb 14;4(2):e497. doi: 10.1038/cddis.2013.4

Figure 4.

Figure 4

The involvement of ROS-mediated p38/JNK activation during canine AD-induced keratinocyte apoptosis. (a) Treatment with the cATSC extract effectively upregulated the AD-inducing decreased redox scavenger genes, GPx3, SEPN1, TXNL1, SOD1 and SOD2 at the transcriptional level. In contrast, the hydrocortisone aceponate treatment was not effective in normalizing the expression of redox scavenging genes other than SEPN1 and SOD2. (b) The involvement of p38/JNK phosphorylation in AD progression. The canine ATSC extract effectively reversed the AD-induced p38/JNK phosphorylation. (c) The involvement of ROS (1′,7′-Dichlodihydrofluorescein diacetate + DCFDA+) during AD-induced pathogenesis and keratinocyte apoptosis. (d) The cATSC extract effectively scavenged the AD-induced, accumulated ROS and protected against ROS-mediated keratinocyte apoptosis (TUNEL+) (*P<0.05, **P<0.01)