Figure 5 : Effects of the KCa3.1 channel inhibitor Senicapoc in CCl4 induced hepatic injury in wt mice.

From: The calcium-activated potassium channel KCa3.1 is an important modulator of hepatic injury

Figure 5

Pharmacological KCa3.1 inhibition in CCl4 induced liver injury in mice led to increased liver fibrosis compared to wt littermates receiving placebo (A–C) and was similarly to the effects seen in KCa3.1−/− mice. Fibrosis was more severe as shown by Sirius red staining (A+B) and collagen-1 gene expression (C). Senicapoc treatment led to increased HSC activation as shown by immunohistochemiacal staining (D+E), as well as by gene expression levels (F) of surrogate marker α-SMA.