Berberine Inhibition of Fibrogenesis in a Rat Model of Liver Fibrosis and in Hepatic Stellate Cells

Figure 5

Activation of AMPK was responsible for BBR inhibition of HSC activation. (a) BBR dose-dependently activated AMPK signalling in HSC. (b) Suppression of AMPK with Compound C attenuated inhibition of α-SMA, Col1A1, and Col4a3 transcripts by BBR. Cells were treated with BBR alone or in combination with AMPK inhibitor Compound C (25 μM) for 24 hr and then RNA was collected. Expression of α-SMA, Col1A1, and Col4a3 mRNA transcripts was analyzed with RT-qPCR. Significant restoration of α-SMA, Col1A1, and Col4a3 mRNA expression was found when BBR was given in combination with Compound C. (c) Inhibition of AMPK reactivated BBR-treated hHSC. Significant reduction of α-SMA distribution was observed in BBR-treated cells, while recovery of α-SMA was found when BBR was given in combination with AMPK inhibitor Compound C (25 μM). (d) hHSC motility was recovered, when cells were treated with BBR in the presence of Compound C (25 μM). versus control. versus the same treatment in the absence of Compound C.

(a)

(b)

(c)

(d)