Fig. 6: NPM downregulated ROS and reduced the apoptosis of HSCs via the Akt pathway. | Cell Death & Disease

Fig. 6: NPM downregulated ROS and reduced the apoptosis of HSCs via the Akt pathway.

From: NPM promotes hepatotoxin-induced fibrosis by inhibiting ROS-induced apoptosis of hepatic stellate cells and upregulating lncMIAT-induced TGF-β2

Fig. 6

CellROX Orange reagent and dihydroethidium were used to label intracellular hydrogen peroxide and superoxide anion. The ROS level and apoptosis of HSCs were detected by flow cytometry. A Flow cytometry results showed that NPM knockdown remarkably reduced hydrogen peroxide and superoxide anion in human LX-2 cells and primary mouse HSCs. B Flow cytometry showed NPM knockdown significantly induced the apoptosis of LX-2 and primary mouse HSCs. C Flow cytometry analysis of primary HSCS isolated from liver tissue of fibrotic mice showed that when VA-lip-siNPM specifically down-regulated the NPM expression of HSC in liver tissue, ROS was up-regulated and apoptosis was increased. When the up-regulated ROS in liver tissue was down-regulated by NAC, the apoptosis of HSC was reduced (n = 3). D Flow cytometry results showed that the ROS inhibitor NAC dose-dependently inhibited CIGB-induced hydrogen peroxide and apoptosis in LX-2 cells. E NAC inhibited CIGB-induced hydrogen peroxide and apoptosis in primary mouse HSCs. F Flow cytometry results showed that NAC reduced MK2206-induced hydrogen peroxide and reduced apoptosis in LX-2 cells. G NAC reduced MK2206-induced hydrogen peroxide and reduced apoptosis in primary mouse HSCs. The data shown are representative of three independent experiments and quantification data were presented as mean ± SEM; MFI mean fluorescence intensity, WT untreated cells, NC negative control, ns non-significant difference, **p < 0.01, ***p < 0.001; T test.

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