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Fig. 8 | Journal of Nanobiotechnology

Fig. 8

From: Exosomes derived from human adipose mesenchymal stem cells ameliorate hepatic fibrosis by inhibiting PI3K/Akt/mTOR pathway and remodeling choline metabolism

Fig. 8

hADMSCs-Exo regulates the choline metabolism, which involved in PI3K/AKT/mTOR signaling pathway to anti-liver fibrosis. A Quantitative analyses of extracellular and intracellular choline content in activated LX-2 cells or incubated with hADMSCs-Exo. B Quantitative analyses of total intracellular betaine, phosphatidylcholine and glycerophosphocholine content. C The mRNA levels of choline metabolism related genes were determined by qRT–PCR in livers of mice. D, E The protein levels of CHPTI were determined by western blotting in the liver tissues of the mice with different treatments and HSCs incubated with hADMSCs-Exo. F, G The expression level of profibrogenic markers (Collagen I, Vimentin and α-SMA) and PI3K/AKT signalling pathway proteins were determined by western blotting in activated LX-2 cells incubated with hADMSCs-Exo and treated (or not treated) with choline or phosphorylcholine. GAPDH was used as a loading control. Exo, exosomes. LFG, liver fibrosis group, REG, regression group. Slc44a1-4, Solute Carrier Family 44 Member. Chka, Choline Kinase Alpha. Chkb, Choline Kinase beta. Pcyt1a, Phosphate Cytidylyltransferase 1A. Pcyt1a, Phosphate Cytidylyltransferase 1B. CHPT1, Choline Phosphotransferase 1. CHPT1, diacylglycerol cholinephosphotransferase 1. PC, phosphorylcholine. Data expressed as the mean ± SEM (n = 3 independent experiments). ns, not significant, *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001

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