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. 2012 Aug 8;7(8):e42490. doi: 10.1371/journal.pone.0042490

Figure 5. CXCL9 and CXCL10 inhibit the expressions of fibrosis associated genes in human HSCs line LX-2 activated with TGF-β and primary HSCs of mice infected with S.japonicum.

Figure 5

LX-2 were co-cultured with TGF-β (2.5 ng/ml) for 12 hours, subsequently stimulated with CXCL9 (2 µg/ml), CXCL10 (4 µg/ml), CXCL11 (2 or 4 µg/ml) or CXCL4 (2 or 4 µg/ml) respectively for 24 hours. Primary HSCs were isolated from mice infected with S.japonicum for 6 weeks. Freshly isolated HSCs were cultured overnight and followed by stimulations of CXCL9 and CXCL10 respectively for 24 hours. (A) Results of Real Time PCR in human HSCs line LX-2 showed that expressions of Col1α1 and Col3α1 were significantly decreased by stimulations of CXCL9 and CXCL10. Expression of α-SMA was deceased by stimulation of CXCL9, but not CXCL10. P values of two tails T-Test statistical analysis were shown. (B) Results of Real Time PCR in human HSCs line LX-2 showed that expressions of Col1α1, Col3α1 and α-SMA were not significantly decreased by stimulations of CXCL11 and CXCL4 (P>0.05). Each treated group (CXCL11 and CXCL4) was compared with TGF- β treated group. (C) In experiments of primary HSCs, results of Real Time PCR showed that expressions of Col1α1, Col3α1 and α-SMA were all inhibited by CXCL9 and CXCL10. Each treated group (CXCL9 and CXCL10) was compared with control group (medium only). One-Way ANOVA statistical analysis (Newman-Keuls Multiple Comparison Test for analysis of two groups) was used. Values (Means±SEM) represented the mean of more than three independent experiments. *, P<0.05; **, P<0.01; ***, P<0.001. NS, no significance.