Consistent with previous studies, we found that hypoxia can promote the progress of hepatic fibrosis (Tables 1 and 2 and Figure 1). Meanwhile, the PPARγ agonist rosiglitazone (RSG) significantly antagonized hypoxia-induced development of hepatic fibrosis. Hypoxia resulted in a trend towards increasing serum markers (HA, LN, PIIINP, and C IV), but also elevated fibrosis histological grade. However, the activation of PPARγ ameliorated this effect (Tables 1 and 2 and Figure 1). To examine the possible correlation of PPARγ with hepatic fibrosis, the correlation between the expression levels of PPARγ and other two markers of fibrosis, α-SMA and desmin, was measured. As shown in Figures 1(b)-1(c), PPARγ was negatively correlated with α-SMA and desmin expression (r = −0.78613, P < 0.001, and r = −0.83517, P = 0.017, resp.). These results suggest that PPARγ is associated with hypoxia-induced hepatic fibrosis.