Then, the expression of α-SMA and desmin were analyzed in HSCs exposed to hypoxia in the presence or absence of the PPARγ agonist, rosiglitazone (RSG, 50 nM), by western blotting and immunofluorescence. As expected, hypoxia exposure to HSCs alone led to significant PPARγ downregulation and α-SMA and desmin rise, whereas cotreatment with hypoxia and RSG reversed these effects (Figure 2(b)), indicating that PPARγ antagonizes HSCs activation caused by hypoxic stress.