It is well known that HSCs are important effectors inducing hepatic fibrosis. Previously, we demonstrated that hypoxia promoted hepatic fibrogenesis through the regulation of PPARγ in vitro. To clarify if HSC is a modulator of this process, HSC was exposed to hypoxic stress with oxygen concentration decreased from 21% to 7% at different time. In comparison to control groups, PPARγ protein level was significantly decreased in a time-dependent manner, accompanied by an obvious increased expression in two markers of fibrosis, α-SMA and desmin (Figure 2(a)). At the same time, based on our observation, the trend reached plateau after 6 hours of hypoxia exposure. These results demonstrated that the early phase of hypoxic stress might cause HSCs activation.