Context:　Pregnane　X　receptor　(PXR)　is　an　important　transcriptional　regulator　that　plays　important　roles　in　the　cell　metabolism　and　cell　growth　by　regulating　the　transcriptional　of　a　sort　of　metabolizing　enzymes.　Objective:　To　investigate　whether　rifampicin　effected　HepG2　cells　growth　and　the　inhibition　was　due　to　the　G0/G1　phase　arrest.　Methods:　PXR-knockdown　experiments　using　RNAi　showed　that　the　cell　cycle　phase　arrest　mediated　by　rifampicin　based　on　activation　of　PXR.　The　results　also　indicated　that　cell　phase　arrest　by　rifampicin　could　protect　cells　form　UVB-induced　DNA　damage.　Retinoid　X　receptor　alpha　(RXRα)　expression　level　in　cells　is　another　key　factor　for　cell　cycle　phase　arrest　mediated　by　rifampicin.　Both　over　expression　and　lacking　expression　of　RXRα　in　cell　reduced　the　cell　arrest　efficiency　mediated　by　rifampicin.　In　the　study,　we　found　that　rifampicin　inhibited　HepG2　cells　growth　and　demonstrated　that　the　inhibition　is　due　to　the　G0/G1　phase　arrest　through　flow　cytometry　analysis.　Conclusion:　The　results　showed　that　RXRα　promote　cell　cycle　phase　transition　rate　of　HepG2.　Competitive　bind　of　rifampicin-activated　PXR　with　RXRα　is　one　main　reason　to　arrest　cell　cycle　phase　through　inhibiting　combination　of　RXRα　with　other　partners.　Rifampicin　could　promote　cell　growth　rate　when　RXRα　expressed　more　excessively　than　PXR　in　cells.　©　2011.