Fuzheng　Qingjie　(FZQJ)　granules,　a　compound　Chinese　medicine,　have　been　used　as　an　adjuvant　therapy　for　alimentary　tract　cancers.　However,　the　underlying　anticancer　mechanisms　are　still　not　well　understood.　In　the　present　study,　HepG2　cells　were　treated　with　FZQJ-containing　serum.　Cell　proliferation　was　evaluated　using　MTT　assay.　Apoptosis　was　analyzed　using　a　flow　cytometer.　Cell　ultrastructure　was　observed　under　a　transmission　electron　microscope.　The　mitochondrial　membrane　potential　(δψ)　was　examined　with　JC-1　dye.　In　H22　tumor-bearing　mice,　CD4+　T　cells,　CD8+　T　cells,　CD3+　T　cells,　and　natural　killer　(NK)　cells　in　peripheral　blood　were　evaluated　cytometrically.　Interleukin　(IL)-2　and　tumor　necrosis　factor　(TNF)-α　levels　were　measured　using　radioimmunoassay.The　mRNA　levels　of　Bax　and　Bcl-2　were　examined　by　reverse　transcription-polymerase　chain　reaction.　The　protein　levels　of　Bax,　Bcl-2,　cytochrome　C,　caspase　3　and　9,　PARP,　and　CD69　were　examined　by　Western　blotting.　The　apoptotic　cells　in　tissues　were　observed　using　TUNEL　method.　Alanine　transaminase　(ALT),　aspartate　transaminase　(AST),　blood　urea　nitrogen　(BUN),　and　creatinine　(CRE)　were　detected　by　an　automatic　biochemical　analyzer.　The　results　showed　that　FZQJ-containing　serum　remarkably　inhibited　proliferation　of　HepG2　cells　in　dose-　and　time-dependent　manners,　induced　HepG2　cell　apoptosis　and　caused　a　decrease　of　δψ.　Analysis　of　tumor　tissue　showed　that　FZQJ-induced　apoptosis　was　accompanied　by　downregulation　of　Bcl-2　and　upregulation　of　Bax,　release　of　cytochrome　c,　activation　of　caspase　3　and　9,　and　cleavage　of　PARP.　In　addition,　FZQJ　increased　the　percentages　of　CD4+　T　and　NK　cells,　the　ratio　of　CD4+/CD8+　T　cells　as　well　as　the　levels　of　serum　TNF-α.　FZQJ　also　increased　CD69　expression　in　tumor　tissue.　No　hepatorenal　toxicity　was　observed　in　H22　tumor-bearing　mice.　These　results　indicated　that　FZQJ　could　inhibit　the　growth　of　hepatoma　cells　via　regulating　immune　function　and　inducing　mitochondria　mediated　apoptosis.　©　The　Author(s)　2015.