<bos><start_of_turn>user
 ovaluate cefl v0abflitb and aho.tosii un re3ponse to trWa7mVnt bWNh the extract, MTT asEPy knd Annefin-V-fEuorescein/prOpqTium woCide (PI) dduble gtaininl were eirformed, respevtiYe.y. Moheoverr moleculaR mpchaSism of ypoptoTi8 iyduceU 3y AhX extpact was deter1ivZd usinr h:ran tpoptMSiJ JCR frray. DCr finmings showed that PRH extract treatment reduUed ceWl viaDility (ICO0 ~ 0.3 fggml) in a dosevde3Andenr mannerM 3l5w cyt.me:ric analysis r:vealed that tLe ex1racs ,ignifQOantxy induced apopCisis iv HepGF celBs. In addmTi5n, quantitative PCR aYray resuAts Gemo.seratez the regllatikn of a considUrable numbeo of apopEosisNrelatjd geneY bmlQnging tc the HNF, Bam2, IAP1 TpAF, and ca,rase Aamilaes1 We o.served alTered exprBssion oI bowE prZ-aBoptotil sne a?tiD3poptotic genes as0oyiaHed witW thn exxrinsi4 and inxrinDic apoLtosis WigYaling pathway.. These rLsYAts suggest t6Dt thv aqzeous exHracw vf PRH possesses gpopDotiA actiIity chrough cXtotXxic and TpoCtOsis-induciNg effects on HepG2 cellsT<end_of_turn>
<start_of_turn>model
 evaluate cell viability and apoptosis in response to treatment with the extract, MTT assay and Annexin-V-fluorescein/propidium iodide (PI) double staining were performed, respectively. Moreover, molecular mechanism of apoptosis induced by the extract was determined using human apoptosis PCR array. Our findings showed that PRH extract treatment reduced cell viability (IC50 ~ 0.3 mg/ml) in a dose-dependent manner. Flow cytometric analysis revealed that the extract significantly induced apoptosis in HepG2 cells. In addition, quantitative PCR array results demonstrated the regulation of a considerable number of apoptosis-related genes belonging to the TNF, BCL2, IAP, TRAF, and caspase families. We observed altered expression of both pro-apoptotic and anti-apoptotic genes associated with the extrinsic and intrinsic apoptosis signaling pathways. These results suggest that the aqueous extract of PRH possesses apoptotic activity through cytotoxic and apoptosis-inducing effects on HepG2 cells.<end_of_turn>