Eighty five percent confluent Hela cells were treated with 0, 10, 20 or 50 μM cisplatin, and with 0 or 1 μM PKC β inhibitor, enzastaurin for 24 h, then the expression of PKC β and Bcl-2, the phosphorylation of PKC β (T642). (A) Western blotting assay for PKC β, Bcl-2 and p-PKC β (with GAPDH as an internal control) in the cisplatin-treated Hela cells; (B, C): Ratio of p-PKC β to PKC β, of Bcl-2 to GAPDH in the cisplatin-treated Hela cells; (D) Western blotting assay for PKC β, Bcl-2 and p-PKC β (with GAPDH as the internal control) in the Hela cells, which were treated with cisplatin and enzastaurin; (E, F) Ratio of p-PKC β to PKC β, Bcl-2 to GAPDH in the cisplatin- and enzastaurin-treated Hela cells. Data are mean ± S.E.M. of three independent experiments; ns, no significance; *P<0.05; **P<0.01 or ***P<0.001.