The aims of the present study were to explore the effects of: (i) scutellarin (Scu) on protein kinase C (PKC) translocation caused by diabetic conditions in diabetic rat thoracic aorta; and (ii) phorbol-12-myristate-13-acetate (PMA) treatment of cultured thoracic aortic smooth muscle cells. Diabetes was induced in rats by streptozotocin and diabetic rats were divided into two groups: (i) an Scu-treated group, administered 0.1 g/kg Scu by gavage; and (ii) an aminoquanidine (AG)-treated group, which received dietary supplementation of 0.1% AG from Week 1 of diabetes induction. After 10 weeks, rats were killed and thoracic aortic smooth muscle cells were isolated and cultured. Cell fractions were obtained by ultracentrifugation and PKC activity was assayed by ELISA, whereas the distribution of PKC was verified by western immunoblotting. The PKC activity in the membrane fraction of thoracic aortic smooth muscle cells was significantly increased in diabetic compared with control rats, whereas the administration of Scu significantly inhibited this increase. Phorbol myristate acetate (100 nmol/L, 10 min) induced the translocation of the PKCα, βI, βII, δ and ε isoforms, whereas 48 h pretreatment of cells with 1 μmol/L Scu significantly inhibited PMA-induced PKCβI, βII and δ translocation. The results of the present study suggest that Scu inhibits the translocation of PKC in vivo and in vitro and may have value as a drug in the treatment of diabetic complications via its inhibition of PKC βI, βII and δ translocation.
© 2011 The Authors. Clinical and Experimental Pharmacology and Physiology © 2011 Blackwell Publishing Asia Pty Ltd.