Antiproliferative Effect of Schisandrin B on Cardiac Fibroblast via Oxidation Mechanism in Rats

Abstract:

Objective: To probe the oxidative mechanism of schisandrin B (Sch B) on antiproliferation of neonatal rat cardiac fibroblast induced by AngII. Method: Cultured neonatal cardiac fibroblast (CFb) cells were randomly divided into control, AngiotensinⅡ (AngⅡ), 10^-1μmol·L^-1) and three doses of Sch B groups (SchB 1, 10, 30 μmol·L^-1).Trypsin digestion and spectrophotometer method were used to measure superoxide dismutase (SOD) activity and malondialdehyde (MDA) level. Flow cytometry was adopted to test mitochondrial membrane potential level. Laser confocal microscope technology was applied to measure intracellular calcium level. Result: SOD activity and MDA level in AngII group was lower and higher than that of control respectively (P<0.01), Sch B (1-30 μmol·L^-1) elevated SOD activity and drop MDA level of CFb (P<0.05 or P<0.01) respectively.mitochondrial membrane potential (MMP, ΔΨm) was increased (Sch B 10, 30 μmol·L^-1) and calcium intensity was declined (1, 30 μmol·L^-1) after Sch B treatment and have dramatic difference compared with that in AngⅡgroup. Conclusion: Sch B can elevate the free radical scavenging ability via enhancing SOD activity and decrease MDA level in CFb, these effects are related to increasing MMP levels and inhibiting the intracellular calcium concentration, therefore suppressing the generation of oxidized substances related to CFb proliferation.