The Effect of Arbutin on The Expression of Tumor Suppressor P53, BAX/BCL2 Ratio and Oxidative Stress Induced by TertButyl Hydroperoxide in Fibroblast and LNcap Cell Lines

Objective Arbutin (phydroxyphenylβDglucopyranoside) possesses beneficial functions including antioxidant, anti inflammatory, and antitumoral activities. Due to the important role of oxidative stress and apoptosis in the successful treatment of cancer, understanding mechanisms that lead to apoptosis in cancer cells, is essential. The purpose of the current study was to evaluate the effect of arbutin on tertbutyl hydroperoxide (tBHP)induced oxidative stress and the related mechanisms in fibroblast and Lymph Node Carcinoma of the Prostate (LNCaP) cells. Materials and Methods In this experimental study, the LNCaP and fibroblast cell lines were pretreated with arbutin (50, 250 and 1000 μM). After 24 hours, tBHP (30 and 35 μM) was added to the cells. Viability was measured (at 24 and 48 hours) using MTT assay. The antioxidant effect of arbutin was measured by FRAP assay. The mRNA expression of P53 and BAX/BCL2 ratio were measured using quantitative polymerase chain reaction (PCR). The percentage of apoptotic or necrotic cells was determined using a double staining annexin V fluorescein isothiocyanate (FITC) apoptosis detection kit. Results Arbutin pretreatment increased the total antioxidative power and cell viability in the MTT assay and reduced BAX/BCL2 ratio, P53 mRNA expression and necrosis in fibroblasts exposed to the oxidative agent (P 0.001). In addition, our results showed that arbutin can decrease cell viability, induce apoptosis and increase BAX/BCL2 ratio in LNCaP cells at some specific concentrations (P 0.001). ConclusionArbutin as a potential functional βDglucopyranoside has strong ability to selectively protect fibroblasts against tBHPinduced cell damage and induce apoptosis in LNCaP cells.