SJSZ glycoprotein (38 kDa) inhibits cell cycle and oxidative stress in N- Methyl-N`-nitro-N-nitrosoguanidine-induced ICR mice
Jin Lee and Kye-Taek Lim
AbstractThe initiation stage in the liver cancer closely relates to the abnormal cell proliferation as a same like other carcinogenesis. Recently, we isolated a glycoprotein from Styrax japonica Siebold et al Zuccarini (SJSZ glycoprotein) which consists of a carbohydrate moiety (52.64%) and a protein moiety (47.36%). The antitumoric mechanism of SJSZ glycoprotein at initiation stage in N-Methyl-N`-nitro-N-nitrosoguanidine (MNNG; 40 mg/kg, BW)-induced ICR was investigated. Firstly, we evaluated the activities of lactate dehydrogenase (LDH), alanine aminotransferase (ALT), thiobarbituric acid-reactive substances (TBARS), and activities of antioxidative enzymes [superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT)] in mouse liver tissue and serum. After that, alpha-fetoprotein (AFP), cell cycle-related factors [cyclin D1/ cyclin dependent kinase (CDK) 4], cell cycle inhibitors (CKIs; p53, p21, and p27), and proliferating cell nuclear antigen (PCNA) were assessed using the Western Blot analysis. The results showed that SJSZ glycoprotein (10 mg/kg, BW) decreased the levels of LDH, ALT, TBARS, and the expression of AFP but it increased the activity of hepatic anti-oxidant enzymes (SOD, GPx and CAT). In the cell cycle factors, SJSZ glycoprotein (10 mg/kg, BW) diminished, cyclin D1/CDK4 and PCNA, whereas it increased the expression of CKIs (p53, p21, and p27). The results in this study indicated that SJSZ glycoprotein has a character of anti-oxidative stress and anti-cell proliferation in MNNG-induced ICR.
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