Title:SJSZ Glycoprotein (38 kDa) Inhibits Cell Cycle and Oxidative Stress in N-Methyl-N`- nitro-N-nitrosoguanidine-induced ICR Mice
Volume: 13
Issue: 4
Author(s): Jin Lee and Kye-Taek Lim
Affiliation:
Keywords:
SJSZ glycoprotein (38 kDa), CDK4/cyclin D1, CKIs, PCNA
Abstract: The initiation stage of liver cancer is closely related to abnormal cell proliferation as observed for other types of
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%). In this study, the antitumoric mechanism of SJSZ glycoprotein during
the initiation stage in N-Methyl-N`-nitro-N-nitrosoguanidine (MNNG; 40 mg/kg, BW)-induced ICR was investigated. First, 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. The 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 then assessed using Western Blot analysis. The results of
this analysis showed that the 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 addition, the SJSZ glycoprotein (10 mg/kg,
BW)was shown to decrease the expression of cyclin D1/CDK4 and PCNA and increase the expression of CKIs (p53, p21, and p27). The
results in this study indicate that the SJSZ glycoprotein displays anti-oxidative stress and anti-cell proliferation activity in MNNGinduced
ICR.
