SHENG Qing-shou, WANG Wu, GUO Hong-wu. Effect and Mechanism of Dihydroartemisinin on Rats with Primary Liver Cancer[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(14): 150-154.
DOI:
SHENG Qing-shou, WANG Wu, GUO Hong-wu. Effect and Mechanism of Dihydroartemisinin on Rats with Primary Liver Cancer[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(14): 150-154. DOI: 10.13422/j.cnki.syfjx.2014140150.
Effect and Mechanism of Dihydroartemisinin on Rats with Primary Liver Cancer
Objective: To study the antitumous effect and mechanism of different doses of dihydroartemisinin(DHA)on rats with diethylnitrosamine(DEN)-induced liver cancer. Method: One hundred twenty SD rats were randomly divided into the normal group and the model group.The rats in model group were administered DEN intragastrically to induce the liver cancer. Then the 100 modeling rats were divided into 5 groups
20 rats in each group
DHA high dose group(60 mg·kg-1)
middle dose group(30 mg·kg-1)
low dose group(15 mg·kg-1)
endostar group and model group.The expression levels of vascular endothelial growth factor(VEGF)in the tumor tissue of rat were detected with immunohistochemisty.The expression levels of VEGF
vascular endothelial growth factor receptor-2(VEGFR-2)and alpha-fetoprotein(AFP)in the serum of rat were detected by ELISA assay. The indicators of liver function including alanine aminotransferase(ALT)
aspartate aminotransferase(AST)and total bilirubin(TBIL)were detected using automatic biochemical analyzer. The overall survival times of remaining rats in each group were recorded
in order to calculate prolonged survival rate. Result: Compared with normal group
the expression of VEGF was decreased obviously in DHA middle and high dose group. The expressions of VEGF
VEGFR-2
AFP in serum were decreased. The survival time of the remaining rats were delayed significantly. The life-prolonging rate was 19.25% and 12.81%. Conclusion: DHA at doses of 30 mg·kg-1 and 60 mg·kg-1 has therapeutic effects on rats with primary liver cancer and can prolong their survival time. The mechanism may inhibit angiogenesis and metastasis in liver cancer through inhibiting the expression of VEGF and its receptors
thus delaying tumor proliferation process and improving liver function.
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