TAILIEUCHUNG - Báo cáo khoa học: Betulinic acid-mediated inhibitory effect on hepatitis B virus by suppression of manganese superoxide dismutase expression

The betulinic acid (BetA) purified fromPulsatilla chinensis(PC) has been found to have selective inhibitory effects on hepatitis B virus (HBV). In hepatocytes from HBV-transgenic mice, we showed that BetA substantially inhibited HBV replication by downregulation of manganese superoxide dismutase (SOD2) expression, with subsequent reactive oxygen species gen-eration and mitochondrial dysfunction. | Betulinic acid-mediated inhibitory effect on hepatitis B virus by suppression of manganese superoxide dismutase expression Dachun Yao1 2 Huawen Li3 Yulan Gou1 4 Haimou Zhang5 Athanasios G. Vlessidis2 Haiyan Zhou4 Nicholaos P. Evmiridis2 and Zhengxiang Liu1 1 InternalMedicine of Tongji Hospital Tongji MedicalCollege Huazhong University of Science and Technology Wuhan China 2 Laboratory of AnalyticalChemistry Department of Chemistry University of Ioannina Greece 3 Department of Nutrition and Food Hygiene Guangdong MedicalCollege China 4 The First Hospitalof Wuhan China 5 Schoolof Life Sciences Hubei University Wuhan China Keywords apoptosis CREB mitochondrial Pulsatilla chinensis reactive oxygen species Correspondence D. Yao and Z. Lin InternalMedicine of Tongji Hospital Tongji MedicalCollege Huazhong University of Science and Technology Wuhan 430030 China Fax 86 27 83662622 Tel 86 27 83662601 E-mail dachun927@ zxliu_tjmu@ Received 3 December 2008 revised 26 February 2009 accepted 27 February 2009 doi The betulinic acid BetA purified from Pulsatilla chinensis PC has been found to have selective inhibitory effects on hepatitis B virus HBV . In hepatocytes from HBV-transgenic mice we showed that BetA substantially inhibited HBV replication by downregulation of manganese superoxide dismutase SOD2 expression with subsequent reactive oxygen species generation and mitochondrial dysfunction. Also the HBV X protein HBx is suppressed and translocated into the mitochondria followed by cytochrome c release. Further investigation revealed that SOD2 expression was suppressed by BetA-induced cAMP-response element-binding protein dephosphorylation at Ser133 which subsequently prevented SOD2 transcription through the cAMP-response element-binding protein-binding motif on the SOD2 promoter. SOD2 overexpression abolished the inhibitory effect of BetA on HBV replication whereas SOD2 knockdown mimicked this effect indicating that .

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