Planta Med 2008; 74(3): 252-257
DOI: 10.1055/s-2008-1034317
Pharmacology
Original Paper
© Georg Thieme Verlag KG Stuttgart · New York

Ampelopsin Prevents Apoptosis Induced by H2O2 in MT-4 Lymphocytes

Jiantao Ye1 [*] , Yongyuan Guan2 [*] , Sa Zeng1 , Deyu Liu1
  • 1School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, People’s Republic of China
  • 2Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, People’s Republic of China
Weitere Informationen

Publikationsverlauf

Received: August 23, 2007 Revised: January 13, 2008

Accepted: January 15, 2008

Publikationsdatum:
26. Februar 2008 (online)

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Abstract

Human immunodeficiency virus (HIV) infection can result in oxidative stress through production of reactive oxygen species (ROS). Simultaneously, oxidative stress is able to activate the replication of virus and lead to the apoptosis of T lymphocytes which is the defense of the immune function. Ampelopsin, belonging to the flavonoids, is a purified component from the root of a Chinese medicinal herb. Our previous studies revealed that ampelopsin could protect sensitive cells against HIV-1 infection and reduce HIV-1 antigen P24 expression. In this study, we determined whether ampelopsin, as an antioxidant, has protective effects on oxidant stress-induced apoptosis in MT-4 cells, a CD4 T lymphocyte cell line. The results indicate that ampelopsin scavenged hydroxyl radicals (·OH) and superoxide radicals (O2 .-) in a concentration-dependent manner. It significantly increased MT-4 cells viability after treatment with H2O2 and inhibited H2O2-induced DNA laddering. The data from flow cytometry analysis showed that ampelopsin remarkably decreased the percentage of apoptotic cells induced by H2O2. In addition, activation of caspase-3 was detected during the course of apoptosis induction. Western blot analysis showed that ampelopsin inhibited the cleavage of caspase-3 induced by H2O2. All these findings might shed new light on the understanding of the anti-AIDS functions of ampelopsin by protecting T cells of persons infected with HIV.

References

1 These authors contributed equally to this work.

Prof. Deyu Liu

School of Pharmaceutical Sciences

Sun Yat-sen University

74 Zhongshan 2 Road

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People’s Republic of China

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eMail: liudeyu@mail.sysu.edu.cn