Ampelopsin prevents apoptosis induced by H2O2 in MT-4 lymphocytes.

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 (O(2).-) in a concentration-dependent manner. It significantly increased MT-4 cells viability after treatment with H(2)O(2) and inhibited H(2)O(2)-induced DNA laddering. The data from flow cytometry analysis showed that ampelopsin remarkably decreased the percentage of apoptotic cells induced by H(2)O(2). 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 H(2)O(2). 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.