Ampelopsin, a flavonoid with a wide variety of
biological activities, has been proposed to be a potent
antitumor agent. However, the mechanism by which
Ampelopsin shows anti-
breast cancer activity remains unclear. Therefore, this study will explore the mechanism of
Ampelopsin's anti-
breast cancer activity by culturing MDA-MB-231 and MCF-7
breast cancer cells. Cell Counting Kit-8 (CCK-8) method and plate cloning method were used to detect the proliferation inhibition of
breast cancer cells. Fluorescence microscopy was used to detect mitochondrial membrane potential (
MMP).
2',7'-Dichlorodihydrofluorescein diacetate (
DCFH-DA) method was used to determine the content of intracellular
reactive oxygen species (ROS).
Hoechst 33258 staining was used to detect the apoptotic morphological changes. Transmission electron microscope was used to observe the mitochondrial structure. Western blot was used to detect the
protein expression of Bax and Bcl-2. The results showed that
Ampelopsin could significantly inhibit the proliferation of
breast cancer cells, and promote cells apoptosis. In addition, the occurrence of apoptosis in
breast cancer cells was associated with
mitochondrial dysfunction, including the loss of mitochondrial membrane potential, the production of large amounts of
reactive oxygen species, and the up-regulation of Bax/Bcl-2 expression. In conclusion,
Ampelopsin-induced mitochondria damage leads to loss of mitochondria membrane potential, overproduction of ROS and activation of Bax, increasing mitochondria membrane permeability and ultimately inducing breast cell apoptosis. These findings provided a new perspective on the role of
Ampelopsin in
breast cancer prevention and treatment.