The Studies On Curcumin Induced-HepG2 Cell Apoptosis

Curcumin is a kind of anticancer dug without toxicity and side effects. It is widely used in cancer prevention and treatment. In this study, we used atomic force microscope (AFM). laser scanning confocal microscope (LSCM), transmission electron microscope (TEM). flow cytometry and QDs labeling technology to investigate the HepG2 cell apoptosis mechanism induced by curcumin. Changes in HepG2 cytoskeleton and CD44 molecule were also investigated because they involved in the cell apoptosis. The results are as follows:1. After being treated with curcumin, HepG2 cell morphology and ultrastructure were changed: cell membrane roughness was declined, cell cycle was arrested at G2 M and cell apoptosis was occurred with mitochondria swelling, mitochondrial membrane potential disorder, intracellular redox unbalance and caspase 3 activation. After being pretreated with NAC, the role of promoting apoptosis of curcumin reduced significantly:The downtrend of mitochondrial membrane potential became gently; the content of caspase 3 was reduced:significantly, the cell apoptosis rate of 30μM group with NAC pretreatment was only 1 5 of the 30μM curcumin group with no NAC pretreated. This study indicated that curcumin was able to induce HepG2 cell apoptosis through ROS mediated-mitochondrial pathway.2. After being treated with curcumin, the expression of CD44 decreased by 25%. By combining the AFM tip modification and the QDs labeling technology, we found the distribution of CD44 molecules was changed. With the increasing of the curcumin concentration, the interaction force between modified-AFM tip and HepG2 cell membrane decreased gradually. In 20μM curcumin-treated group, the force was almost 1/2 of the control group. These demonstrated that HepG2 cell apoptosis had some thing to do with CD44 molecules. The combination of AFM and LSCM is a favorable and convenient method to detect the distribution of surface molecules and investigate the interaction between surface ligand and receptor.3. Cytoskeleton contributes to keeping cell original morphology and supporting cell movement. Our study found HepG2 cytoskeleton was aggregated and rearranged in curcumin-induced apoptosis. Actin filaments and the amount of F-actin were decreased. Meanwhile, the Young's modulus of HepG2 cells was nearly 1/3 of the control group after being treated with 20μM curcumin. This study indicated that cytoskeleton had closely connection with curcumin-induced HepG2 cell apoptosis. Meanwhile, our results demonstrated that there were other modulation of actin homeostasis, not only F-actin stabilization, could affect the cell death program. Simultaneously it might facilitate to develop new anti-cancer drugs that could effectively decrease the actin-dependent cell motility or cell death.In conclusion, curcumin is kind of phytochrome with low toxicity, high efficiency, wide source and low price. It is able to kill hepatumor cells effectively by changing intracellular ROS level, cytoskeleton structure and CD44 molecular expression and distribution. This muti-targets and multi-channel antitumor mechanism of curcumin can contribute to cancer prevention and treatment. It is a kind of anticancer dug with very wide application prospect.