ABSTRACT
Autophagy is a crucial biological process in eukaryotes, which is involved in cell growth, survival and energy metabolism. It has been confirmed that autophagy mediates toxicity of anticancer drugs, especially in heart, liver and neuron. It is important to understand the function and mechanism of autophagy in anticancer drugs-induced toxicity. Given that autophagy is a double-edged sword in the maintenance of the function of heart, liver and neuron, the autophagy-mediated toxicity are very complicated in the body. We provide a review on the concept of autophagy and current status about autophagy-mediated toxicity of anticancer drugs. The knowledge is crucial in the basic study of anticancer drugs-induced toxicity, and provides some strategies for the development of alleviating the toxicity of anticancer drugs.
ABSTRACT
AIM To observe the effect of artesunate on content of progesterone, estrogen and decidua of pregnant rats and study the efficacy and mechanism of artesunate for termination of early pregnancy. METHODS Serum content of progesterone, estrogen and TNF-α were measured with RIA. The effects of artesunate on the ovary, decidua and fetus of pregnant rats were studied using histochemistry techniques. Decidual cells were estimated using cell culture. RESULTS Artesunate 40 mg*kg-1 sc on day 6-10 of gestation significantly decreased the concentration of serum progesterone in early pregnant rats; decidual cells and fetus of treated groups were found to be degenerated at d 11. Artesunate was shown to directly damage the decidual cells. Cultured human decidual cells were exposed to artesunate for 48 h, the LC50 was found to be 25±3 mL*L-1. CONCLUSION The damage of artesunate on decidua and placenta may be the mechanisms of its contragestational action.