RESUMEN
Interactions between host and pathogenic microorganisms are common in nature and have a significant impact on host health, often leading to several types of infections. These interactions have evolved as a result of the ongoing battle between the host's defense mechanisms and the pathogens' invasion strategies. In this chapter, we will explore the evolution of host-pathogen interactions, explore their molecular mechanisms, examine the different stages of interaction, and discuss the development of pharmacological treatments. Understanding these interactions is crucial for improving public health, as it enables us to develop effective strategies to prevent and control infectious diseases. By gaining insights into the intricate dynamics between pathogens and their hosts, we can work towards reducing the burden of such diseases on society.
Asunto(s)
Interacciones Huésped-Patógeno , Salud Pública , BiologíaRESUMEN
Breast cancer is one of the leading causes of mortality among women worldwide due to aggressive behavior, early metastasis, resistance to existing chemotherapeutic agent and high mortality rate. Doxorubicin (Dox) is a powerful antitumoral drug. It is one of the most active agents for treatment of breast cancer. The aim of the present study was to evaluate the influence of Dox in apoptosis and oxidative stress in the breast cancer cell lines MCF-10F, MCF-7 and MDA-MB-231. These studies showed that Dox decreased anti-apoptotic Bcl-2 protein expression and affected oxidative stress by increasing hydrogen peroxide production and simultaneously decreasing NF-κB gene and protein expression in MCF-7, a tumorigenic triple-positive cell line. Results also indicated that Dox induced apoptosis by upregulating Bax, caspase-8 and caspase-3 and downregulation of Bcl-2 protein expression. On the contrary, ROS damage decreased by increasing SOD2 gene and protein expression and hydrogen peroxide production with parallel NF-κB protein expression decrease in MDA-MB-231, a tumorigenic triple-negative breast cancer cell line. It can be concluded that Dox activated apoptosis by inducing proteolytic processing of Bcl-2 family, caspases and simultaneously decreased oxidative stress by influencing ROS damage in MCF-7 and MDA-MB-231 cell lines.