Expression of p16INK4a in the Brain of Animal Model of D-Galactose Induced Aging

Abstract

Aging is a complex natural phenomenon associated with a continuous decline in a number of pathophysiological processes, manifested by degenerative changes in structure and function of cells. Significant amount of data was found to prove that aging process has a strong correlation with the continuously declining antioxidant function, contrasting to the highly accumulating oxidant products and mitochondrial ROS (reactive oxygen species). [1][2][3] Aging has become a global problem, as the aging population continues to increase. How to slow down the aging process is a major challenge in clinical and biological research. Recent study of aging at the molecular level has been comprehensively reviewed worldwide to understand the basic mechanisms of aging as well as the pathophysiological effects and behavior of aging. 4 Animal aging models are important for aging studies, because not all molecular mechanisms can be studied in humans and limitation of ethical problems. Some standard models have been studied including fish, birds, mice, and dogs. 5,6 The use of accelerated aging models are considered common due to the practical conditions of the research project, such as duration and budget. 7,8,9 D-galactose causes oxidative stress in various tissues by increasing the production of ROS and AGEs (Advanced glycation end products) which also occurs in normal aging. Research aging models with administration of D-galactose can moreover be utilized to study aging in the brain.