PCB118引言部分.docVIP

Polychlorinated biphenyls 118 (PCB118) induced oxidative stress and MAPK signaling mediates its pro-apoptotic effects in islet beta cells Introduction With the increasing incidence of diabetes and the growing awareness of the medical complication, the study on the pathogenesis of diabetes became a valuable topic. Plenty of research[1] showed that insulin resistance and dysfunction of pancreatic β-cells were the main mechanism of type 2 diabetes mellitus (T2DM). The insulin resistance is initial factor, while the dysfunction of pancreatic β-cells is decisive factor. All of the diabetic patients were associated with dysfunctional β-cells. The apoptosis of β-cells result from internal and external factors directly lead to seriously damage of pancreas. Afterwards deficiency of insulin secretion played an important role in the process of diabetes. However the specific mechanism of β-cells apoptosis is not fully elucidated. Oxidative stress and endoplasmic reticulum stress were two probable theories in the present study stage. Owing to the serious environmental pollution, some nonbiodegradable and bioaccumulative toxic substances such as polychlorinated biphenyls(PCBs) might have a bad influence in endocrine system and immune system. PCBs was synthetic organic compounds which was insulative and antiflaming. The feature of stable chemical property and the ability to resist pyrolysis were principal reason why it could widely used in industrial production. Recent epidemiological studies [2]showed that exposure to environmental toxins was an important factor for the development of T2DM and there was close relationship between diabetes and environmental toxins such as PCBs. The mechanism may be that PCBs induced islet cells apoptosis and insulin secretion capacity was weakened, then diabetes was induced or aggravated. In order to explore the specific mechanism on islet cell apoptosis, our research use rat INS-1 cells as observation subject and treated with PCB118. The results