糖尿病是一種由於體內胰島素分泌不足或作用不良而導致血糖升高的疾病，此慢性病會造成周邊神經病變，影響周邊神經的傳導。本實驗以大白鼠為研究對象，首先將大白鼠分為兩組，一組以腹腔注射streptozotocin (STZ, 60-80 mg/kg)，破壞其胰臟之β細胞；令另一組腹腔注射生理食鹽水作為對照組。經過4-6 週，測量其血糖。其中注射STZ 的一組，依照血糖改變分為兩組，一組是高血糖(>126mg/dl)，另一組是正常血糖組(<126mg/dl)，並進行行為反應測試神經反應。待實驗結束後，犧牲大白鼠，並取出其背根神經節，以做分析。本實驗針對高血糖之下，是否增加氧化壓力，進而造成DRG 神經細胞之凋亡，此現象是否和內質網路徑或粒線體途徑有關。主要分析幾種內質網壓力的指標蛋白質，包括procaspases-12、BIP、CHOP，以及粒線體途徑的指標蛋白質caspase 3。此外也觀察α-synuclein 是否和高血糖引起神經病變有關。截至目前的結果顯示，高血糖的老鼠之背根神經節有細胞凋亡的發生，內質網壓力及粒線體途徑參與高血糖引起之細胞凋亡。Diabetes Mellitus (DM) is a chronic disease caused by improper use or abnormal production of insulin, which results in elevated plasma glucose levels. Neuropathy in peripheral nervous system is commonly observed in DM patients. The aim of the present study was to investigate the involvement of endoplasmic reticulum (ER) stress and mitochondrial pathway in dorsal root ganglion (DRG) in STZ-injected rats. Male adult Sprague-Dawley rats were randomly divided into two groups, one group was intraperitoneally injected with streptozotocin (STZ, 60-80 mg/kg) to destroy their pancreatic β-cells and the other group was given saline as control. 4-6 weeks after STZ injection, blood glucose level was measured and rats receiving STZ were divided into two groups, one group had elevated blood glucose level (>126 mg/dl), and the other had normal blood glucose level (<126 mg/kg). Behavioral studies were performed to test the nerve conductivity. At the end of experiment, rats were sacrificed and DRG were removed for further analysis. Several hallmark proteins of ER stress and mitochondrial pathway, including procaspases-12, BIP, CHOP, caspase 3, were studied. Furthermore, -synuclein, a protein involved in neurodegeneration was investigated in DRG of STZ-injected rats. My preliminary data show that apoptosis happened in dorsal roots ganglions of STZ-induced DM rats; ER stress and mitochondrial pathway are involved in apoptosis.