The Research On Aging Effects Of Endoplasmic Reticulum Stress By The Exposure Of The PM2.5

Objective:Young mice and aged mice were exposed to PM2.5, measure the endoplasmic reticulum stress(ERS) related proteins, and then clarify whether PM2.5 causes endoplasmic reticulum stress and the effect of aging on the endoplasmic reticulum stress.Methods:A total of 24 healthy male C57BL/6 mice were randomly divided into a normal young control group(N1 group), a normal aged control group(N2 group), a young mouse atomized PM2.5 group(Q1 group), and an aged mouse atomized PM2.5 group(L1 group) with 6 mice in each group. The mice in the Q1 group and L1 group were placed into mineral water bottles with the bottom covers removed, and the mouse head stretched out of the bottleneck and the tail was plugged. PM2.5 solution(concentration:1.5 mg/Kg and 40 mg/ml) was added into a medicine cup in an ultrasonic nebulizer and the mice inhaled atomized PM2.5 at once per day for seven consecutive days. Mice in the N1 and N2 groups inhaled atomized normal saline at a same dose by the same method.Seven days later, the mouse right upper lobe was taken for RT-PCR to detect GRP78、IRE1 and caspase12 protein expressions at the transcription levels; and the mouse lower lobe was taken for immunohistochemistry to observe the expressions of p-e IF2α、CHOP and GRP78 proteins.Results:By comparing group Q1 with group N1 and group L1 with group N2, GRP78、IRE1 and caspase12 m RNA levels were significantly up-regulated, p-e IF2α、CHOP and RP78 protein expressions were significantly increased(all P < 0.05). By comparing with group L1, the m RNA expressions of ERS marker protein GRP78, the downstream signaling pathway related proteins IRE1, and the apoptosis-related protein caspase12 in group Q1 were lower. While the immunohistochemistry showed the expressions of p-e IF2α、CHOP and GRP78 proteins were significantly increased in group L1 compared with group Q1.Conclusion : PM2.5 causes lung tissue damage, which activates ERS and downstream signaling pathways. Mice in the aged group were more prone to produce ERS overactivation, which enabled the alveolar epithelial cell apoptosis, etc. The pathogenesis of idiopathic pulmonary fibrosis is unclear, this research is expected to further clarify the pathogenesis and susceptibility of the aged, and providing a certain basis for the prevention and treatment of idiopathic pulmonary fibrosis.