Endoplasmic reticulum stress and apoptosis via PERK-eIF2α-CHOP signaling in the methamphetamine-induced chronic pulmonary injury

- Severe ERS is involved in MA-induced the chronic pulmonary injury.
- PERK pathway is activated in MA-induced the chronic pulmonary injury.
- ERS-mediated apoptosis via PERK signaling in chronic pulmonary injury by MA.

Methamphetamine (MA) leads to multiple organs lesions and apoptosis. The aim of this study is to investigate if endoplasmic reticulum stress (ERS) - initiated apoptosis is involved in the chronic pulmonary injury induced by MA. In this study, rats were divided into a control group, methamphetamine 5 mg/kg group and methamphetamine 10 mg/kg group. This study found that the protein level of GRP78 is higher in M10 group than in control group. PERK signaling and the relevant apoptosis factors were also activated. Morphological measurements showed that protein BAX and CHOP accumulated in the alveolar epithelium and the alveolar walls with epithelium were damaged and that the number of pulmonary alveoli decreased. The findings showed that ERS and PERK pathway are activated and eventually lead to apoptosis. Severe ERS mediated the apoptosis of alveolar epithelium cells as well as decreasing numbers of pulmonary alveoli.