Endoplasmic reticulum stress within the primary motor cortex in hypobaric hypoxia-induced acute urinary retention.

Purpose: Acute urinary retention (AUR) is a prevalent clinical challenge following rapid exposure to hypobaric hypoxia (HH). Neurons are highly sensitive to HH, and the destruction or damage of primary motor cortex (M1) neurons will lead to micturition dysfunction and subsequent urinary retention. The aim of this study is to elucidate the potential mechanism of HH induced AUR in M1. Methods: Mice were subjected to a simulated HH environment to establish AUR model. ELISA is used to detect inflammatory markers, Nissl and TUNEL staining is used to detect neuronal damage and apoptosis, and western blot is used to detect the expression of endoplasmic reticulum stress (ERS) and apoptosis related proteins. Results: Compared to the normoxic group, mice in the HH group exhibited AUR, characterized by diminished urine output and frequency and increased single voiding volume. Simultaneously, the levels of inflammatory cytokines (IL-1β, IL-6, TNF-α) also significantly increased. Nissl staining and TUNEL staining showed more severe neuronal damage and apoptosis caused by HH. Western blot results confirmed that the increased expression of pro-apoptotic markers caspase-3 and Bax, while decreased expression of anti-apoptotic marker Bcl-2, indicating an increase in neuronal apoptosis. However, administration of endoplasmic reticulum stress inhibitor 4-PBA significantly improved AUR, reduced neuroinflammation, neuronal damage and apoptosis. Conclusion: These findings confirm that ERS plays a key role in HH induced AUR.