Salidroside Ameliorates Lung Injury Induced by PM2.5 by Regulating SIRT1-PGC-1α in Mice

Objective This study aimed to clarify the intervention effect of salidroside (SAL) on lung injury caused by PM2.5 in mice and illuminate the function of SIRT1-PGC-1 alpha axis. Methods Specific pathogen-free (SPF) grade male C57BL/6 mice were randomly assigned to the following groups: control group, SAL group, PM2.5 group, SAL+PM2.5 group. On the first day, SAL was given by gavage, and on the second day, PM2.5 suspension was given by intratracheal instillation. The whole experiment consist of a total of 10 cycles, lasting 20 days. At the end of treatment, blood samples and lung tissues were collected and analyzed. Observation of pathological changes in lung tissue using inverted microscopy and transmission electron microscopy. The expression of inflammatory, antioxidants, apoptosis, and SIRT1-PGC-1 alpha proteins were detected by Western blotting. Results Exposure to PM2.5 leads to obvious morphological and pathologica changes in the lung of mice. PM2.5 caused a decline in levels of antioxidant-related enzymes and protein expressions of HO-1, Nrf2, SOD2, SIRT1 and PGC-1 alpha, and an increase in the protein expressions of IL-6, IL-1 beta, Bax, caspase-9 and cleaved caspase-3. However, SAL reversed the aforementioned changes caused by PM2.5 by activating the SIRT1-PGC-1 alpha pathway. Conclusion SAL can activate SIRT1-PGC-1 alpha to ameliorate PM2.5-induced lung injury.