To investigate the effect of salvianolate (SAL) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and the possible mechanism involved.

ALI was induced in mice by intranasal drip of LPS. SAL intervention was performed by intraperitoneal injection of different doses of drugs (15 mg/kg, 30 mg/kg, and 60 mg/kg) 1 h before modeling. Twenty-four hours after modeling, HE staining was used to detect the pathological changes of lung tissue. The wet/dry weight ratio and myeloperoxidase (MPO) activity were measured in lung tissue. The activities of superoxide dismutase (SOD) and catalase (CAT), and the content of malondialdehyde (MDA) were detected by colorimetry in bronchoalveolar lavage fluid (BALF). Levels of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) in BALF were measured by enzyme-linked immunosorbent assay. The expression levels of nuclear factor E2 related factor (Nrf2) and hemo-oxygenase-1 (HO-1) in lung tissue were detected by Western blot.

Compared with the blank control group, the lung tissue structure of the ALI group was damaged, and the lung wet/dry weight ratio significantly increased. The MPO activity was also strengthened in the ALI group (P＜0.01). Compared with the ALI group, SAL pretreatment at a doses of 30 mg/kg and 60 mg/kg significantly improved the pathological changes of lung tissue in mice, and the wet/dry weight ratio and the MPO activity were decreased in those two SAL groups (P＜0.01). Compared with the blank control group, the activities of SOD and CAT in BALF significantly decreased in the ALI group (P＜0.01). Meanwhile, the contents of MDA and inflammatory factors, including TNF-α and IL-1β, were significantly increased in the ALI group (P＜0.01). Compared with the ALI group, the activities of SOD and CAT in BALF of mice in the medium- and high-dose SAL groups were significantly increased (P＜0.01), while the content of MDA was significantly decreased (P＜0.01), and the contents of TNF-α and IL-1β were significantly down-regulated (P＜0.01). The protective effect of SAL was related to the Nrf2/HO-1 signaling pathway. The expression levels of Nrf2 and HO-1 in lung tissue in the ALI group were significantly lower than those in the blank control group (P＜0.01), while the expression levels of Nrf2 and HO-1 in lung tissue in the medium- and high-dose SAL groups were higher than those in the ALI group (P＜0.01). Low-dose SAL pretreatment had no significant effect in improving the pathological condition of lung tissue, oxidative stress injury, or inflammatory response.

SAL can reduce oxidative stress injury in lung tissue and inhibit the local inflammatory response by activating the Nrf2/HO-1 signal pathway, thus alleviating LPS-induced ALI symptoms in mice.