Effects of calcium gluconate on lipopolysaccharide-induced acute lung injury in mice

Lipopolysaccharide (LPS), which can cause acute airway inflammatory reactions, constitutes one of the most common substances to establish acute lung injury (ALI) models in mice. Studies suggest that calcium gluconate offers the possibility of suppressing the immune response, and this study was intended to explore the effects of calcium gluconate on LPS-induced ALI in mice. Mice inhaled with LPS were intraperitoneally injected with calcium gluconate (12.5, 25, 50 mg/kg). IL-1β, IL-6 and TNF-α levels in bronchoalveolar lavage fluid (BALF) were determined by ELISA. The expression of signaling proteins, phosphorylation extracellular regulated protein kinases (p-ERK), was detected using Western Blot in lung tissues. In our study, the release of inflammatory cytokines IL-1β, IL-6 and TNF-α in BALF increased after inhalation of LPS. Post-treatment with calcium gluconate inhibited LPS-induced airway inflammatory injury and the release of inflammatory cytokines. In addition, LPS promoted the expression of signaling protein p-ERK while calcium gluconate was capable of reversing this change. Overall, calcium gluconate inhibits LPS-induced ALI in mice, which may take effects through the inhibition of ERK phosphorylation.

Acute lung injury; Calcium gluconate; Lipopolysaccharide.