Niacin attenuates the production of pro-inflammatory cytokines in LPS-induced mouse alveolar macrophages by HCA2 dependent mechanisms

• Niacin reduced the levels of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β in LPS-challenged mouse alveolar macrophages.
• Niacin inhibited NF-κB activation in LPS-challenged alveolar macrophages.
• Silencing HCA2 abrogated the effect of niacin on the production of pro-inflammatory cytokines induced by LPS.

Niacin has been reported to have potent anti-inflammatory effects in LPS-induced acute lung injury. However, the molecular mechanism of niacin has not been fully understood. The aim of the present study was to investigate the effects of niacin on the production of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β in LPS-induced mouse alveolar macrophages and explore its underlying mechanism. Mouse alveolar macrophages were incubated in the presence or absence of various concentrations of niacin (1, 10, 100 μmol/l) 1 h before LPS (1 μg/ml) challenge. The results showed that niacin reduced the levels of TNF-α, IL-6 and IL-1β in LPS-challenged alveolar macrophages. Furthermore, NF-κB activation was inhibited by niacin through blocking the phosphorylation of NF-κB p65 and IκBα. In addition, silencing HCA2 abrogated the effect of niacin on the production of pro-inflammatory cytokines. These findings suggested that niacin attenuated the LPS-induced pro-inflammatory cytokines possibly mediated by HCA2 in LPS-challenged alveolar macrophages.