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Apelin‑36 is able to mediate a range of effects on various diseases, and is upregulated in lipopolysaccharide (LPS)‑induced acute lung injury (ALI). However, to the best of our knowledge, whether apelin‑36 is able to regulate LPS‑induced ALI has yet to be investigated. The present study aimed to investigate the role of apelin‑36 in LPS‑induced ALI, and the putative underlying mechanisms. Rats were assigned to one of four treatment groups: The Control group, apelin‑36 group, LPS group and LPS + apelin‑36 group. At 4 h after intratracheal instillation of LPS (5 mg/kg), rats were intraperitoneally treated with 10 nmol/kg apelin‑36. Subsequently, pathological manifestations and the extent of inflammation and apoptosis of the lung tissues were assessed. Untransfected and apoptosis signal‑regulating kinase 1 (ASK1)‑overexpressing Beas‑2B cells were treated with LPS in the absence or presence of apelin‑36, and subsequently the levels of inflammation and apoptosis were assessed. The results obtained showed that the level of apelin‑36 was increased in the bronchoalveolar lavage fluid (BALF) of LPS‑treated rats. Co‑treatment with apelin‑36 alleviated LPS‑induced lung injury and pulmonary edema, reduced the levels of pro‑inflammatory cytokines, including interleukin‑6, monocyte chemoattractant protein‑1 and tumor necrosis factor‑α, in BALF, and inhibited apoptosis in the lung tissues. The presence of apelin‑36 also blocked the activation of LPS‑induced ASK1, p38, c‑Jun N‑terminal kinase and extracellular signal‑regulated kinase in lung tissues. &lt;em&gt;In vitro&lt;/em&gt; studies performed with Beas‑2B cells showed that the addition of apelin‑36 led to an increase in the cell viability of LPS‑induced Beas‑2B cells in a concentration‑dependent manner. Additionally, co‑treatment with 1 &lt;em&gt;µ&lt;/em&gt;M apelin‑36 prevented LPS‑induced inflammation and apoptosis. However, overexpression of ASK1 significantly reversed the inhibitory effects of apelin‑36 on LPS‑induced inflammation and apoptosis. Taken together, the results of the present study demonstrated that apelin‑36 was able to protect against LPS‑induced lung injury both &lt;em&gt;in vivo&lt;/em&gt; and &lt;em&gt;in vitro&lt;/em&gt;, and these actions may be dependent on inhibition of the ASK1/mitogen‑activated protein kinase signaling pathway.

Apelin‑36 protects against lipopolysaccharide‑induced acute lung injury by inhibiting the ASK1/MAPK signaling pathway