Polydatin alleviates sepsis‑induced acute lung injury via downregulation of Spi‑B

Abstract

Sepsis‑induced acute lung injury (ALI) is related to the dysregulation of inflammatory responses. Polydatin supplement was reported to exhibit anti‑inflammatory effects in several diseases. The present study aimed to investigate the role of polydatin in sepsis‑induced ALI. A cecum ligation and puncture (CLP)‑induced mouse ALI model was established first and the pathological changes of lung tissues were assessed using hematoxylin and eosin staining. Meanwhile, to mimic sepsis‑induced ALI in vitro, pulmonary microvascular endothelial cells (PMVECs) were treated with lipopolysaccharide (LPS). Pro‑inflammatory cytokines levels were measured in lung tissues and PMVECs using ELISA. Reverse transcription‑quantitative PCR was used to measure the mRNA levels of Spi‑B in lung tissues and PMVECs. Moreover, the expression levels of Spi‑B, p‑PI3K, p‑Akt, and p‑NF‑κB in lung tissues and PMVECs were determined using western blotting. The data revealed that polydatin attenuated CLP‑induced lung injury and inhibited sepsis‑induced inflammatory responses in mice. Furthermore, polydatin significantly inhibited the expression of Spi‑B, p‑PI3K, p‑Akt, and p‑NF‑κB in lung tissues of mice subjected to CLP‑induced ALI, while this phenomenon was reversed through Spi‑B overexpression. Consistently, the anti‑inflammatory effect of polydatin was abolished by Spi‑B overexpression. Taken together, the current findings revealed that polydatin alleviated sepsis‑induced ALI via the downregulation of Spi‑B.