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.