Octreotide is a synthetic octapeptide of natural
somatostatin. We aimed to investigate the influence of
Octreotide on
lipopolysaccharide (LPS)-stimulated human pulmonary epithelial cell damage. After stimulated by LPS, BEAS-2B cells were treated with various concentrations of
Octreotide.
CCK-8 assay and LDH kits were to evaluate cell cytotoxicity. ELISA kits were to analyze the levels of inflammatory factors. TUNEL staining was to measure cell apoptosis. Western blot assay was used to assess the expression of apoptosis-related
proteins,
autophagy-related proteins and AKT/mTOR signaling-related
proteins. Then,
3-methyladenine (3-MA) was adopted for treating BEAS-2B cells to determine its effects on
inflammation and apoptosis. Afterward, adding AKT agonist (SC79) or mTOR antagonist (
rapamycin) to explore the impact of
Octreotide on autophagy. Results revealed that
Octreotide notably enhanced cell viability and reduced LDH activity. The levels of inflammatory factors were significantly decreased following
Octreotide treatment. Additionally,
Octreotide attenuated the apoptotic capacity of LPS-induced BEAS-2B cells, led to the up-regulation of Bcl-2
protein level while cut down the
protein levels of Bax and cleaved caspase3. Remarkably, the expression of
autophagy-related protein LC3II/I and
Beclin1 was elevated after
Octreotide administration. Importantly, the suppressive effects of
Octreotide on the
inflammation and apoptosis of LPS-induced BEAS-2B cells was abrogated by 3-MA. Further experiments suggested that
Octreotide downregulated p-AKT and mTOR expression in LPS-stimulated BEAS-2B cells. SC79 addition inhibited autophagy, evidenced by downregulated LC3II/I and
Beclin1 expression while
rapamycin presented the opposite effects. To conclude,
Octreotide activates autophagy to alleviate LPS-induced pulmonary epithelial cell injury by inhibiting the AKT/mTOR signaling.