Introduction: Acute lung injury (ALI) is the critical respiratory condition. Syringin with anti-inflammatory and anti-oxidant properties can exhibit the lung protective effects. SIRT1 and STAT6 can exert protective roles against lung injury by inhibiting ferroptosis.
Methods: In the current study, A549 lung epithelial cells were treated with 200 μM HO for 2 h to establish an in vitro ALI model. Then, HO-stimulated A549 cells were treated with syringin to identify the biological role of syringin in ROS-induced ALI. Moreover, HO-stimulated A549 cells were further treated with SIRT1 inhibitor EX527 or ferroptosis activator erastin to elucidate whether syringin could exert protective effects against ROS-induced ALI depending on SIRT1/STAT6 signaling-mediated ferroptosis inhibition.
Results: It was verified that syringin treatment improved the impaired viability and mitigated inflammatory response and oxidative stress of HO-stimulated A549 lung epithelial cells by activating SIRT1/STAT6 signaling pathway. Syringin treatment inhibited the ferroptosis of HO-stimulated A549 lung epithelial cells by activating SIRT1/STAT6 signaling pathway. Treatment with SIRT1 inhibitor EX527 or ferroptosis activator erastin both reversed the alleviating effect of syringin on HO-induced A549 lung epithelial cell injury.
Conclusion: To sum up, syringin treatment alleviates HO-induced lung epithelial cell injury by activating SIRT1/STAT6 signaling pathway to inhibit ferroptosis.
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| http://dx.doi.org/10.1016/j.tice.2024.102698 | DOI Listing |
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