Isorhamnetin alleviates lipopolysaccharide-induced acute lung injury by inhibiting mTOR signaling pathway

Aim: Acute Lung Injury (ALI) is an acute hypoxic respiratory insufficiency caused by various traumatic factors, manifested as progressive hypoxemia and respiratory distress, and lung imaging shows a heterogeneous osmotic outbreak. Isorhamnetin (ISO) is a flavonoid compound isolated and purified from medicinal plants, such as Hippophae rhamnoides L. and Ginkgo, and has multiple pharmacological functions, such as anti-tumor, anti-myocardial hypoxia, and cardiovascular protection. Our previous study has shown that ISO could attenuate lipopolysaccharide (LPS)-induced acute lung injury in mice, but its mechanism is not clear. Methods: In this study, we used LPS-induced mouse and cell models to research the mechanism of ISO alleviating acute lung injury. Results: The results showed that ISO could attenuate the injury of type II alveolar epithelial cells by inhibiting the TLR4/NF-kappa B pathway. Further studies showed that ISO could inhibit the activation of mTOR signal in vivo and in vitro and promote autophagy in alveolar epithelial cells to reduce lung injury caused by LPS. In addition, ISO could inhibit LPS-induced epithelial cell apoptosis. Conclusion: Overall, ISO could suppress injury and apoptosis of epithelial cells and activate autophagy to protect epithelial cells via inhibiting mTOR signal and attenuating LPS-induced acute lung injury in mice.

Automated summary

Isorhamnetin can attenuate the injury of type II alveolar epithelial cells by inhibiting the TLR4/NF-κB pathway, promote autophagy to reduce lung injury caused by LPS, and inhibit LPS-induced epithelial cell apoptosis.