Tetramethylpyrazine mitigates lipopolysaccharide-induced acute lung injury by inhibiting the HMGB1/TLR4/NF-κB signaling pathway in mice.

Background: Tetramethylpyrazine (TMP) possesses anti-inflammatory and antioxidant properties and plays a crucial role in mitigating acute lung injury (ALI). However, the specific underlying mechanisms remain elusive. High mobility group box 1 (HMGB1), a pro-inflammatory factor, can bind to Toll-like receptor 4 (TLR4), activating downstream signaling pathways, which in turn activate nuclear factor kappa-B (NF-κB). This study aims to explore the preventive effects of TMP on lipopolysaccharide (LPS)-induced ALI and its influence on the HMGB1/TLR4/NF-κB signaling pathway. Methods: C57BL/6 mice were randomly divided into a control group (CON group), a model group (LPS group), a heparin (Hep) group, and a TMP group. In the model group, mice received an initial intraperitoneal injection of LPS followed by a second airway injection three hours later to induce ALI. In the TMP group, LPS was administered 30 minutes before the first intraperitoneal injection and followed by intratracheal atomization of LPS. TMP was injected intraperitoneally 30 minutes after the second LPS administration. The Hep group received heparin at 200 IU/kg following the same schedule as the TMP group. Peripheral capillary oxygen saturation (SpO Results: Compared to the control group, the model group showed reduced SpO Conclusions: TMP can alleviate LPS-induced ALI in mice by reducing lung inflammatory response through inhibiting the HMGB1/TLR4/NF-κB pathway.