Total flavonoids of (P. Beauv.) Spring ameliorates diabetes-induced acute lung injury via activating Nrf2/HO-1.

OBJECTIVES

This investigation explored the mechanism by which the total flavonoids of (P.Beauv.) Spring (TFST) mitigate oxidative stress through the activation of the heme oxygenase-1 (HO-1) signaling pathway mediated by nuclear factor erythroid 2-related factor 2 (Nrf2), thereby ameliorating acute lung injury (ALI) induced by diabetes.

MATERIALS AND METHODS

Male mice weighing 20-25 grams were divided into four groups: a control group, a diabetic group, a diabetic group treated with TFST, and a diabetic group treated with TFST and ML385. Various biological specimens were collected for analysis, including bronchoalveolar lavage fluid (BALF), blood, and tissue samples. These were subjected to a range of assessments covering hematological and BALF parameters tumor necrosis factor-alpha (TNF-α), interleukin-6 [IL-6]), biochemical markers (malondialdehyde [MDA], superoxide dismutase [SOD], glutathione peroxidase [GSH], Nrf2, and HO-1 levels), along with histopathological evaluations.

RESULTS

Pre-treatment with TFST demonstrated a significant decrease in pulmonary tissue damage, evidenced by decreased wet-to-dry (W/D) lung ratios (<0.001), reduced lung injury scores (<0.0001), and lower levels of TNF-α, IL-6 (<0.0001), as well as oxidative stress markers like MDA (<0.05). Moreover, there was an elevation in the activity of anti-oxidative enzymes, specifically SOD and GSH (<0.05), coupled with an enhanced expression of Nrf2 and HO-1 in the diabetic group (<0.01).

CONCLUSION

The study findings demonstrate that TFST can suppress oxidative stress by modulating the Nrf2 pathway and up-regulating HO-1 activity, thereby ameliorating diabetes-induced acute lung injury.