Kaempferol pretreatment modulates systemic inflammation and oxidative stress following hemorrhagic shock in mice

Kaempferol has been reported as beneficial for both acute and chronic inflammatory diseases. This study aims to investigate whether kaempferol affects systemic inflammation and oxidative stress in the heart, lung, and liver after hemorrhagic shock in mice.

Male C57/BL6 mice underwent hemorrhagic shock (mean arterial pressure of 35 mmHg for 90 min) and were arbitrarily divided into Sham, hemorrhagic shock (HS), and Kae groups (n = 10 in each group). Mice in the Kae groups received a kaempferol (10-mg/kg body weight) injection 12 h prior to (Group Kae PT) or 90 min after (Group Kae T) the initiation of hemorrhagic shock. Plasma proinflammatory cytokines (TNF-α and IL-6), organ myeloperoxidase (MPO) and superoxide dismutase (SOD) activities, and organ malondialdehyde (MDA) concentrations and heme oxygenase-1 (HO-1) expression levels were assessed by enzyme-linked immunosorbent assay (ELISA) or western blot assay.

Compared with the HS group and the Kae T group, pretreatment with kaempferol significantly decreased proinflammatory cytokines TNF-α (P = 0.012 and 0.015, respectively) and IL-6 (P = 0.023 and 0.014, respectively) following hemorrhagic shock. Kae pretreatment reverted MPO, SOD, and MDA to basal levels in the heart, lung, and liver (Ps < 0.05), while the Kae T group showed no significant differences in these biomarkers compared with the HS group (Ps > 0.05). HO-1 expression was significantly increased in the Kae PT group compared with the other groups (P = 0.011 vs. HS group and P = 0.02 vs. Kae T group).

Pretreatment of hemorrhagic shock mice with kaempferol significantly decreased plasma levels of TNF-α and IL-6; reverted MPO, SOD, and MDA in the heart, lung, and liver; and increased expression of HO-1 in the same organs.