Mastitis is a disease involved in
inflammation of breast which affects human and animals.
Wogonin is one bioactive compound from many Chinese
herbal medicines, which have multiple properties, including anti-inflammatory activity. However, the roles of
wogonin in
mastitis progression are largely undefined.
Mastitis models were established using LPS-treated mice and mammary epithelial cells (MECs). Infiltration of inflammatory cells was analyzed by
hematoxylin-
eosin staining and
myeloperoxidase (MPO) activity. Inflammatory
cytokine (TNF-α and IL-1β) levels were detected via ELISA. The phosphorylation and total of Akt and NF-κB levels and content of Nrf2 and HO-1 were measured via western blot. Cell viability was examined by
CCK-8 assay. Oxidative stress was assessed by ROS generation and levels of MDA, GSH, and SOD.
Wogonin attenuated LPS-induced infiltration of inflammatory cells, increase of MPO activity and levels of TNF-α and IL-1β, and activation of the Akt/NF-κB pathway in murine mammary gland tissues, and promoted activation of Nrf2/HO-1 signaling.
Wogonin did not affect MEC viability, but mitigated LPS-induced
inflammation in MECs by reducing TNF-α and IL-1β levels.
Wogonin relieved LPS-induced oxidative stress in MECs through decreasing ROS generation and MDA level and increasing GSH and SOD levels.
Wogonin repressed LPS-induced activation of the Akt/NF-κB pathway in MECs and increased Nrf2/HO-1 signaling activation. Activated Akt/NF-κB signaling or Nrf2/HO-1 signaling inactivation reversed the suppressive effects of
wogonin on LPS-induced
inflammation and oxidative stress in MECs.
Wogonin mitigates LPS-induced
inflammation and oxidative stress of MECs via suppressing activation of the Akt/NF-κB signaling and activating Nrf2/HO-1 pathway, indicating the therapeutic potential of
wogonin in
mastitis.