Baicalin attenuates lipopolysaccharide induced inflammation and apoptosis of cow mammary epithelial cells by regulating NF-κB and HSP72

•We investigated the impact of baicalin and its mechanism on inflammation response and apoptosis induced by LPS in CMECs.•Baicalin ameliorates inflammation response and apoptosis of the cell by up-regulating HSP72 and down-regulating NF-κB.•Our study provided a theoretical basis for use of baicalin to treat or prevent cow mastitis in clinical practice.

Baicalin is the main ingredient of traditional Chinese herbal medicine, Scutellaria baicalensis, which has been widely used clinically as an anti-inflammatory agent. However, molecular mechanism of action of this drug is not yet clear. In the present study, the protective mechanism of baicalin against lipopolysaccharide (LPS) induced inflammatory injury in cow mammary epithelial cells (CMECs) was explored. For this purpose, in vitro cultured CMECs were treated with baicalin (10 μg/mL) and LPS (10 μg/mL) for 24 and 12 h, respectively, and the cell viability was measured by using cell counting kit-8 (CCK-8). The results revealed that LPS induced inflammatory responses, as p-p65/p65 and p-IκBα/IκBα ratios and TNF-α and IL-1β production was increased in the CMECs. Both Bcl-2/Bax ratio and cell viability were decreased and caspase-3 cleaved following LPS treatment, indicating apoptosis of CMECs. Moreover, both LPS and baicalin increased HSP72 expression of the CMECs. However, cellular inflammatory responses and apoptosis were significantly reduced in baicalin treated CMECs. In conclusion, baicalin ameliorated inflammation and apoptosis of the CMECs induced by LPS via inhibiting NF-κB activation and up regulation of HSP72.