Objective: To investigate the effect of baicalin on Phosphatidylinositol 3-kinase/threonine protein kinase/nuclear factor-κB (PI3K/Akt/NF-κB) signaling pathways in cell inflammation models of human colon carcinoma epithelial cell line (HT-29). Method: Tumor necrosis factor-α (TNF-α) and lipopolysaccharides (LPS) were used to induce HT-29 cells and establish cells inflammation models. This experiment was divided into six groups: complete medium was used in the blank control group

without any drug intervention during experiment

the cells in model control group were incubated with hTNF(20 μg·L-1) for 12 h

then incubated with LPS (1 mg·L-1) for 15 h

the cells in positive medicine group were also incubated with salazosulfapyridine (SASP

500 μmol·L-1) for 24 h on the basis of the processing method in model group

cells in baicalin groups were incubated with different doses (1

10

100 μg·L-1) of baicalin for 24 h on the basis of the processing method in model group. MTT assay was used to detect the effect of baicalin (1

10

100 μg·L-1) on cell growth

Western blot was used to measure the effect of baicalin (1

10

100 μg·L-1) on protein expression levels of PI3K

Akt and NF-κB

enzyme linked immunosorbent assay (ELISA) was used to measure the effect of baicalin (1

10

100 μg·L-1) on TNF-α

interleukin (IL)-6 levels in cell supernatant. Result: As compared with the model group

the secretion levels of TNF-α

IL-6

IL-8

and IL-1 in the cell supernatant were reduced in baicalin (1

10

100 μg·L-1) groups and SASP (500 μmol·L-1)group (P<0.05)

and the combined application of these two medicines reduced more secretion of TNF-α

IL-6

IL-8

and IL-1 levels in the cell supernatant (P<0.01). As compared with the model group

the PI3K protein phosphorylation levels

phosphorylated Akt levels and the activated NF-κB levels were reduced in baicalin groups (1

10

100 μg·L-1)

and SASP (500 μmol·L-1) group (P<0.05). As compared with the model group

the cyclooxygenase-2 (Cox-2)

β-catenin

Caspase-9 and FasL protein expression levels were reduced in baicalin (1

10

100 μg·L-1)groups and SASP (500 μmol·L-1) group (P<0.05). Conclusion: Baicalin can reduce HT-29 cell inflammation

inhibit PI3K phosphorylation

down-regulate Akt activation

inhibit the activation of NF-κB

and thus inhibit the secretion of TNF-α

IL-6 and other inflammatory factors to play its anti-inflammatory effect. It suggested that baicalin may play its anti-inflammatory effect by inhibiting the activation of Akt and inhibiting NF-κB signaling pathways.