A inflammatory model of RAW264.7 cell induced with lipopolysaccharide （LPS） was established in vitro to study the effects and mechanism of baicalin （BCN） against LPS-induced inflammatory injury in mice. The cellular phagocytic ability， nitric oxide （NO） release， and mRNA expression to inflammatory cytokines and TGF-β/SMAD2 pathways related genes were measured. Experiments in vivo were conducted using different concentrations of baicalin to establish an inflammatory model in BALB/c mice after 7 consecutive days of gastric lavage and intraperitoneal injection of LPS. The spleen index， subgroups and immune balance of T cell in mice were detected. RT-qPCR was used to determine the mRNA expression of inflammatory cytokines and TGF-β/SMAD2 pathways related genes in the spleen. Results showed that baicalin had no effect on inhibiting the proliferation of RAW264.7 cell within the range of 0-25 μg/mL. When the LPS concentration was 1 mg/mL， the survival rate of RAW264.7 cell was 54.55%. Different concentrations of baicalin enhanced the phagocytic ability（P<0.05） and reduced NO release （P<0.05） of RAW264.7 cells. The mRNA expression of inflammatory cytokines related genes increased （P<0.05） while the mRNA expression of TGF-β/SMAD2 pathways related genes decreased after LPS stimulation. The mRNA expression of above genes was reversed after intervention with baicalin. The spleen index of mice significantly increased（P<0.05） after LPS treatment， and different doses of baicalin groups improved this situation（P<0.05）. Results of flow cytometry showed that baicalin improved the differentiation of CD4⁺ and CD8⁺ cells stimulated by LPS， reduced the ratio of CD4⁺/CD8⁺， and restored the imbalance of Th17/Treg balance axis induced by LPS. It is indicated that baicalin alleviates the LPS induced inflammation in mice， and its mechanism may be related to the activation of TGF-β/SMAD2 signaling pathway， the inhibition of inflammatory cytokines expression， and the restoration of Th17/Treg balance axis.