Baicalin alleviates TNBS‑induced colitis by inhibiting PI3K/AKT pathway activation
Lei Zhu, Hong Shen, Pei‐Qing Gu, Yajun Liu, Lu Zhang, Jia‑Fei Cheng
Abstract
Inflammatory bowel diseases (IBDs) are chronic immunological disorders of the intestinal tract characterized by persistent inflammation. Baicalin, a type of flavonoid, has exhibited a wide range of pharmacological activities, including immunomodulation and anti‑inflammation. However, little is known about the therapeutic role of baicalin in IBD. The aim of the present study was to ascertain whether baicalin could be a therapeutic drug of IBD and investigate its specific mechanisms. In the present study, the results revealed that baicalin not only significantly alleviated TNBS‑induced colitis by reducing the release of IL‑6, TNF‑α and IL‑1β and increasing the level of IL‑10, but promoted the expression of tight‑junction proteins ZO‑1 and β‑catenin, which may have been achieved by blockage of the PI3K/AKT signaling pathway. In vitro, the results demonstrated that baicalin clearly inhibited the release of TNF‑α, IL‑6 and IL‑1β and promoted the expression of IL‑10 in LPS‑induced HT‑29 cells, and significantly decreased LPS‑induced HT‑29 cell apoptosis by blockage of the PI3K/AKT signaling pathway. In conclusion, the present research revealed for the first time that baicalin acted as a therapeutic drug in IBD by suppression of the PI3K/AKT signaling pathway.