OBJECTIVE To investigate the mechanism of baicalin in alleviating the intestinal mucosal barrier injury in rats with intraperitoneal infection-induced sepsis through the vitamin D receptor (VDR)/nuclear factor E2-related factor 2 (Nrf2)/haemoglobin oxygenase-1 (HO-1) signalling pathway.

METHODS Twenty-four SD rats were randomly divided into a sham-surgery group, a model group, an ulinastatin group and a baicalin group, with six rats in each group. Sepsis models were established via cecal ligation and puncture (CLP) in rats in each groups except for the sham surgery group. Six hours after modeling, the sham-surgery and the model groups received intraperitoneal saline, while the ulinastatin and baicalin groups were administered ulinastatin at 20, 000 U/kg and baicalin at 100 mg/kg, respectively, via intraperitoneal injection once daily for 5 consecutive days. The histopathological changes in the ileum tissue of rats in each group were observed, and the levels of oxidative stress, inflammatory factors, and the expression of related mRNA and proteins in the VDR/Nrf2/HO-1 signalling pathway were compared.

RESULTS Compared with the sham-surgery group, the model group showed disordered villus arrangement, severe intestinal mucosal atrophy and inflammatory cell infiltration, with necrotic epithelial cell shedding. Additionally, in the model group, the total antioxidant capacity (T-AOC), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) levels reduced, while the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β significantly increased, and the expression of VDR mRNA, Nrf2 mRNA, HO-1 mRNA, and VDR, Nrf2, and HO-1 proteins were downregulated (P < 0.05). Compared with the model group, the ulinastatin group and the baicalin group showed that villus arrangement, intestinal mucosal atrophy and inflammatory cell infiltration got improved, the levels of T-AOC, SOD, and GSH-PX elevated, the levels of TNF-α, IL-6, and IL-1β decreased, and expressions of VDR mRNA, Nrf2 mRNA, HO-1 mRNA, and VDR, Nrf2, and HO-1 proteins were upregulated. Moreover, all indicators in the baicalin group were superior to those in the ulinastatin group (P < 0.05).

CONCLUSION Baicalin can inhibit the expression of inflammatory factors and regulate the balance of oxidative stress in vivo by up-regulating the VDR/Nrf2/HO-1 signaling pathway, thereby alleviate the intestinal mucosal barrier dysfunction caused by intraperitoneal infection-induced sepsis.