Objective: To investigate the inhibitory effect of shikonin on severe acute pancreatitis (SAP) and associated acute lung injury (ALI) in rats.
Methods: Twenty-four male SD rats were equally randomized into the control group, model group and treatment group. Rats in both model group and treatment group underwent SAP induction by retrograde pancreaticobiliary duct injection of 4% sodium taurocholate, while those in control group underwent a sham operation. Rats in treatment group were administered with shikonin (50 mg/kg) by gavage 2 h before model creation, while rats in the other two groups received vehicle of the same volume by the same fashion. Six hours after operation, rats in each group were sacrificed and the blood samples as well as the pancreatic and lung tissue specimens were collected. The pathological changes in pancreatic and lung tissues were observed, the lung wet/dry weight ratio, the serum levels of TNF-α IL-6, and the expression levels of PI3K, phosphorylated PI3K (p-PI3K) and NF-κB in lung tissue were determined.
Results: No abnormalities were observed in the pancreatic and lung tissues from control group, while evident pathological lesions were found in the pancreatic and lung tissues from either model group or treatment group, but the degrees of pathological changes in both pancreatic and lung tissues from treatment group were milder than those from model group. There were significant differences in the pathological scores for pancreatic and lung tissues among the groups (all P<0.05). The serum levels of TNF-α and IL-6, the lung wet/dry weight ratios, as well as the p-PI3K/PI3K and NF-κB expression levels in the lung tissues in both model group and treatment group were significantly increased compared with control group (all P<0.05), but the changing amplitudes of above variables in treatment group were smaller than those in model group (all P<0.05).
Conclusion: Shikonin has inhibitory effect against both SAP and associated ALI in rats. The mechanism may be related to its reducing the release of inflammatory factors and suppressing the activation of PI3K-Akt-NF-κB pathway in the lung tissue.