Da-Cheng-Qi decoction improves severe acute pancreatitis-associated acute lung injury by interfering with intestinal lymphatic pathway and reducing HMGB1-induced inflammatory response in rats

Context: Da-Cheng-Qi Decoction (DCQD) has a significant effect on Severe Acute Pancreatitis-Associated Acute Lung Injury (SAP-ALI).Objective: To explore the mechanism of DCQD in the treatment of SAP-ALI based on intestinal barrier function and intestinal lymphatic pathway. Materials and methods: Forty-five Sprague-Dawley rats were divided into three groups: sham operation, model, and DCQD. The SAP model was induced by a retrograde infusion of 5.0% sodium taurocholate solution (1 mg/kg) at a constant rate of 12 mL/h using an infusion pump into the bile-pancreatic duct. Sham operation and model group were given 0.9% normal saline, while DCQD group was given DCQD (5.99 g/kg/d) by gavage 1 h before operation and 1, 11 and 23 h after operation. The levels of HMGB1, RAGE, TNF-a, IL-6, ICAM-1, D-LA, DAO in blood and MPO in lung were detected using ELISA. The expres-sion of HMGB1, RAGE, NF-jB p65 in mesenteric lymph nodes and lung were determined.Results: Compared with SAP group, DCQD significantly reduced the histopathological scoring of pancre-atic tissue (SAP, 2.80 +/- 0.42; DCQD, 2.58 +/- 0.52), intestine (SAP, 3.30 +/- 0.68; DCQD, 2.50 +/- 0.80) and lung (SAP, 3.30 +/- 0.68; DCQD, 2.42 +/- 0.52). DCQD reduced serum HMGB1 level (SAP, 134.09 +/- 19.79; DCQD, 88.05 +/- 9.19), RAGE level (SAP, 5.05 +/- 1.44; DCQD, 2.13 +/- 0.54). WB and RT-PCR showed HMGB1-RAGE path-way was inhibited by DCQD (p < 0.01).Discussion and conclusions: DCQD improves SAP-ALI in rats by interfering with intestinal lymphatic pathway and reducing HMGB1-induced inflammatory response.

Automated summary

The study aimed to explore the mechanism of Da-Cheng-Qi Decoction (DCQD) in treating Severe Acute Pancreatitis-Associated Acute Lung Injury (SAP-ALI), focusing on intestinal barrier function and intestinal lymphatic pathway. The results showed that DCQD improved SAP-ALI in rats by interfering with intestinal lymphatic pathway and reducing HMGB1-induced inflammatory response.