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. 2023 Dec;61(1):144-154.
doi: 10.1080/13880209.2022.2160768.

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

Xiaowen Liu  1 , Lin Yuan  2 , Yishuang Tang  1 , Yue Wu  1 , Jing Kong  1 , Bingduo Zhou  1 , Xiaosu Wang  1 , Min Lin  2 , Yading Li  1 , Gaofan Xu  1 , Yi Wang  1 , Tingting Xu  1 , Cong He  1 , Shengquan Fang  1 , Shengliang Zhu  1
Affiliations

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

Xiaowen Liu et al. Pharm Biol. 2023 Dec.

Abstract

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-α, IL-6, ICAM-1, d-LA, DAO in blood and MPO in lung were detected using ELISA. The expression of HMGB1, RAGE, NF-κB p65 in mesenteric lymph nodes and lung were determined.

Results: Compared with SAP group, DCQD significantly reduced the histopathological scoring of pancreatic 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 pathway 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.

Keywords: Intestinal barrier function; NF-κB p65; traditional Chinese medicine.

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Conflict of interest statement

No potential conflict of interest was reported by the author(s).

Figures

Figure 1.
Figure 1.
Experimental design. Forty-five Sprague-Dawley rats were divided into three groups: SO, SAP and DCQD groups (n = 15). The SAP model was induced by a standard 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. The SO and SAP 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 h, 11 h and 23 h after operation. 24 h after operation, samples were taken for detection.
Figure 2.
Figure 2.
Impact of DCQD on STC-induced pancreatic injury. (A) Images of H&E staining, 200 × magnifications of pancreas tissues of each experimental group. (B) Pathological score of pancreas tissues of each experimental group. ***p < 0.001, compared with the SO group; ###p < 0.001, compared with the SAP group. n = 10–14.
Figure 3.
Figure 3.
Impact of DCQD on SAP-associated lung injury. (A) Images of H&E staining, 200 × magnifications of lung tissues of each experimental group. (B) Pathological score of lung tissues of each experimental group. (C) MPO activity in lung tissues of each experimental group. ***p < 0.001, compared with the SO group; ###p < 0.001, compared with the SAP group. n = 10–14.
Figure 4.
Figure 4.
Impact of DCQD on SAP-associated intestinal injury. (A) Electron microscopic images of intestinal tissue of each experimental group (2 µm). (B) Serum d-LA levels of each experimental group. (C) Serum DAO levels of each experimental group. ***p < 0.001, compared with the SO group; ###p < 0.001, compared with the SAP group. n = 10–14.
Figure 5.
Figure 5.
Impact of DCQD on the expression of HMGB1, RAGE and NF-κB p65 at the mRNA and protein levels in lung tissues. (A) RT-PCR analysis of HMGB1, RAGE and NF-κB p65 mRNA expression in lung tissues. (B) Western blot results of HMGB1, RAGE and NF-κB p65 protein expression in lung tissues. (C) Statistical results of B scanning densitometry. **p < 0.01, ***p < 0.001, compared with the SO group; #p < 0.05, ##p < 0.01, ###p < 0.001, compared with the SAP group. n = 10–14.
Figure 6.
Figure 6.
Impact of DCQD on the levels of inflammatory factors in serum. ELISA data of HMGB1, RAGE, TNF-α, IL-6 and ICAM1 in serum. ***p < 0.001, compared with the SO group; ###p < 0.001, compared with the SAP group. n = 10–14.
Figure 7.
Figure 7.
Impact of DCQD on the levels of inflammatory factors in mesenteric lymph node. RT-PCR analysis of HMGB1, RAGE, TNF-α and ICAM1 mRNA in mesenteric lymph node. ***p < 0.001, compared with the SO group; ###p < 0.001, compared with the SAP group. n = 10–14.
Figure 8.
Figure 8.
DCQD can improve SAP-ALI by improving intestinal barrier function, reducing the translocation of inflammatory factors through intestinal lymphatic pathway and regulating HMGB1 mediated inflammatory response. DCQD: Da-Cheng-Qi decoction; SAP-ALI: severe acute pancreatitis-associated acute lung injury; HMGB1: high mobility group box 1. RAGE: receptor of advanced glycation end products; NF-κB: nuclear factor kappa-B; TNF-α: tumour necrosis factor alpha; DAO: diamine oxidase; d-LA: d-lactate.
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