Traditional Chinese medicine, Qing Ying Tang, ameliorates the severity of acute lung injury induced by severe acute pancreatitis in rats via the upregulation of aquaporin-1

Abstract

Aquaporin-1 (AQP-1) is expressed in lung endothelial cells and regulates water transport; thus, AQP-1 plays an important role in a number of edema-associated lung diseases. Qing Yin Tang (QYT), a traditional Chinese medicine, has been shown to effectively reduce the mortality rate of acute lung injury (ALI) induced by severe acute pancreatitis (SAP). The current study aimed to investigate the detailed mechanisms underlying the effects of QYT on ALI induced by SAP, particularly the effects on the expression levels of AQP-1 in the lung tissue. ALI was established in Wister rats who were subsequently divided into four groups: SHAM, ALI, dexamethasone (DEX) and QYT groups (n=8 per group). In the QYT group, 20 ml/kg QYT was administered by gavage immediately following the induction of SAP. Blood and lung tissues were collected 8 h following the induction of pancreatitis. The lung wet/dry ratio, as well as the levels of blood gases, serum amylase and tumor necrosis factor-α (TNF-α), were measured at 4, 8 and 12 h following SAP-associated ALI induction surgery. The expression levels of AQP-1 in the lung tissue were detected by quantitative polymerase chain reaction, immunohistochemistry and western blot analysis. No statistically significant differences were observed with regard to the levels of serum amylase, wet/dry ratio, partial pressure of oxygen, serum TNF-α and pathological changes in the pulmonary tissue between the QYT and DEX groups; however, a statistically significant difference was observed when compared with the ALI group. The expression levels of AQP-1 significantly increased (P<0.05) and lung edema was alleviated in the QYT and DEX groups, when compared with ALI group. Therefore, the expression level of AQP-1 is associated with pulmonary edema. QYT protects the lungs from injury induced by SAP via the upregulation of AQP-1, which suppresses TNF-α expression.

Emodin ameliorates acute lung injury induced by severe acute pancreatitis through the up‐regulated expressions of AQP1 and AQP5 in lung

“…Many studies have demonstrated that emodin intervention could significantly decrease the production of serum amylase and inflammatory mediators/cytokines in lung tissues, such as TNF-α, IL-6 levels, as well as lower MPO activity. 18,26,27 DEX was a non-specific immune inhibitor, it inhibited gene synthesis of numerous inflammatory mediators and increased the synthesis of anti-inflammatory proteins, its good therapeutic benefit in SAP-associated ALI has been confirmed. 28,29 In this study, emodin and DEX have a similar effect on ALI, and there were no differences between them, which further demonstrated the effectiveness of emodin.…”

“…Emodin, derived from the traditional Chinese medicine, rhubarb, has a long history of use in anti‐inflammation. Many studies have demonstrated that emodin intervention could significantly decrease the production of serum amylase and inflammatory mediators/cytokines in lung tissues, such as TNF‐α, IL‐6 levels, as well as lower MPO activity . DEX was a non‐specific immune inhibitor, it inhibited gene synthesis of numerous inflammatory mediators and increased the synthesis of anti‐inflammatory proteins, its good therapeutic benefit in SAP‐associated ALI has been confirmed .…”

“…Ying Tang, a traditional Chinese medicine, of which the major active ingredient is emodin, as previously described 18,19 it could protect the lungs from injury induced by SAP via up-regulating AQP1, AQP5 and Cav-1 expression. However, as Qing Ying Tang was a compound prescription, the exact protective mechanism in ALI was unclear.…”

“…In addition, it was also reported that emodin could inhibit the production of inflammatory cytokines such as tumor necrosis factor‐α (TNF‐α) . Qing Ying Tang, a traditional Chinese medicine, of which the major active ingredient is emodin, as previously described it could protect the lungs from injury induced by SAP via up‐regulating AQP1, AQP5 and Cav‐1 expression. However, as Qing Ying Tang was a compound prescription, the exact protective mechanism in ALI was unclear.…”

Expression of phosphatidylinositol-3 kinase and effects of inhibitor Wortmannin on expression of tumor necrosis factor-α in severe acute pancreatitis associated with acute lung injury

“…It can develop into acute respiratory distress syndrome (ARDS) without timely intervention. [1] Wu et al [2][3][4] reported that ALI is a kind of medium disease. The activation, invasion and massive release of infl ammatory mediators of neutrophils can cause damage to lung tissue and capillaries, thus aggravaing lung injury.…”