Emodin protects against intestinal and lung injury induced by acute intestinal injury by modulating SP-A and TLR4/NF-κB pathway.

Jingli Qian,Chunfang Ma,Xiaosheng Jin,Guoping Li,Wanru Cai,Jisheng Zheng,Na Jiang

doi:10.1042/bsr20201605

Abstract

Objective: Our aim was to investigate the effect of emodin on intestinal and lung injury induced by acute intestinal injury in rats and explore potential molecular mechanisms.Methods: Healthy male Sprague–Dawley (SD) rats were randomly divided into five groups (n=10, each group): normal group; saline group; acute intestinal injury model group; model + emodin group; model+NF-κB inhibitor pynolidine dithiocarbamate (PDTC) group. Histopathological changes in intestine/lung tissues were observed by Hematoxylin and Eosin (H&E) and terminal deoxynucleotidyl transferase biotin-dUTP nick-end labeling (TUNEL) staining. Serum IKBα, p-IKBα, surfactant protein-A (SP-A) and toll-like receptor 4 (TLR4) levels were examined using enzyme-linked immunosorbent assay (ELISA). RT-qPCR was performed to detect the mRNA expression levels of IKBα, SP-A and TLR4 in intestine/lung tissues. Furthermore, the protein expression levels of IKBα, p-IKBα, SP-A and TLR4 were detected by Western blot.Results: The pathological injury of intestinal/lung tissues was remarkedly ameliorated in models treated with emodin and PDTC. Furthermore, the intestinal/lung injury scores were significantly decreased after emodin or PDTC treatment. TUNEL results showed that both emodin and PDTC treatment distinctly attenuated the apoptosis of intestine/lung tissues induced by acute intestinal injury. At the mRNA level, emodin significantly increased the expression levels of SP-A and decreased the expression levels of IKBα and TLR4 in intestine/lung tissues. According to ELISA and Western blot, emodin remarkedly inhibited the expression of p-IKBα protein and elevated the expression of SP-A and TLR4 in serum and intestine/lung tissues induced by acute intestinal injury.Conclusion: Our findings suggested that emodin could protect against intestinal and lung injury induced by acute intestinal injury by modulating SP-A and TLR4/NF-κB pathway.

Highlights

Acute intestinal injury is a serious but common clinical event, based on the pathological basis of ischemic edema of the intestinal wall and increased permeability of the intestinal mucosa, with or without intra-abdominal hypertension syndrome [1]
We found that emodin not pynolidine dithiocarbamate (PDTC) treatment distinctly elevated the mRNA expression levels of surfactant protein-A (SP-A) (Figure 6A)
Our results showed that emodin could ameliorate the intestinal and lung injury induced by acute intestinal injury in rats

Summary

Introduction

Acute intestinal injury is a serious but common clinical event, based on the pathological basis of ischemic edema of the intestinal wall and increased permeability of the intestinal mucosa, with or without intra-abdominal hypertension syndrome [1]. Studies have confirmed that acute intestinal injury can be caused by a variety of factors (such as trauma, shock, severe infection, sepsis, and excessive fluid resuscitation). If the ischemic edema is not corrected in time, the permeability of the intestinal mucosa would further increase, eventually leading to acute intestinal injury syndrome or even multiple organ dysfunction syndrome (MODS) [2,3]. It has been confirmed that lung is the most vulnerably affected organs by MODS, with a high mortality, of approximately 40% [4–6]. There is currently no effective med License 4.0 (CC BY). Emodin is one of the effective ingredients of rhubarb, which belongs to the class of hydroxyanthraquinones [7–9]

Methods

Results

Conclusion