Abstract
BackgroundIntestinal mucosa barrier dysfunction after burn injury is an important factor for causing mortality of burn patients. The current study established a burn model in rats and used a free radical scavenger edaravone (ED) to treat the rats, so as to investigate the effect of edaravone on intestinal mucosa barrier after burn injury.MethodsAnesthetized rats were subjected to 40% total body surface area water burn immediately, followed by treatment with ED, scrambled antagomir, or antagomiR-320. Intestinal mucosa damage was observed by hematoxylin-eosin staining and graded by colon mucosal damage index (CMDI) score. The contents of total sulfhydryl (TSH), superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) were determined by spectrophotometry. Cell apoptosis, protein relative expression,and the in situ expressions of p-Akt and p-Bad were detected by flow cytometry, Western blotting and immunohistochemistry, respectively. The miR-320 expression was determined by quantitative real-time polymerase chain reaction.ResultsED alleviated intestinal mucosal damage caused by burn injury, down-regulated the levels of MDA, cytochrome C, cleaved caspase-9 and cleaved caspase-3, but up-regulated the levels of TSH, SOD, CAT and Bcl-2. We also found that ED could reduce oxidative stress, inhibit cell apoptosis, increase the expressions of p-Akt, p-Bad and miR-320, and decrease PTEN expression. PTEN was predicted to be the target gene for miR-320, and cell apoptosis could be promoted by inhibiting miR-320 expression.ConclusionED regulates Akt/Bad/Caspase signaling cascade to reduce apoptosis and oxidative stress through up-regulating miR-320 expression and down-regulating PTEN expression, thus protecting the intestinal mucosal barrier of rats from burn injury.
Highlights
Intestinal mucosa barrier dysfunction after burn injury is an important factor for causing mortality of burn patients
The rats were anesthetized by intraperitoneal injection of sodium pentobarbital (50 mg/kg), those in sham group were exposed to water at 25 °C for 15 s, while those in model group, ED group, scrambled group and antago group were exposed to boiled water at 100 °C for 15 s to create the burn model with 40% total body surface area (TBSA)
The HE staining results (Fig. 1b) showed a clear structure of intestinal villi and mucosa and intact epithelial cells in the sham group, in the model group, the intestinal villi were arranged in disorder and some structures were completely destroyed, the epithelial cells were degenerated and necrotic, a large amount of necrotic and exfoliated tissues and mucus were observed in the intestinal cavity of the rats
Summary
Intestinal mucosa barrier dysfunction after burn injury is an important factor for causing mortality of burn patients. The current study established a burn model in rats and used a free radical scavenger edaravone (ED) to treat the rats, so as to investigate the effect of edaravone on intestinal mucosa barrier after burn injury. Physiological barrier injury caused by intestinal damage after burn injury is an important factor for causing the mortality of burn patients (Grimes et al, 2016; Ng et al, 2016). Protecting the function of intestinal mucosal barrier after burn injury could be effective to the prevention and treatment of intestinal infection and multiple organ dysfunctions. ED scavenges free radicals, inhibits lipid peroxidation and alleviates ischemia-reperfusion injury
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