An experimental study of emodin assisted early enteral nutrition for the treatment of severe acute pancreatitis.

BACKGROUND/AIMS: Both emodin and early enteral nutrition (EEN) have been affirmed as effective means to restore the intestinal mucosal function and abate the severity of severe acute pancreatitis (SAP). However, whether a combined strategy applying both is more effective than either one alone is still undetermined. In this study, we investigated the feasibility and efficacy of emodin assisted early enteral nutrition (EAEEN) for the treatment of SAP.

METHODOLOGY

Sixty male Wistar rats were randomly divided into four groups (n=15). SAP was induced in all the rats by a retrograde infusion of 5.0% sodium taurocholate into the pancreatic main duct. Rats in group A received no further intervention, group B with emodin alone, group C with early enteral nutrition (EEN) alone, and group D with emodin assisted early enteral nutrition (EAEEN), respectively, all through an enteral nutrition tube incubated after the induction of SAP. 72 hours after SAP induction, all surviving animals were sacrificed to collect blood and tissue samples for the following measurements: serum amylase, tumor necrosis factor-alpha (TNF-alpha), angiotensin II (AngII) and maleic dialdehyde (MDA), intestinal mucosal secretory IgA (SIgA), pancreatic myeloper oxidase (MPO) activity, and the wet-dry weight ratio of pancreatic tissue (pww/dw). The severity of pancreatic destruction was analyzed by pathological grading and scoring. The severity of intestinal mucosal damage was assessed by the wet-dry weight ratio of ileum (iww/dw), plasma D-lactate and plasma endotoxin.

RESULTS

The results of every index in group B, C and D were significantly better than those in group A (P<0.05). Compared with group B and C, group D had significantly reduced levels of serum amylase, TNF-alpha, Ang-II and MDA (P<0.05). Group D also had significantly lowered plasma D-lactate and endotoxin, and decreased pancreatic MPO activity (P<0.05). The pww/dw and iww/dw ratios were decreased, while the SIgA level increased in this group, both with statistical significance (P<0.05). Furthermore, group D had significantly better pancreatic pathologic scores over group B and group C (P<0.05).

CONCLUSIONS

Our results suggested that EAEEN could obviously abate the severity of experimental SAP in rats. This combined strategy was rational, safe and more effective than either EEN or emodin used alone, and has a broad potential for future clinical application.