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Fucoidan improves intestinal peristaltic function in rats with postoperative ileus
Baoguo He1, Zhenming Zhu1, Zibin Tian1
1Department of Gastroenterology, the Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266000, China.
Abstract:
The effect of fucoidan on postoperative ileus (POI) has not been studied. In this study, how fucoidan ameliorates POI in a rat POI model was investigated. The results showed that in the model animals, when the first defecation time was prolonged, the amount of food consumed decreased, the small intestinal propulsion rate dramatically slowed, and the motility index (MI%) of the small intestine decreased. In vitro experiments revealed that the contractile response of small intestinal smooth muscle strips to carbachol (CCh) was reduced. Immunohistochemistry revealed evident macrophage infiltration in the intestinal muscularis. However, after oral pretreatment with fucoidan, the time to first defecation decreased, and food intake, the small intestinal propulsion rate, and MI% of the small intestine increased. Additionally, the contractile response of the intestinal strips to CCh became stronger, and macrophage infiltration decreased. Mechanistically, fucoidan alleviated POI by exerting anti-inflammatory and antioxidant effects as well as likely through the TrkB/ERK1/2/Akt signalling pathways. When POI occurred, the expression levels of inflammatory factors in the intestines significantly increased while the phosphorylation of TrkB, ERK1/2, and Akt significantly decreased; malondialdehyde (MDA) levels in the intestines increased but the levels of superoxide dismutase (SOD) and glutathione (GSH) decreased. In contrast, after pretreatment with fucoidan, the expression levels of inflammatory factors decreased; the phosphorylation levels of TrkB, ERK1/2, and Akt increased; the MDA level decreased; and SOD and GSH levels increased. Thus, fucoidan alleviated POI-induced impairment of rat intestinal motility through anti-inflammatory and antioxidant effects possibly associated with the TrkB/ERK1/2 and Akt signalling pathways.
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