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P023. Therapy with FREMS (Frequency Rhythmic Electrical Modulation System)

R. Pola1, M. Massari2, I. Gatto1, I. Giarretta1, G. Costamagna3, 1Catholic University School of Medicine, Medicine, Rome, Italy, 2Catholic University School of Medicine, Surgery, Rome, Italy, 3Catholic University School of Medicine, Endoscopic Surgery, Rome, Italy

Background

Frequency Rhythmic Electrical Modulation System (FREMS) is a recently developed treatment for painful diabetic neuropathy and chronic painful leg ulcers. Among the mechanisms underlying the beneficial effects of this therapy is the enhancement of microvascular blood flow and the modulation of the expression of angiogenic growth factors and cytokines. In this study, we investigated the effects of FREMS in an experimental model of acute inflammatory colitis.

Methods

We used a model of TNBS-induced colitis in guinea pigs. Colitis was induced by trans-anal administration of TNBS (15 mg/250 g of body weight in 30% ethanol) in 14 animals. An additional group of guinea pigs (n = 3) did not received TNBS and was used as normal control. Successful induction of colitis was confirmed in all cases by positive fecal occult blood tests. One week after the induction of colitis, animals were randomized to the FREMS therapy group (n = 7) or the control group (n = 7). After 3 weeks, animals in the FREMS and control group were sacrificed and colons were harvested and used for further analyses.

Results

Treatment with FREMS significantly decreased the severity of TNBS-induced colonic damages, both macroscopically and histologically, as assesed by using established scoring systems that account for parameters of mucosal ulceration and atrophy, edema of the submucosa, inflammatory cell infiltration, and vascular dilatation. The macroscopic score of colonic damage was 2.1 in the FREMS group and 7.5 in the control group (P < 0.01). The histological score of colonic damage was 2.1 in the FREMS group and 6.6 in the control group (P < 0.01). FREMS therapy also normalizes colonic vascularization and increases the number of regenerating nerve fibers, as assessed by GAP43 immunostaining (P < 0.001). Finally, the expression of TNF-alfa, a prototypical inflammatory molecule in inflammatory bowel diseases, in the colon of animals treated with FREMS was more than 3 times lower than in the control group (4.1 vs. 14.8 pg/ml, P < 0.0001).

Conclusion

FREMS has significant beneficial effects in an experimental model of acute inflammatory colitis. It reduces both macroscopic and histological parameters of inflammation, normalizes colon vascularization, increases the number of regenerating nerve fibers, and reduces the expression of TNF-alfa. FREMS merits further investigation as novel therapeutic strategy in inflammatory bowel diseases.