Apple polyphenols extract (APE) improves colon damage in a rat model of colitis

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• 作者：Giuseppe D&rsquo ; Argenio^a ; ^b ; ^{dargenio@unina.it} ; Giovanna Mazzone^a ; Concetta Tuccillo^c ; Maria T. Ribecco^a ; Giulia Graziani^d ; Antonietta G. Gravina^c ; Sergio Caserta^e ; ^f ; Stefano Guido^e ; ^f ; Vincenzo Fogliano^d ; Nicola Caporaso^a ; Marco Romano^c
• 关键词：Apple polyphenols ; Calpain ; Rat colitis ; Tissue transglutaminase
• 刊名：Digestive and Liver Disease
• 出版年：2012
• 期刊代码：79_15908658
• 类别：med
• 出版时间：July, 2012
• 卷：44
• 期：7
• 页码：555-562
• 文件大小：1195 K

摘要

Background and aim

Searching for alternative therapies that are effective, safe and less expensive of those currently used for ulcerative colitis, we investigated the efficacy of a polyphenol extract from apple in rat colitis.

Methods

Rats with trinitrobenzensulphonic acid-induced colitis were treated daily with rectal administration of apple polyphenols 10^鈭? M for 14 days. COX-2, TNF-伪, tissue transglutaminase and calpain in colon mucosa samples were assessed by reverse transcription-polymerase chain reaction and western blot analyses. To ascertain the role of tissue transglutaminase in mucosal healing, wounded rat fibroblasts were incubated with cystamine (a tissue transglutaminase activity inhibitor).

Results

Colitis was associated with increased COX-2, TNF-伪, calpain, and tissue transglutaminase mRNA. The protein expression of COX-2, TNF-伪 and calpain was increased whilst tissue transglutaminase was decreased. Apple extract treatment reduced the severity of colitis (p < 0.05) and restored all the considered biomarkers at the baseline level. Apple polyphenols reduced the degradation of tissue transglutaminase protein occurring through calpain action. Apple polyphenols-treated wounded fibroblast recovered within 24 h showing intense immunoreactivity for tissue transglutaminase.

Conclusion

The efficacy of apple extract is mediated by its effects on COX-2 and TNF-伪. The unbalance between calpain and tissue transglutaminase may play a role in colonic damage and future therapeutic interventions in ulcerative colitis can target this mechanisms.