Mentha longifolia protects against acetic-acid induced colitis in rats

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• 作者：Hussam A.S. Murad^a ; ^b ; ¹ ; ^{muradha2000@yahoo.com" class="auth_mail" title="E-mail the corresponding author} ; ^{hamurad@kau.edu.sa" class="auth_mail" title="E-mail the corresponding author} ; ^{HussamMurad@med.asu.edu.eg" class="auth_mail" title="E-mail the corresponding author} ; Hossam M. Abdallah^c ; ^d ; ² ; ^{hmafifi2013@gmail.com" class="auth_mail" title="E-mail the corresponding author} ; Soad S. Ali^e ; ³ ; ^{soadshaker@gmail.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Sulfasalazine (PubChem CID ; 5359476) ; Eucalyptol (1 ; 8-Cineole) (PubChem CID ; 2758) ; Acetic acid (PubChem CID ; 176)
• 刊名：Journal of Ethnopharmacology
• 出版年：2016
• 出版时间：22 August 2016
• 年：2016
• 卷：190
• 期：Complete
• 页码：354-361
• 全文大小：3010 K

文摘

Mentha longifolia L (Wild Mint or Habak) (ML) is used in traditional medicine in treatment of many gastrointestinal disorders.

Aim of the study

This study aimed to evaluate potential protecting effect of ML and its major constituent, eucalyptol, against acetic acid-induced colitis in rats, a model of human inflammatory bowel disease (IBD).

Materials and methods

Rats were divided into ten groups (n=8) given orally for three days (mg/kg/day) the following: normal control, acetic acid-induced colitis (un-treated, positive control), vehicle (DMSO), sulfasalazine (500), ML extract (100, 500, 1000), and eucalyptol (100, 200, 400). After 24 h-fasting, two ML of acetic acid (3%) was administered intrarectally. On the fifth day, serum and colonic biochemical markers, and histopathological changes were evaluated.

Results

Colitis significantly increased colonic myeloperoxidase activity and malonaldehyde level, and serum tumor necrosis factor-α, interleukin-6, and malonaldehyde levels while significantly decreased colonic and serum glutathione levels. All treatments (except ML 100, ML 1000, and eucalyptol 100) significantly reversed these changes where eucalyptol (400) showed the highest activity in a dose-dependent manner. The colitis-induced histopathological changes were mild in sulfasalazine and eucalyptol 400 groups, moderate in ML 500 and eucalyptol 200 groups, and severe in ML 100, ML 1000, and eucalyptol 100 groups nearly similar to colitis-untreated rats.

Conclusion

ML (in moderate doses) and eucalyptol (dose-dependently) exerted protective effects against acetic acid-induced colitis in rats possibly through antioxidant and antiinflammatory properties suggesting a potential benefit in treatments of IBD. To our knowledge this is the first report addressing this point.