Pharmaceutical Biology (Jan 2018)

Assessing the effect of Mentha longifolia essential oils on COX-2 expression in animal model of sepsis induced by caecal ligation and puncture

  • Abolfazl Dadkhah,
  • Faezeh Fatemi,
  • Azadeh Rasooli,
  • Mohammad Reza Mohammadi Malayeri,
  • Fatemeh Torabi

DOI
https://doi.org/10.1080/13880209.2018.1510972
Journal volume & issue
Vol. 56, no. 1
pp. 495 – 504

Abstract

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Context: Mentha longifolia L. (Lamiaceae), a traditional Iranian plant, possesses antimicrobial and antioxidant activities. Objective: We investigated the potential protective effects of M. longifolia essential oils (E.Os) on caecal ligation and puncture (CLP) induced liver injury. Materials and methods: Wistar Albino rats (n = 50) were grouped as follows: (1) a laparotomy group (LAP); (2) a CLP group (CLP); (3) the treatment groups received orally the E.Os (50 and 100 mg/kg b.w) and indomethacin (2 mg/kg b.w) for 2 weeks. The oxidative stress parameters, liver enzymes and prostaglandin E2 (PGE2) level were measured in liver and plasma tissues. The liver was also harvested for the real time PCR of cyclooxygenase (COX-2) expression following histopathological examinations. Results: The results indicated that the CLP operation significantly increased lipid peroxidation (LP) [1.79-fold], myeloperoxidase (MPO) [2.76-fold], PGE2 [1.56-fold] besides plasma aspartate aminotransferase (AST) [2.4-fold] and alanine aminotransferase (ALT) activities [2.22-fold], while, markedly reduced glutathione (GSH) [0.63-fold] and ferric reducing ability of plasma (FRAP) levels [0.63-fold]. Even COX2 expression significantly increased in the CLP group as compared to the LAP group. Treatments of rats with the E.Os could return all the hepatic and plasma biomarkers to the normal levels. These results were further confirmed by pathological examination on liver indicating that E.Os could successfully improve the CLP-induced liver injuries. Discussion and conclusions: Our findings suggest that E.Os is able to protect liver injuries against sepsis via modulating the oxidative stress parameters concomitant with the suppression of inflammatory reactions such as PGE2 and COX-2.

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