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Toxicology Mechanisms and Methods 2006

Biochemical and histopathological evidences for beneficial effects of satureja khuzestanica jamzad essential oil on the mouse model of inflammatory bowel diseases.

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Ghazal Ghazanfari
Bagher Minaie
Narges Yasa
Leila Ashtaral Nakhai
Azadeh Mohammadirad
Shekoufeh Nikfar
Gholamreza Dehghan
Vahid Shetab Boushehri
Hamidreza Jamshidi
Reza Khorasani

Sleutelwoorden

Abstract

The essential oil from Satureja Khuzestanica Jamzad (SKEO), an endemic plant from Iran, was evaluated for its activity against inflammatory bowel disease (IBD). SKEO was examined on the experimental mouse model of inflammatory bowel disease, which is acetic acid-induced colitis. Prednisolone was used as the standard drug for comparison. Biochemical, macroscopic, and microscopic examinations of colon were performed. Lipid peroxidation significantly increased in acetic acid-treated mice in comparison to the normal group (4.88 vs. 3.02 mumol/g) and was significantly restored by SKEO (500, 1000, 1500 ppm) and prednisolone treatment. The mean percentage of decreases of lipid peroxidation in SKEO (500, 1000, 1500 ppm)- and prednisolone-treated groups were 10.5, 28.5, 42.85, and 33.33 of control, respectively. The myeloperoxidase activity significantly increased in acetic acid-treated mice in comparison to the normal group (4.1 vs. 0.8 U/g) and significantly restored in SKEO (1000 and 1500 ppm)- and prednisolone-treated groups. The mean percentage of decreases of myeloperoxidase activity in SKEO (1000 and 1500 ppm)- and prednisolone-treated groups were 24.56, 50, and 52.63 of control, respectively. SKEO (1000 and 1500 ppm)- and prednisolone-treated groups showed significantly lower score values of macroscopic and microscopic characters when compared to the acetic acid-treated group. The beneficial effect of SKEO (1500 ppm) was comparable to that of prednisolone. Known antioxidant, antimicrobial, antiinflammatory, and antispasmodic potentials of Satureja Khuzestanica may be the mechanisms by which this plant protects animals against experimentally induced IBD. Proper clinical investigation should be carried out to confirm the activity in human disease.

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