Protection by Ziziphora clinopoides of acetic acid-induced toxic bowel inflammation through reduction of cellular lipid peroxidation and myeloperoxidase activity.
Inflammatory bowel disease (IBD) is a chronic condition of the intestine with unknown etiology involving multiple immune, genetic and environmental factors. We were interested in examining the effect of a total extract from Ziziphora clinopoides, an Iranian folk herbal medicine, in the prevention and control of experimental mouse IBD. Z. clinopoides was administered (75, 150, 300 mg/kg) through drinking water to mice, which dispensed a toxic dose of acetic acid intrarectally. Prednisolone was used as the standard drug for comparison. Biochemical, macroscopic and microscopic examinations of the colon were performed. Biochemical evaluation of the inflamed colon was carried out using assays of myeloperoxidase (MPO) activity and thiobarbituric acid reacting substances (TBARS) as indicators of free radical activity and cellular lipid peroxidation. Results indicated that the activity of MPO and lipid peroxidation products (TBARS) increased in acetic acid-treated groups, while recovered by pretreatment of animals with Z. clinopoides (75-300 mg/kg) and prednisolone. All doses of Z. clinopoides and prednisolone-treated groups showed significant lower score values of macroscopic and microscopic characters when compared to the acetic acid-treated group. The beneficial effect of Z. clinopoides (300 mg/kg) was comparable to that of prednisolone. It is concluded that Z. clinopoides inhibits acetic acid toxic reactions in the mouse bowel through inhibition of cellular oxidative stress. Proper clinical investigation should be carried out to confirm the same activity in human.
Ghafari
H
H
Department of Toxicology and Pharmacology, Laboratory of Toxicology, Faculty of Pharmacy, and Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Yasa
N
N
Mohammadirad
A
A
Dehghan
G
G
Zamani
M J
MJ
Nikfar
S
S
Khorasani
R
R
Minaie
B
B
Abdollahi
M
M
D019342:Acetic Acid / Q000037:antagonists & inhibitors* / Q000633:toxicity; D000818:Animals; D007202:Indicators and Reagents / Q000633:toxicity*; D015212:Inflammatory Bowel Diseases / Q000139:chemically induced / Q000201:enzymology / Q000517:prevention & control*; D015227:Lipid Peroxidation / Q000187:drug effects*; D051379:Mice; D009195:Peroxidase / Q000378:metabolism*; D008517:Phytotherapy / Q000379:methods*; D028321:Plant Preparations / Q000627:therapeutic use*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D007202:Indicators and Reagents; D028321:Plant Preparations; D017392:Thiobarbituric Acid Reactive Substances; D009195:Peroxidase; D019342:Acetic Acid