PT  - JOURNAL ARTICLE
AU  - Meyrem Ozkan
AU  - Aysun Sengul
AU  - Ceyla Eraldemir
AU  - Leman Huseynova
AU  - Firuzan Akar
TI  - Evaluation of antiinflammatory and antioxidant effect of mepenzolate in subacute cigarette exposure mouse model
AID  - 10.1183/13993003.congress-2015.PA3576
DP  - 2015 Sep 01
TA  - European Respiratory Journal
PG  - PA3576
VI  - 46
IP  - suppl 59
4099  - http://erj.ersjournals.com/content/46/suppl_59/PA3576.short
4100  - http://erj.ersjournals.com/content/46/suppl_59/PA3576.full
SO  - Eur Respir J2015 Sep 01; 46
AB  - Aim: Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease mainly caused by tobacco smoke inhalation. We aimed to evaluate antiinflamatory and antioxidant effect of mepenzolate bromide which is a muscarinic antagonist in subacute cigarette exposure mice model.Method: Forty seven healthy 25-40 gram male mices were categorized into 4 groups: (A) control group (n=7), (B) exposed to cigarette smoke (CS) (n=18), and (C) exposed to CS treated with 400 mikrogram/kg/ day mepenzolate group(n=14),( D) treated with 400 mikrogram/kg/ day mepenzolate group (n=8). After 5 weeks, mepenzolate or saline was given to mices during two weeks by inhalation. Mices were anesthetized, broncoalveolar lavage (BAL) was performed, lung tissues was removed. Interleukin-1β (IL1β), macrophage inflammatory protein-1 (MIP 1), tumor necrosis factor alpha (TNF α) measurements were evaluated in BAL fluid and total oxidant and antioxsidant status (TAS-TOS) were measured in lung tissues.Results: We found that cigarettes exposure significantly decreased TAS and increased TOS (p<0,001; p<0,001). TOS and TOS/TAS ratio was significantly improved by using mepenzolat (p<0.05). Furthermore, mepenzolate significantly improved IL 1 β and MIP 1 levels (p<0.05), but not TNF α.Conclusions: Mepenzolate may be a promising therapeutic choice to reduce oxidative effect and to control inflammation due to cigarette exposure.