| Abstrak/Abstract |
Chronic obstructive pulmonary disease (COPD) is an incurable disease which causes disability and death. The main
pathogenesis of COPD is oxidative stress due to cigarette smoke which initiates various reactions and lead to lung elastic
fibers destruction. Statins are known to have antioxidant effects and reduce mortality in COPD. We studied the effects of
cigarette smoke exposure cessation and rosuvastatin on oxidative stress and the level of elastic fiber destruction in COPD
model rats. Thirty 10-week old male Sprague-Dawley rats were divided into 2 groups: Control (n=6, did not received
fumigation nor treatment) and Smoking (n=24, received fumigation for 70 days) groups. Afterwards, the smoking group
was divided into 4 groups: Sham, R2, R5,R10, and received 0.9% NaCl, 2.5, 5 and 10 mg/kg/day of rosuvastatin,
respectively. Examination of malondialdehyde (MDA) and desmosine serum were conducted to measure oxidative stress
and elastic fiber degradation level, respectively. After smoke exposure, MDA and desmosine levels of COPD rats were found
to be significantly higher (p=0.000 and 0.000) than controls. The MDA level in Sham, R2, R5 and R10 groups decreased
significantly after therapy (p=0.000; 0.033; 0.015; 0.002). However, the post-treatment desmosine level was increase
significantly in Sham and R2 groups (p=0.006 dan 0.012) and insignificantly (p=0.117 dan 0.278) in the R5 and R10 groups.
It can be concluded that the cessation of exposure to cigarette smoke can reduce oxidative stress, but not elastic
degradation process. The administration of rosuvastatin of 5 or 10 mg/kg/day attenuated elastic degradation process. |
