We investigated the biochemical and histopathological effects of
caffeic acid phenethyl ester (CAPE) against oxidative stress causing
lung injury induced by
pneumoperitoneum. Twenty-eight rats were selected at random and seven rats were assigned to each of the following groups. The control group (S) was subjected to a
sham operation without
pneumoperitoneum. The other groups were subjected to CO2
pneumoperitoneum 15 mmHg for 60 min. The laparoscopy group (L) had no additional drugs administered, the laparoscopy + alcohol (LA) group had 1 ml of 70%
ethyl alcohol administered 1 h before the desufflation period, and the laparoscopy + CAPE (LC) group had CAPE administered
at 10 μmol/kg 1 h before the desufflation period. The total oxidative status levels of lung and plasma were significantly increased in the LA group as compared with the LC and S group. When the LC group was compared with the L group, there was a decrease in the level of total
oxidant status and increase in the levels of total
antioxidant status and
paraoxonase in lung tissue. The level of total antioxidative status in the S group was increased compared with the L group in lung tissue and bronchoalveolar lavage fluid. TNF-α and
IL-6 were found significantly elevated in the L group compared with the LC and S groups in bronchoalveolar lavage fluid. There was a similar increase in plasma levels of
IL-6. These results were supported by histopathological examination. CAPE was found to considerably reduce oxidative stress and
inflammation induced by
pneumoperitoneum.