Effects of epigallocatechin gallate on smoke-induced oxidative stress and apoptosis in rat lung in vivo

Abstract

BACKGROUND: Cigarette smoking is the major risk factor for the development of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) is a rich source of oxidants, and is thought to disrupt the oxidant-antioxidant balance in the lung, thus inducing apoptosis. Epigallocatechin gallate (EGCG), a natural compound found mainly in green tea, is considered as an antioxidant. The aim of this study is to explore the role of EGCG on CS-induced oxidative stress and apoptosis in a rat model of passive smoking. METHODS: Thirty-two male Sprague Dawley rats were randomly divided into four groups: Control, CS alone, EGCG alone, and combination of CS and EGCG. The control group was exposed to sham air, while the CS group was exposed to 4% CS for 1 hour daily. The EGCG and EGCG + CS groups were given EGCG (50 mg/kg; oral gavage) every other day. Rats were sacrificed 56 days later and protein was extracted from lung tissue. Protein expressions of the antioxidant enzyme quinone oxidoreductase 1 (NQO1), and apoptosisrelated protein caspase-3 (total and cleaved) and Bcl-2 were detected by Western analysis. RESULTS: CS exposure alone caused an increase in protein expression of NQO1, Bcl-2 and cleaved-caspase-3 in comparison to control group. EGCG alone increased NQO1 but has no effect on Bcl-2 or caspase-3 (total and cleaved). The combination of EGCG and CS normalized the levels of NQO1 and Bcl-2 protein expression. CONCLUSION: Our data reinforce the defensive role of EGCG against oxidative stress and apoptosis. The protective role of EGCG in reversing apoptosis in the CS-exposed rat lungs is thought to be mediated through induction of antioxidant mechanisms.