Jump to Main Content
(-)-Epigallocatechin-3-gallate suppresses cigarette smoke-induced inflammation in human cardiomyocytes via ROS-mediated MAPK and NF-κB pathways
- Yingmin Liang, Mary Sau Man Ip, Judith Choi Wo Mak
- Phytomedicine 2019 v.58 pp. 152768
- Camellia sinensis, Western blotting, acetylcysteine, apoptosis, cardiomyocytes, cardioprotective agents, cardiovascular diseases, catechin, chemokines, cigarettes, enzyme-linked immunosorbent assay, epigallocatechin gallate, flow cytometry, green tea, humans, inflammation, interleukins, leaves, mitochondria, mitogen-activated protein kinase, oxidative stress, reactive oxygen species, smoking (habit), transcription factor NF-kappa B
- Cigarette smoking is the leading cause for the initiation and development of cardiovascular disease (CVD). Oxidative stress and inflammatory responses play important roles in the pathophysiological processes of smoking-induced cardiac injury. (-)-epigallocatechin-3-gallate (EGCG), the most abundant catechin in green tea, which is made from Camellia sinensis leaves, has been reported to possess potent anti-oxidant property.This study aims to investigate whether the antioxidant EGCG could alleviate cigarette smoke medium (CSM)-induced inflammation in human AC16 cardiomyocytes in vitro.Human AC16 cardiomyocytes were pre-treated with EGCG, N-acetyl-L-cysteine (NAC), or specific inhibitors for 30 min before 4% CSM was added. Supernatant was collected for determination of interleukin (IL)-8 by ELISA and cells were collected for flow cytometry, biochemical assays and Western blot analysis.EGCG treatment significantly attenuated CSM-induced oxidative stress as evidenced by reducing intracellular and mitochondrial reactive oxygen species (ROS) generations and preventing antioxidant depletion. EGCG treatment reduced CSM-induced inflammatory chemokine interleukin (IL)-8 productions in the supernatant via the inhibition of ERK1/2, p38 MAPK and NF-κB pathways. EGCG treatment further inhibited CSM-induced cell apoptosis.Taken together, EGCG protected against CSM-induced inflammation and cell apoptosis by attenuating oxidative stress via inhibiting ERK1/2, p38 MAPK, and NF-κB activation in AC16 cardiomyocytes. These findings suggest that EGCG with its antioxidant, anti-inflammatory and anti-apoptotic properties may act as a promising cardioprotective agent against ROS-mediated cardiac injury.