Epigallocatechin-3-gallate inhibits angiotensin II and interleukin-6-induced C-reactive protein production in macrophages

• Published in: Pharmacological reports 2012-07, Vol.64 (4), p.912-918
• Main Authors: Li, Ming, Liu, Jun-Tian, Pang, Xiao-Ming, Han, Chun-Jie, Mao, Jun-Jun
• Format: Article
• Language: English
• Subjects: angiotensin II; Angiotensin II - genetics; Angiotensin II - metabolism; Anti-Inflammatory Agents - pharmacology; C-reactive protein; C-Reactive Protein - biosynthesis; C-Reactive Protein - genetics; Cardiovascular Diseases - drug therapy; Cardiovascular Diseases - genetics; Cardiovascular Diseases - metabolism; Catechin - analogs & derivatives; Catechin - pharmacology; Cell Line, Tumor; Drug Safety and Pharmacovigilance; epigallocatechin-3-gallate; Humans; Inflammation - drug therapy; Inflammation - genetics; Inflammation - metabolism; interleukin-6; Interleukin-6 - genetics; Interleukin-6 - metabolism; macrophages; Macrophages - drug effects; Macrophages - metabolism; Pharmacotherapy; Pharmacy; Reactive Oxygen Species - metabolism; RNA, Messenger - genetics; Tea; U937 Cells
• ISSN: 1734-1140; 2299-5684
• DOI: 10.1016/S1734-1140(12)70886-1

Consumption of green tea has been associated with health benefits against multiple diseases including cardiovascular diseases. However, the action mechanisms of green tea and its major ingredient epigallocatechin-3-gallate (EGCG) against cardiovascular diseases are still unclear. Emerging evidence has suggested a common role for C-reactive protein (CRP) in the pathogenesis of inflammation and atherosclerosis. Therefore, the effect of EGCG on angiotensin II (Ang II)- and interleukin-6 (IL-6)-induced CRP production in U937 macrophages and the possible mechanisms were observed. U937 macrophages were cultured, and Ang II and IL-6 were used as stimulants for generation of CRP. U937 macrophages were preincubated with EGCG at 1,3,10µM for 1h prior to the stimulation. mRNA expression and protein level were determined by RT-PCR and ELISA, respectively. ROS production was observed by a fluorescence microscope. Pretreatment of macrophages with EGCG prior to the stimulation concentration-dependently inhibited Ang II- and IL-6-induced expression of CRP both in protein and mRNA levels. Meanwhile, EGCG reduced Ang II- and IL-6-stimulated generation of ROS in macrophages. EGCG is able to inhibit Ang II- and IL-6-stimulated CRP expression in macrophages to produce an anti-inflammation by interfering with ROS generation. The finding is helpful to update understanding of anti-atherosclerotic effects of EGCG.