Inflammation and breast cancer prevention by phyllostachys edulis extract

Abstract

Obesity affects roughly one-third of American adults, in which chronic inflammation and lipotoxicity are disorders that are frequently found in conjunction. An estimated 232,340 American women are predicted to be diagnosed with breast cancer (BrCa) in 2013, and 39,620 are expected to die from it. Obesity does not guarantee that a woman will develop BrCa, but it increases her risk of developing it. This dissertation focuses on the potential therapeutic effects of an extract from the bamboo Phyllostachys edulis as related to lipotoxicity-induced inflammation and breast cancer. Bamboo extract (BEX) has previously demonstrated anti-lipotoxic effects. In the present study, which used in vitro cell culture models mimicking lipotoxic conditions, BEX was found to decrease production of the inflammatory cytokines IL-6 and MCP-1, inhibit nuclear translocation of the proinflammatory transcription factors NF-κB and AP-1, and increase activity of the antiinflammatory transcription factors Nrf2 and PPARγ. An in vivo study showed that BEX could also inhibit MCP-1 production in mice when supplemented into a high fat diet. Tricin and 7-O-methyl tricin (7MT) were isolated from BEX, and both compounds had inhibitory effects on lipotoxicity-induced MCP-1 production. On the topic of breast cancer, BEX showed inhibitory effects on multiple BrCa cell lines while showing minimal toxicity to MCF-10A, a non-carcinoma mammary cell line. BEX appeared to induce protective effects in MCF-10A cells by increasing expression of genes involved with DNA damage and repair and inducing antioxidant signaling and activity. BrCa cell lines showed varied responses to inhibition by tricin, 7MT, and other compounds reportedly isolated from P. edulis. BEX did not bind to or activate estrogen receptor alpha at physiological levels. A proteomics study carried out on MCF7 cells treated with BEX, tricin, and 7MT suggested that BEX and its compounds may alter cytoskeletal structures, and inhibit mTOR and IGF-1R signaling.