Phyllostachys edulis Compounds Inhibit Palmitic Acid-Induced Monocyte Chemoattractant Protein 1 (MCP-1) Production

Abstract

Background Phyllostachys edulis Carriere (Poaceae) is a bamboo species that is part of the traditional Chinese medicine pharmacopoeia. Compounds and extracts from this species have shown potential applications towards several diseases. One of many complications found in obesity and diabetes is the link between elevated circulatory free fatty acids (FFAs) and chronic inflammation. This study aims to present a possible application of P. edulis extract in relieving inflammation caused by FFAs. Monocyte chemoattractant protein 1 (MCP-1/CCL2) is a pro-inflammatory cytokine implicated in chronic inflammation. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and activator protein 1 (AP-1) are transcription factors activated in response to inflammatory stimuli, and upregulate pro-inflammatory cytokines such as MCP-1. This study examines the effect of P. edulis extract on cellular production of MCP-1 and on the NF-κB and AP-1 pathways in response to treatment with palmitic acid (PA), a FFA.Methodology/Principal FindingsMCP-1 protein was measured by cytometric bead assay. NF-κB and AP-1 nuclear localization was detected by colorimetric DNA-binding ELISA. Relative MCP-1 mRNA was measured by real-time quantitative PCR. Murine cells were treated with PA to induce inflammation. PA increased expression of MCP-1 mRNA and protein, and increased nuclear localization of NF-κB and AP-1. Adding bamboo extract (BEX) inhibited the effects of PA, reduced MCP-1 production, and inhibited nuclear translocation of NF-κB and AP-1 subunits. Compounds isolated from BEX inhibited MCP-1 secretion with different potencies.Conclusions/SignificancePA induced MCP-1 production in murine adipose, muscle, and liver cells. BEX ameliorated PA-induced production of MCP-1 by inhibiting nuclear translocation of NF-κB and AP-1. Two O-methylated flavones were isolated from BEX with functional effects on MCP-1 production. These results may represent a possible therapeutic application of BEX and its compounds toward alleviating chronic inflammation caused by elevated circulatory FFAs.

Carrot juice ingestion attenuates high fructose‐induced circulatory pro‐inflammatory mediators in weanling Wistar rats

“…Although the underlying mechanism is not clear, the reduction in plasma FFA levels supports our contention that carrot juice attenuated the pro‐inflammatory condition induced by high fructose diet. Previously, both in vivo and in vitro studies have demonstrated FFA‐induced activation of nuclear factor k B (NF‐ k B), thereby resulting in over‐expression of pro‐inflammatory cytokines TNF α , interleukin 6 (IL‐6) and IL‐1 β and elevation of MCP1 levels . Our present data on plasma FFA and MCP1 levels are in line with these reports.…”

Overexpression of juxtaposed with another zinc finger gene 1 reduces proinflammatory cytokine release via inhibition of stress‐activated protein kinases and nuclear factor‐κB

“…time-dependent and concentration-dependent manner, suggesting that PA led to the release of proinflammatory cytokines and inflammatory responses. A growing body of evidence suggests that alterations of several stress-activated signaling pathways, including JNK/SAPK, p38 MAPK, ERK1/2, and NF-jB, are associated with the transcripts of some proinflammatory factors [28,[35][36][37][38][39][40][41][42][43]. In agreement with previous findings, we have found that, accompanied by increased TNF-a, MCP-1 and IL-8 transcript levels, PA treatment activates JNK, p38 MAPK and ERK1/2 signaling, and increases the degradation of IjBa, an NF-jB-inhibitory protein [44], suggesting that PA may have promoted the release of proinflammatory cytokines and inflammatory responses by inducing the activation or degradation of these signal molecules.…”

Anti-inflammatory Function of Phyllostachys Edulis Extract in the Hippocampus of HIV-1 Transgenic Rats

“…Bioactivity-guided fractionation revealed that flavonoids such as tricin and 7-O-methyltricin were among the anti-inflammatory compounds in BEX (Higa et al, 2012). In the present study, BEX inhibited the increases of both mRNA and protein levels of IL1β in the hippocampus of the HIV-1 TG rats, and meanwhile lowered the protein levels of p65 and c-Jun, implicating the inhibition of both NFκB and AP-1 pathways.…”