The untreated systemic chronic
inflammation leads to
autoimmune diseases,
hyperglycemia,
cardiovascular diseases,
type 2 diabetes,
hypertension,
osteoporosis, and so on.
Phytochemicals effectively inhibit the
inflammation, and numerous studies have proved that the phytocomponents possess anti-inflammatory property via inhibiting the
cyclooxygenase and
lipoxygenase signaling pathways.
Rhaponticin is one such
phytochemical obtained from the perennial plant Rheum rhaponticum L. belonging to Polygonaceae family. We assessed the anti-inflammatory potency of
rhaponticin in endothelial cells induced with
lipopolysaccharides (LPS). Four different endothelial cells induced with LPS were treated with
rhaponticin and assessed for the
nitric oxide generation. The cytotoxic potency of
rhaponticin was evaluated in endothelial cells using the 3-(4,5-dimethylthizaol-2yl)-2,5-diphenyl tetrazolium
bromide assay. The
tumor necrosis factor-α (TNF-α) synthesis was quantified using the commercially available assay kit. The inflammatory signaling
protein gene expression of TNF-α,
inducible nitric oxide synthase (iNOS),
cyclooxygenase-2 (COX2), and interleukin-1β (IL-1β) was analyzed with quantitative polymerase chain reaction (PCR) analysis. The gene expression of
NADPH oxidase (NOX) cytoplasmic catalytic subunits gp91phox , p47phox , and p22phox was assessed with real-time PCR analysis. Finally, to confirm the anti-inflammatory potency of
rhaponticin, the
nuclear factor kappa B (NFκB) and
mitogen-activated protein kinase (MAPK) signaling
protein expression was analyzed with immunoblotting analysis.
Rhaponticin treatment significantly decreased the levels of
nitric oxide and TNF-α synthesis in LPS-induced endothelial cells. It significantly decreased the gene expression of inflammatory
proteins and NOX signaling
protein. The
protein expression of NFκB and MAPK signaling
proteins was drastically decreased in
rhaponticin-treated endothelial cells induced with LPS. Overall, our results confirm that
rhaponticin effectively inhibited the
inflammation triggered by LPS in endothelial cells via downregulating iNOS, COX2, and NFκB and MAPK signaling pathways.