Chrysanthemum coronarium L (CC)., a leafy vegetable, has various biological properties, including anti-oxidative, antiinflammatory, antiproliferative, and anti-osteoporosis effects. However, the vascular protective effects of CC remain poorly understood. In this study, we identified the vascular protective effect of CC against ferroptosis in aortic thoracic smooth muscle A7r5 cells. The vascular protective effects of CC against erastin (Era)-induced A7r5 cells were assessed by estimating cell viability, glutathione (GSH) levels, lipid peroxidation, mitochondrial morphological change, and using western blot analysis. The CC treatment effectively ameliorated Era-induced ferroptotic cytotoxicity, including cellular death. The treatment also suppressed mitochondrial morphological change in the Era-induced A7r5 cells. CC significantly regulated Era-induced abnormal mechanisms related to GSH, lipid peroxidation, cysteine/glutamate antiporter SLC7A11 (xCT), and glutathione peroxidase 4 (GPX4) protein expression in A7r5 cells. In conclusion, these findings indicate that CC shows potential as a functional food supplement, nutraceutical, or medicinal food, with protective effects with respect to vascular health by regulating ferroptosis.

Porphyromonas gingivalis, a foremost periodontal pathogen, has been known to cause periodontal diseases. Epidemiologic evidences have indicated the involvement of P. gingivalis in the development of cardiovascular diseases. In this study, we show that the P. gingivalis lipopolysaccharide increases the mRNA expression and protein secretion of interleukin-6 in vascular smooth muscle cells. We demonstrate that P. gingivalis LPS activates the extracellular signalregulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and Akt, which mediate the IL-6 expression in vascular smooth muscle cells. Also, P. gingivalis LPS stimulates the vascular smooth muscle cell migration, which is a critical step for the progression of atherosclerosis. Moreover, neutralization of the IL-6 function inhibits the migration of vascular smooth muscle cells induced by P. gingivalis LPS. Taken together, these results indicate that P. gingivalis LPS promotes the expression of IL-6, which in turn increases the migration of vascular smooth muscle cells.

It is study was designed to characterize endotoxin-induced prostaglandin production in primary cultured rat vascular smooth muscle cells (VSMC). The time course for prostag)andim synthesis in lipopolysaccharide (LPS)-stimulated VSMC showed that the maximum production was reached in 12 hours. LPS induced prostaglandin H2 synthase (PGHS) activity in VSMC and the time course profile in the changes of PGHS activity paralleled that of total prostaglandin production. Differential treatment showed that 4 hours' exposure to LPS was enough for the maximum effect on the prostaglandin production and this effect was completely inhibited by the co-treatment of actinomycin D, a transcription inhibitor. These results suggest that LPS effect might be determined within 4 hours. Actinomycin D increased PGHS activity without affecting prostaglandin production if added 4 hours after LPS treatment. On the other hand, cycloheximide, a translation inhibitor, augmented LPS-induced prostaglandin production if treated during first four hours, but it inhibited LPS-induced PGHS activity regardless of treatment schedule. These results suggeat the existence of multiple regulating mechanisms in the LPS-induced prostaglandin synthesis.