Plantamajoside (PMS) is a phenylpropanoid glycoside isolated from Plantago asiatica L.(Plantaginaceae). Plantamajoside ameliorated the lung injury that was induced by LPS. Plantamajoside suppressed the production of IL-1β, IL-6 and TNF-α in a dose-dependent manner. Plantamajoside inhibited the phosphorylation of IκBα, p65, p38, JNK and ERK. Plantamajoside has protective effect on LPS-induced ALI (acute lung injury) in mice and in RAW264.7 cells[3]. In vitro, PMS inhibited the ISO(isoproterenol)-induced increase in H9c2 cell surface area and the mRNA expression of ANP, BNP and Myh7. In vivo, PMS improved the ISO-induced decrease in cardiac function, inhibited the increase in cardiac anatomical parameters and alleviated the histopathological changes in cardiac tissues[4]. PMS inhibited the invasion, migration and viability of malignant melanoma cells. In addition, PMS induced apoptosis by regulating the expression levels of apoptotic-related genes and the activation of the PI3K/AKT signaling pathway, thereby exerting anti-malignant melanoma effects[5]. Plantamajoside decreased the production of PGE2, NO, IL-6, and IL-8 in LPS-stimulated HGFs. LPS-induced NF-κB p65 and IκB phosphorylation were also suppressed by plantamajoside. Furthermore, plantamajoside inhibited LPS-induced PI3K and AKT phosphorylation[6]. PMS protected against myocardial I/R injury via attenuating oxidative stress, inflammatory response and apoptosis[7].
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