Parthenolide is a sesquiterpene lactone from the plant feverfew (T. parthenium) with multiple biological functions. Parthenolide inhibits the growth of the promastigote form of L. amazonensis with IC50 of 3.6 μg/mL, induces apoptosis in cancer cells and blocks inflammation by inhibiting signaling through NF-κB.
Parthenolide (PTL) is a sesquiterpene lactone which can induce apoptosis in cancer cells and eradicate cancer stem cells such as leukemia stem cells, prostate tumor-initiating cells and so on. Parthenolide (PTL) has a dose-dependent growth inhibition effect on NSCLC cells Calu-1, H1792, A549, H1299, H157, and H460. Moreover, induction of apoptosis, Parthenolide also induces G0/G1 cell cycle arrest in a concentration-dependent manner in A549 cells and G2/M cell cycle arrest in H1792 cells[3]. Parthenolide increased cell viability and inhibited the apoptosis of H2O2‑induced osteoblasts. Parthenolide decreased the levels of reactive oxygen species, MDA (malondialdehyde), LDH (lactate dehydrogenase) and ALP (alkaline phosphatase). SOD (superoxide dismutase) and GPX (glutathione peroxidase) levels were increased by parthenolide in H2O2‑induced osteoblasts[4]. PTL reduced the cell viability and migration rate of lung fibroblasts and inhibited the expression of EMT-related (epithelial-mesenchymal transition) transcription factors in lung epithelial cells. PTL attenuated BLM-induced pulmonary fibrosis and improved the body weight and pathological changes of BLM-treated mice[5]. In addition, PTL directly or indirectly attenuates neuropathy symptoms and promotes M2 microglia/macrophages polarization[6].
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