Tormentic acid, a natural product isolated and purified from the herb of Potentilla tormentilla with anti-allodynic, anti-inflammatory, anticancer,anti-atherogenic activities, has protective effect against lipopolysaccharide/D-galactosamine induced fulminant hepatic failure in mice.
Tormentic acid, a triterpene isolated from Rosa rugosa, exerts anti-inflammatory, antihyperlipidemic, and anti-atherogenic properties. Tormentic acid inhibits LPS-induced iNOS, COX-2, and TNF-α expression through inactivation of the nuclear factor-κb pathway in RAW 264.7 macrophages[3]. Tormentic acid significantly supresses the proliferation of HeLa cells in dose dependence. Tormentic acid also induced remarkable morphological changes in HeLa cells, indicative of apoptosis. Tormentic acid induced G2/M phase cell cycle arrest and its effectiveness increased with increased doses. The expression of tormentic acid on mTOR/PI3K/AKT pathway revealed blocking of this pathway with a concentration-dependent manner[4]. Intraperitoneal administration of TA (Tormentic acid) attenuated memory deficits in amyloid β precursor protein/presenilin 1 transgenic mice, with a marked decrease in amyloid plaque deposition. TA also reduced microglial activation and decreased the secretion of pro‑inflammatory factors in AD mice. Furthermore, pre‑treatment with TA suppressed the production of pro‑inflammatory markers, as well as the nuclear translocation of nuclear factor‑κB (NF‑κB) p65 induced by Aβ exposure in BV2 cells. TA also reduced inhibited neurotoxicity and improved neuron survival in a neuron‑microglia co‑culture system[5]. TA inhibited reactive oxygen species (ROS) generation, induced H2O2 in RVSMCs (rat vascular smooth muscle cells), and inhibited H2O2-induced expression of inducible nitric oxide synthase (iNOS) and NADPH oxidase (NOX) in RVSMCs[6].
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