Demethylzeylasteral, a natural product isolated and purified from the herb of Tripterygium wilfordii Hook.f., has strong immunosuppressive activity, that can be used in the fields of organ transplantation and autoimmune disorders. It increases both activation and inactivation time constants of Ca(2+) currents, and inhibits significantly the sperm acrosome reaction initiated by progesterone.
Demethylzeylasteral (T-96) is a triterpene compound isolated from Tripterygium wilfordii Hook F, with anti-inflammatory, immunosuppressive and anti-tumor activities. T-96 inhibited TGF-β-induced migration and epithelial-mesenchymal transition both in vitro and in vivo. T-96 inhibited invasion of MDA-MB-231 and 4T1 cells via suppressing the canonical and non-canonical TGF-β signaling pathways[3]. T-96 significantly inhibited glioma cell growth and induced cell cycle arrest in G1 phase but did not induce apoptosis. Cell invasion and migration were dramatically suppressed after treatment with T-96[4]. Compared with the rats in the unilateral ureteral obstruction model group, demethylzeylasteral treatment markedly inhibited the increased concentrations of serum creatinine and blood urea nitrogen, urinary protein/creatinine ratio, and concentrations of high‑density lipoprotein and low‑density lipoprotein cholesterol, and prevented kidney damage. In addition, demethylzeylasteral inhibited the levels of TNF‑α andIL‑6 and suppressed the protein expression levels of COX‑2 (cyclooxygenase) and ICAM‑1 (intercellular adhesion molecule‑1) in the kidneys of the rats in the unilateral ureteral obstruction model. Demethylzeylasteral also significantly suppressed the protein expression of NF‑κB p65[5]. Demethylzeylasteral not only inhibits cell proliferation through cell cycle arrest at S phase, but also induces cell apoptosis in melanoma cells[6].
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