Explore the vast range of titles available.

异硫氰酸酯（isothiocyanate,ITC）是由硫代葡萄糖苷经黑芥子酶水解形成的天然小分子,广泛存在于十字花科蔬菜中。大量研究证明异硫氰酸酯可以通过诱导肿瘤细胞周期阻滞、促进肿瘤细胞凋亡、诱导活性氧的产生等多种机制抑制肿瘤细胞在体内、体外的增殖。近期研究发现异硫氰酸酯还可以抑制肿瘤细胞侵袭转移、诱导内质网应激和细胞自噬。本文对异硫氰酸酯的抗肿瘤作用机制进行综述。

背景与目的异硫氰酸酯是广泛存在于十字花科蔬菜中的天然抗癌物质，具有抑制多种肿瘤细胞生长的特性。本文研究其对肺腺癌A549细胞生长的影响，并初步探讨其作用机理。 方法我们选取了二种异硫氰酸酯，即异硫氰酸苄酯（BITC）和异硫氰酸苯乙酯（PEITC），检测其对肺腺癌A549细胞生长和细胞周期的影响，对细胞氧化一还原平衡的调节，及对转录因子的调控。

Aim： α-Naphthylisothiocyanate （ANIT） is a well-characterized cholestatic agent for rats. The aim of this study was to examine whether resveratrol could attenuate ANIT-induced acute cholestasis and liver injury in rats. Methods： SD rats were treated with resveratrol （15 or 30 mg/kg, ip） or a positive control drug ursodeoxycholic acid （100 mg/kg, po） for 5 consecutive days followed by a single dose of ANIT （60 mg/kg, po）. Bile flow, and serum biochemical markers and bile constituents were measured 48 h after ANIT administration. Hepatic levels of oxidative repair enzymes （glutathione peroxidase, catalase and MnSOD）, myeloperoxidase activity, TNF-α, IL-6, and ATP content, as well as the expression of liver transporter genes and proteins were assayed. Results： ANIT exposure resulted in serious cholestasis and liver injury, as shown by marked neutrophil infiltration in liver, dramatically increased serum levels of ALT, AST, GGT, ALP, TBA, TBIL, IBIL, and DBIL, and significantly decreased bile excretion and biliary output of GSH and HCO3-. ANIT significantly increased TNF-α and IL-6 release and myeloperoxidase activity, decreased mitochondrial biogenesis in liver, but had little effect on hepatic oxidative repair enzymes and ATP content. Furthermore, ANIT significantly decreased the expression of Mrp2, FXR, and CypTal, markedly increased Mrp3 expression in liver. Pretreatment with resveratrol attenuated ANIT- induced acute cholestasis and liver injury, and other pathological changes. Pretreatment with ursodeoxycholic acid was less effective. Conclusion： Resveratrol effectively attenuates ANIT-induced acute cholestasis and liver injury in rats, possibly through suppression of neutrophil infiltration, as well as upregulation of expression of hepatic transporters and enzymes, thus decreasing accumulation of bile acids.