7β-hydroxy Cholesterol is an oxysterol formed by enzymatic and non-enzymatic oxidation of cholesterol [1]. 7β-hydroxy Cholesterol increases the permeability of vascular endothelium to LDL and promotes the adhesion and extravasation of monocytes and lymphocytes by triggering endothelial cell apoptosis, IL-1β secretion and/or adhesion molecule expression [2-3]. 7β-hydroxy Cholesterol has anti-tumor activity [4].
In human umbilical venous endothelial cells (HUVECs), treatment of HUVECs with 7β-hydroxy Cholesterol (50 and 100μM; 20 and 48h) induced apoptosis in a concentration- and time-dependent manner [1]. In Caco-2 cells, 7β-hydroxy Cholesterol (30μM; 32h) inhibits Caco-2 cell proliferation [4]. In U937 cells, 7β-hydroxy Cholesterol (30μM; 24h) triggers apoptosis by enhancing Ca2+ influx through dihydropyridine-sensitive channels [5]. In U937 cells, 7β-hydroxy Cholesterol (30μM; 24h) exerts cytotoxic effects by inducing apoptosis and reducing cell viability and glutathione levels [6]. In HUVECs, 7β-hydroxy Cholesterol (2.5, 12.5, and 25μM; 15h) produces antiapoptotic and proliferative effects via activation of ERK [7].
References:
[1]. Lemaire S, Lizard G, Monier S, et al. Different patterns of IL-1β secretion, adhesion molecule expression and apoptosis induction in human endothelial cells treated with 7α-, 7β-hydroxycholesterol, or 7-ketocholesterol. FEBS letters. 1998 Dec 4; 440(3): 434-439.
[2]. Lizard G, Monier S, Cordelet C, et al. Characterization and comparison of the mode of cell death, apoptosis versus necrosis, induced by 7β-hydroxycholesterol and 7-ketocholesterol in the cells of the vascular wall. Arteriosclerosis, thrombosis, and vascular biology. 1999 May; 19(5): 1190-1200.
[3]. Ziedén B, Kaminskas A, Kristenson M, et al. Increased plasma 7β-hydroxycholesterol concentrations in a population with a high risk for cardiovascular disease. Arteriosclerosis, thrombosis, and vascular biology. 1999 Apr; 19(4): 967-971.
[4]. Roussi S, Winter A, Gosse F, et al. Different apoptotic mechanisms are involved in the antiproliferative effects of 7beta-hydroxysitosterol and 7beta-hydroxycholesterol in human colon cancer cells. Cell Death Differ. 2005 Feb; 12(2): 128-135.
[5]. Lordan S, O'Brien NM, Mackrill JJ. The role of calcium in apoptosis induced by 7β‐hydroxycholesterol and cholesterol‐5β, 6β‐epoxide. Journal of biochemical and molecular toxicology. 2009 Sep; 23(5): 324-332.
[6]. Maguire L, Konoplyannikov M, Ford A, et al. Comparison of the cytotoxic effects of β-sitosterol oxides and a cholesterol oxide, 7β-hydroxycholesterol, in cultured mammalian cells. British Journal of Nutrition. 2003 Oct; 90(4): 767-775.
[7]. Trevisi L, Bertoldo A, Agnoletto L, et al. Antiapoptotic and proliferative effects of low concentrations of 7β-hydroxycholesterol in human endothelial cells via ERK activation. Journal of vascular research. 2010 Apr 1; 47(3): 241-251.
7β-hydroxy Cholesterol是由胆固醇经酶促和非酶促氧化形成的氧固醇 [1]。7β-hydroxy Cholesterol可增加血管内皮细胞对低密度脂蛋白（LDL）的通透性，并通过诱发内皮细胞凋亡、IL-1β分泌和/或粘附分子表达，促进单核细胞和淋巴细胞的粘附和外渗 [2-3]。7β-hydroxy Cholesterol具有抗肿瘤活性 [4]。
在人脐静脉内皮细胞（HUVEC）培养中，用7β-hydroxy Cholesterol（50和100μM；20和48h）处理HUVEC，以浓度和时间依赖性方式诱导细胞凋亡 [1]。在Caco-2细胞中，7β-hydroxy Cholesterol（30μM；32h）可抑制Caco-2细胞增殖 [4]。在U937细胞中，7β-hydroxy Cholesterol（30μM；24h）通过二氢吡啶敏感通道增强Ca2+内流，从而引发细胞凋亡 [5]。在U937细胞中，7β-hydroxy Cholesterol（30μM；24h）通过诱导细胞凋亡、降低细胞活力和谷胱甘肽水平发挥细胞毒作用 [6]。在HUVEC中，7β-hydroxy Cholesterol（2.5、12.5和25μM；15h）通过激活ERK产生抗凋亡和增殖作用 [7]。