College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, People's Republic of China.
Biol Trace Elem Res. 2013 Aug;154(2):275-80. doi: 10.1007/s12011-013-9729-1. Epub 2013 Jun 18.
The aim of this study was to investigate the effect of norepinephrine (NE) on spleen lymphocytes exposed to aluminum trichloride (AlCl3). In this experiment, lymphocytes were isolated from spleens of healthy Wistar rats weighing about 130 g and cultured with RPMI-1640 medium containing the final concentration of 0.552 mmol/L AlCl3. NE was added to the cultured cells at the final concentrations of 0 (control group), 0.1 (low-dose group), 1 (mid-dose group), and 10 (high-dose group) nmol/L. No addition of both AlCl3 and NE serviced as blank (BG). The T lymphocyte proliferation; the contents of IL-2, TNF-α, and T lymphocyte subsets; immunoglobulin G (IgG) and intracellular cyclic adenosine monophosphate (cAMP) concentrations; and β2-adrenergic receptor (β2-AR) density were measured at the end of the culture. The result showed that NE decreased T lymphocyte proliferation and the contents of IL-2, TNF-α, and T lymphocyte subsets whereas increased the concentrations of IgG and intracellular cAMP and β2-AR density of the lymphocyte exposed to AlCl3. AlCl3 exposure without adding NE showed the similar impacts on these measures compared with BG. The results suggested that NE aggravated AlCl3 immunotoxicity on the lymphocytes and disordered the immune functions of the lymphocyte through the β2-AR-cAMP signal pathway.
本研究旨在探讨去甲肾上腺素(NE)对暴露于三氯化铝(AlCl3)的脾淋巴细胞的影响。在该实验中,从体重约 130 g 的健康 Wistar 大鼠的脾脏中分离淋巴细胞,并在含有终浓度为 0.552 mmol/L AlCl3 的 RPMI-1640 培养基中进行培养。将 NE 添加到培养细胞中,终浓度分别为 0(对照组)、0.1(低剂量组)、1(中剂量组)和 10(高剂量组)nmol/L。不添加 AlCl3 和 NE 作为空白(BG)。培养结束时,测量 T 淋巴细胞增殖、IL-2、TNF-α 和 T 淋巴细胞亚群含量、免疫球蛋白 G(IgG)和细胞内环磷酸腺苷(cAMP)浓度以及β2-肾上腺素能受体(β2-AR)密度。结果表明,NE 降低了暴露于 AlCl3 的 T 淋巴细胞增殖和 IL-2、TNF-α 和 T 淋巴细胞亚群含量,而增加了 IgG 和细胞内 cAMP 浓度以及β2-AR 的密度。不添加 NE 暴露于 AlCl3 显示出对这些措施的类似影响,与 BG 相比。结果表明,NE 通过β2-AR-cAMP 信号通路加重了 AlCl3 对淋巴细胞的免疫毒性,并扰乱了淋巴细胞的免疫功能。