Coffey R G, Snella E, Johnson K, Pross S
Department of Pharmacology and Therapeutics, University of South Florida College of Medicine, Tampa 33612, USA.
Int J Immunopharmacol. 1996 Dec;18(12):749-52. doi: 10.1016/s0192-0561(97)85557-9.
delta 9-Tetrahydrocannabinol (THC, 10 micrograms) was administered intraperitoneally to thioglycollate-treated mice. After 18 h, peritoneal macrophages were harvested and nitric oxide (NO.) production was induced by lipopolysaccharide (LPS, 1 microgram/ml) and interferon-gamma (IFN-gamma, 0.1-10 U/ml). Macrophages from THC-treated mice produced about half as much NO. as controls. THC (1 microgram/ml) added in vitro caused further inhibition. Greater inhibition was observed at the lower (0.1-0.3 U/ml) IFN-gamma concentrations. The results suggest that the use of THC can reduce NO. production and thereby affect host defense mechanisms, inflammation and autoimmune responses.
将δ9-四氢大麻酚（THC，10微克）腹腔注射给经巯基乙酸盐处理的小鼠。18小时后，收集腹腔巨噬细胞，并用脂多糖（LPS，1微克/毫升）和干扰素-γ（IFN-γ，0.1 - 10单位/毫升）诱导一氧化氮（NO.）生成。来自经THC处理小鼠的巨噬细胞产生的NO.约为对照组的一半。体外添加THC（1微克/毫升）会导致进一步抑制。在较低的（0.1 - 0.3单位/毫升）IFN-γ浓度下观察到更大的抑制作用。结果表明，使用THC可减少NO.生成，从而影响宿主防御机制、炎症和自身免疫反应。
