Hu Z L, Qian D H
Research Laboratory of Natural and Synthetic Drugs, College of Pharmacy, Second Military Medical University, Shanghai, China.
Zhongguo Yao Li Xue Bao. 1993 Mar;14(2):183-6.
The effects of protein kinase C (PKC) activator 1-O-tetradecanoylphorbol-13-acetate (TPA) and inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) and quercetin were studied on release of tumor necrosis factor (TNF) from mouse peritoneal macrophages primed with Propionibacterium acnes (PA). The results showed that TPA (1-100 ng.ml-1) and lipopolysaccharides (LPS) (1-100 ng.ml-1) induced the release of TNF from PA-primed mouse peritoneal macrophages in dose- and time-dependent manners in vitro, and the effects of TPA and LPS were inhibited by H-7 (12.5-100 mumol.L-1) or quercetin (6.25-25 mumol.L-1) in a dose-dependent manner. After ip H-7 (50 mg.kg-1), LPS-induced release of TNF in vivo decreased significantly. These results suggest that PKC may play a critical role in release of TNF from PA-primed macrophages.
研究了蛋白激酶C（PKC）激活剂1-十四酰佛波醇-13-乙酸酯（TPA）、抑制剂1-（5-异喹啉磺酰基）-2-甲基哌嗪（H-7）和槲皮素对经痤疮丙酸杆菌（PA）致敏的小鼠腹腔巨噬细胞释放肿瘤坏死因子（TNF）的影响。结果表明，TPA（1-100 ng.ml-1）和脂多糖（LPS）（1-100 ng.ml-1）在体外以剂量和时间依赖性方式诱导经PA致敏的小鼠腹腔巨噬细胞释放TNF，且TPA和LPS的作用被H-7（12.5-100 μmol.L-1）或槲皮素（6.25-25 μmol.L-1）以剂量依赖性方式抑制。腹腔注射H-7（50 mg.kg-1）后，LPS诱导的体内TNF释放显著降低。这些结果表明，PKC可能在经PA致敏的巨噬细胞释放TNF中起关键作用。
