Xu Jianjun, Zhao Yongxin, Aisa Haji Akber
a Key Laboratory of Chemistry of Plant Resources in Arid Regions , Xinjiang Technical Institute of Physics and Chemistry, Chinese Academy of Sciences , Urumqi , China.
b University of Chinese Academy of Sciences , Beijing , China.
Pharm Biol. 2017 Dec;55(1):2095-2101. doi: 10.1080/13880209.2017.1357737.
Punica granatum L (Punicaceae) flower is an important diabetes treatment in oriental herbal medicine.
This study investigates the inflammation effects of pomegranate flower (PFE) ethanol extract in LPS-induced RAW264.7 cells.
PFE (10, 25, 50, 100 μg/mL) was applied to 1 μg/mL LPS-induced RAW 264.7 macrophages in vitro. Levels of nitric oxide (NO), prostaglandin E (PGE) and pro-inflammatory cytokines interleukin (IL)-1β (IL-1β), interleukin (IL)-6 (IL-6) and tumor necrosis factor (TNF-α) in the supernatant fraction were determined using enzyme-linked immunosorbent assay (ELISA). Expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), phosphorylation of mitogen-activated protein kinase (MAPK) subgroups extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and P38, as well as nuclear factor-κB (NF-κB) activation in extracts were detected via Western blot.
10-100 μg/mL PFE decreased the production of NO (IC value = 31.8 μg/mL), PGE (IC value = 54.5 μg/mL), IL-6 (IC value = 48.7 μg/mL), IL-1β (IC value = 71.3 μg/mL) and TNF-α (IC value = 62.5 μg/mL) in LPS-stimulated RAW 264.7 cells significantly. A mechanism-based study showed that phosphorylation of ERK1/2, p38, JNK and translocation of the NF-B p65 subunit into nuclei were inhibited by the PFE treatment.
These results show that PFE produced potential anti-inflammatory effect through modulating the synthesis of several mediators and cytokines involved in the inflammatory process.
石榴（石榴科）花是东方草药中一种重要的糖尿病治疗药物。
本研究探讨石榴花（PFE）乙醇提取物对脂多糖（LPS）诱导的RAW264.7细胞的炎症作用。
将PFE（10、25、50、100μg/mL）应用于体外1μg/mL LPS诱导的RAW 264.7巨噬细胞。使用酶联免疫吸附测定（ELISA）法测定上清液中一氧化氮（NO）、前列腺素E（PGE）和促炎细胞因子白细胞介素（IL）-1β（IL-1β）、白细胞介素（IL）-6（IL-6）和肿瘤坏死因子（TNF-α）的水平。通过蛋白质印迹法检测提取物中环氧合酶-2（COX-2）和诱导型一氧化氮合酶（iNOS）的表达、丝裂原活化蛋白激酶（MAPK）亚组细胞外信号调节激酶（ERK）、c-Jun氨基末端激酶（JNK）和P38的磷酸化，以及核因子-κB（NF-κB）的活化。
10-100μg/mL PFE显著降低了LPS刺激的RAW 264.7细胞中NO（半数抑制浓度值=31.8μg/mL）、PGE（半数抑制浓度值=54.5μg/mL）、IL-6（半数抑制浓度值=48.7μg/mL）、IL-1β（半数抑制浓度值=71.3μg/mL）和TNF-α（半数抑制浓度值=62.5μg/mL）的产生。一项基于机制的研究表明，PFE处理可抑制ERK1/2、p38、JNK的磷酸化以及NF-κB p65亚基向细胞核的转位。
这些结果表明，PFE通过调节参与炎症过程的多种介质和细胞因子的合成产生了潜在的抗炎作用。
