β-Caryophyllene attenuates dextran sulfate sodium-induced colitis in mice via modulation of gene expression associated mainly with colon inflammation.
β-Caryophyllene attenuates dextran sulfate sodium-induced colitis in mice via modulation of gene expression associated mainly with colon inflammation.
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DOI：
10.1016/j.toxrep.2015.07.018
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发表时间：
2015
影响因子：
--
通讯作者：
Chun HS
中科院分区：
文献类型：
--
作者：
Cho JY;Kim HY;Kim SK;Park JHY;Lee HJ;Chun HS
我们在葡聚糖硫酸钠（DSS）诱导的结肠炎模型中检测了β-香芹烯（CA）的调节活性和结肠炎组织中的基因表达。通过将雄性BALB/c小鼠暴露于饮用水中的5%DSS 7天来诱导实验性结肠炎。CA（30或300 mg/kg）与DSS一起每日一次经口给药。CA给药减弱了DSS治疗小鼠的疾病活动指数、结肠重量/长度比、炎症评分和髓过氧化物酶活性的增加。微阵列分析表明，CA管理调节炎症相关基因，包括细胞因子和趋化因子在结肠组织中的表达（Ccl 2、Ccl 7、Ccl 11、Ifitm 3、IL-1β、IL-28、Tnfrsf 1b、Tnfrsf 12 a）;急性期蛋白（S100 a8，Saa 3，Hp）;粘附分子（Cd 14，Cd 55，Cd 68，Mmp 3，Mmp 10，Sema 6 b，Sema 7a，Anax 13）;和DSS诱导的信号调节蛋白。CA显著抑制NF-κB活性，其介导不同基因组的表达。这些结果表明，CA减轻DSS诱导的结肠炎，可能是通过调节基因的表达，主要与结肠炎症通过抑制DSS诱导的NF-κB活性。
We examined the modulatory activity of β-caryophyllene (CA) and gene expression in colitic colon tissues in a dextran sulfate sodium (DSS)-induced colitis model. Experimental colitis was induced by exposing male BALB/c mice to 5% DSS in drinking water for 7 days. CA (30 or 300 mg/kg) was administered orally once a day together with DSS. CA administration attenuated the increases in the disease activity index, colon weight/length ratio, inflammation score, and myeloperoxidase activity in DSS-treated mice. Microarray analysis showed that CA administration regulated the expression in colon tissue of inflammation-related genes including those for cytokines and chemokines (Ccl2, Ccl7, Ccl11, Ifitm3, IL-1β, IL-28, Tnfrsf1b, Tnfrsf12a); acute-phase proteins (S100a8, Saa3, Hp); adhesion molecules (Cd14, Cd55, Cd68, Mmp3, Mmp10, Sema6b, Sema7a, Anax13); and signal regulatory proteins induced by DSS. CA significantly suppressed NF-κB activity, which mediates the expression of a different set of genes. These results suggest that CA attenuates DSS-induced colitis, possibly by modulating the expression of genes associated mainly with colon inflammation through inhibition of DSS-induced NF-κB activity.