Monoterpenoid perillaldehyde (PA) is the major component in Perilla frutescens leaf essential oil, but its function regarding anti-inflammatory effect is unclear. We explored the anti-inflammatory activity of PA in a dextran sulfate sodium (DSS)-induced colitis mouse model using relief of bodyweight loss (avg. 49.2% mitigation; P = 0.094) and colon damage (avg. 35.3% mitigation; P < 0.05) by administration of PA at a 100 mg/kg dosage. The PA administration resulted in suppression of DSS-induced expression of pro-inflammatory cytokine genes and matrix metalloproteinase-9 in the colon (e.g., avg. 60.6% mitigation for TNF-α mRNA levels; P < 0.05). These effects were confirmed in macrophage RAW264.7 cells stimulated with lipopolysaccharide (LPS). Application of PA induced cell suppression of LPS-induced expressions of genes and proteins of pro-inflammatory cytokines and induced activation of c-Jun N-terminal kinases (JNKs, p54 and p46; P < 0.05) but not nuclear factor-κB p65. The half maximal inhibitory concentration for decreased expression levels of TNF-α mRNA was 171.7 μM. We discuss the in vivo function of PA in amelioration of intestinal inflammation via JNK-mediated cytokine regulation.

中文翻译：

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紫苏醛的肠道抗炎活性

单萜类紫苏醛（PA）是紫苏叶精油中的主要成分，但其抗炎作用的功能尚不清楚。我们通过减轻体重减轻（平均减轻49.2％；P = 0.094）和结肠损伤（减轻平均35.3％；P < 0.05）通过以100 mg / kg的剂量施用PA。PA给药可抑制DSS诱导的结肠炎性细胞因子基因和基质金属蛋白酶9的表达（例如，TNF- αmRNA水平平均降低60.6％；P<0.05）。在用脂多糖（LPS）刺激的巨噬细胞RAW264.7细胞中证实了这些作用。PA的应用可抑制LPS诱导的促炎性细胞因子基因和蛋白质表达，并诱导c-Jun N端激酶（JNKs，p54和p46；P <0.05）活化，但不能抑制核因子-κBp65活化。降低的TNF- αmRNA表达水平的最大半数抑制浓度为171.7μM。我们讨论了PA通过JNK介导的细胞因子调节改善肠道炎症的体内功能。