目的 研究犁头草醇提物（VIEE）对脂多糖（LPS）所致小鼠急性炎症模型的抗炎作用，并探究其作用机制。方法 36只C57BL/6小鼠随机分为对照组、模型组、地塞米松组(阳性药，5 mg·kg^-1)和VIEE低、中、高剂量(2、4、8 g·kg^-1)组，各组小鼠连续ig给药14 d，对照组和模型组ig等体积纯水，末次给药1 h后，ip LPS 15 mg·kg^-1，建立小鼠炎症模型，12 h后采集样本。ELISA法检测小鼠血清NO、白细胞介素（IL）-1β、IL-6和肿瘤坏死因子（TNF）-α水平；检测小鼠血清丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）水平；苏木素-伊红染色法观察小鼠肝脏组织、脾脏组织病理变化；实时荧光定量PCR（qRT-PCR）法检测小鼠肝脏、脾脏组织诱导型一氧化氮合酶（iNOS）、环氧化酶-2（COX-2）、IL-6、IL-1β和TNF-α m RNA表达；Western blotting法检测小鼠肝脏、脾脏组织蛋白激酶B（Akt）、p-Akt、p65、p-p65、人核因子κB抑制蛋白α（IκBα）、p-IκBα、Toll样受体4（TLR4）、髓分化因子88（MyD88）蛋白表达。结果 与对照组比较，模型组小鼠血清NO、IL-6、IL-1β、TNF-α、ALT和AST水平升高（P<0.01），肝脏、脾脏组织均可见一定程度病理改变，肝脏、脾脏组织i NOS、COX-2、IL-6、IL-1β和TNF-α mRNA表达升高（P<0.01），肝脏、脾脏组织p-Akt、p-p65、p-IκBα、TLR4、MyD88蛋白表达上调（P<0.01）；与模型组比较，VIEE组小鼠血清NO、IL-6、IL-1β、TNF-α、ALT和AST水平降低（P<0.05、0.01），肝脏、脾脏组织病理损伤明显改善，肝脏、脾脏组织i NOS、COX-2、IL-6、IL-1β和TNF-α m RNA表达降低（P<0.05、0.01），肝脏、脾脏组织p-Akt、p-p65、p-IκBα、TLR4、MyD88蛋白表达下调（P<0.05、0.01）。结论 VIEE能够改善LPS诱导的小鼠炎症，具有良好的抗炎效应，其抗炎机制可能与抑制TLR4/MyD88/NF-κB和Akt信号通路激活有关。

Objective To investigate the anti-inflammatory effects of Viola inconspicua ethanol extract（VIEE） in an acute LPSinduced mouse inflammation model and explore its underlying mechanisms. Methods Thirty-six C57 BL/6 mice were randomly divided into a control group, a model group, a dexamethasone group(positive control, 5 mg·kg^-1), and low, medium, and high-dose VIEE groups(2, 4, 8 g·kg^-1). Mice in each group received continuous ig administration for 14 days. The control group and model group received ig administration of pure water of equal volume. One hour after the last administration, mice were ip injected with LPS(15 mg·kg^-1) to establish an inflammation model in mice. Samples were collected after 12 hours. The levels of NO, interleukin（IL）-1β, IL-6, and tumor necrosis factor（TNF）-α in the serum of mice were detected by ELISA. The levels of alanine aminotransferase（ALT） and aspartate aminotransferase（AST） in the serum of mice were also measured. Hematoxylin-eosin staining was used to observe the pathological changes in the liver and spleen tissues of mice. Real-time quantitative PCR（qRT-PCR） was used to detect the mRNA expression of inducible nitric oxide synthase（iNOS）, cyclooxygenase-2（COX-2）, IL-6, IL-1β, and TNF-α in the liver and spleen tissues of mice. Western blotting was used to detect the protein expression of protein kinase B（Akt）, p-Akt, p65, p-p65, inhibitor κB α（IκBα）, p-IκBα, Toll-like receptor 4（TLR4）, and myeloid differentiation factor 88（MyD88） in the liver and spleen tissues of mice. Results Compared with the normal group, serum levels of NO, IL-6, IL-1β, TNF-α, ALT and AST were elevated in the model group（P < 0.01）. Pathological alterations were observed in both liver and spleen tissues. mRNA expression of iNOS, COX-2, IL-6, IL-1β, and TNF-α m RNA expression in liver and spleen tissues were elevated（P < 0.01）, and p-Akt, p-p65, p-IκBα, TLR4, and MyD88 protein expression in liver and spleen tissues were up-regulated（P < 0.01）. Compared with the model group, serum NO, IL-6, IL-1β, TNF-α, ALT and AST levels were reduced in the VIEE groups（P < 0.05, and 0.01）. Pathological damage in liver and spleen tissues were significantly improved, while mRNA expression of iNOS, COX-2, IL-6, IL-1β, and TNF-α mRNA expression in liver and spleen tissues decreased（P < 0.05, and 0.01）, and p-Akt, p-p65, p-IκBα, TLR4, and MyD88 protein expression in liver and spleen tissues were down-regulated（P < 0.05, and 0.01）. Conclusion VIEE ameliorates LPS-induced inflammation in mice, demonstrating potent anti-inflammatory effects. Its anti-inflammatory mechanism may be associated with the inhibition of TLR4/MyD88/NF-κB/and Akt signaling pathway activation.

R965

广西壮瑶药重点实验室项目(桂科基字[2014]32号); 广西高校中青年教师科研基础能力提升项目(2024KY0332); 钟文全国老药工传承工作室(国中医药人教函[2024]255号); 黄瑞松全国名老中医药专家传承工作室(国中医药人教函[2022]75号)