慢性肠炎是畜牧业中常见的疾病，严重影响着经济效益和畜牧业的发展。血管生成在慢性肠炎发展中起着重要的作用。本课题用硫酸葡聚糖（DSS）诱导小鼠慢性肠炎模型，通过观察小鼠的肠炎程度和血管增生程度证明山奈酚对慢性肠炎和血管生成的抑制作用。在细胞试验中，以LPS+TNF-α诱导的原代肠微血管内皮细胞作为模型，通过检测细胞增殖、通透性、迁移、成管作用及血管内皮生长因子分泌，从细胞层面探究山奈酚抑制血管生成的作用。在此基础上，检测内皮细胞VEGFR2通路关键蛋白（ERK、p38 MAPK、Akt）及其磷酸化的水平，探究山奈酚抑制血管生成的分子机制，并利用蛋白抑制剂加以验证。本研究将从血管生成的角度揭示山奈酚治疗慢性肠炎的作用机制，为中兽药抗炎研究提供新的角度和思路。

Chronic enteritis is a common disease in animal husbandry, which seriously affects the economic benefits and the development of animal husbandry. Angiogenesis plays an important role in the development of chronic enteritis. In this study, dextran sulfate (DSS)- induced mice will be used as chronic enteritis models. The anti-inflammatory and antiangiogenic effects of kaempferol will be demonstrated by observing the inflammation and vascular proliferation in mice. The LPS + TNF-alpha-induced primary intestinal microvascular endothelial cells will be used as the cell model. The antiangiogenic effects of kaempferol will be explored at the cellular level by detecting cell proliferation, permeability, migration, endothelial tube formation and secretion of vascular endothelial growth factor. On this basis, key proteins of the VEGFR2 pathway (ERK, p38 MAPK, Akt) and their phosphorylation levels were detected in endothelial cells to explore the molecular mechanism of kaempferol inhibiting angiogenesis. Then the mechanism will be verified by using protein inhibitors. This study will reveal the mechanism of kaempferol in the treatment of chronic enteritis from the perspective of angiogenesis, and provide a new perspective and idea for the research on the anti-inflammatory effect of traditional Chinese veterinary medicine.