Studies on the bronchial vascular bed have revealed that the number of blood vessels in the lamina propria and under the mucosa of the lung tissue increases in patients suffering from mild to severe asthma. Thus, in this study, a new strategy was employed in respiratory system disorders by angiogenesis inhibition in an ovalbumin (OVA)-induced rat model of asthma. Twenty-one male Wistar albino rats, 8 weeks old, were randomly divided into three groups (n = 7 in each group), including (1) control group, (2) OVA-treated group, and (3) OVA + Bmab (bevacizumab drug). On days 1 and 8, 1 mg of OVA and aluminum hydroxide in sterile phosphate-buffered saline (PBS) were intraperitoneally injected to rats in groups 2 and 3. The control group was only subject to intraperitoneal injection of saline on days 1 and 8. One week after the last injection, the rats (groups 2 and 3) were exposed to OVA inhalation for 30 min at 2-day intervals from days 15 to 25. After sensitization and challenge with OVA, the OVA + Bmab group (group 3) were treated with a 5 mg/kg bevacizumab drug. Genes and protein expression of IL-1β and TNF-α and the expression of vascular endothelial growth factor (VEGF) protein were assessed by real-time PCR and immunohistochemistry respectively, in lung tissue. OVA exposure increased mucosal secretion and inflammatory cell populations in lung tissue and OVA-specific IgE level in serum. Also, VEGF and cytokine factor expression were significantly elevated in the OVA-induced asthma model (p ≤ 0.05). However, rats in OVA + Bmab group showed significantly a decrease in VEGF and IL-1β and TNF-α genes as well as proteins (p ≤ 0.05). The results showed that bevacizumab efficiently diminished bronchial inflammation via downregulation of VEGF expression, followed by inflammatory cells population and cytokines reduction. Angiogenesis inhibition in rats with induced asthma not only suppresses the inflammatory process through blocking VEGF expression but also inhibits the development of new blood vessels and progressing asthmatic attacks.

对支气管血管床的研究表明，轻度至重度哮喘患者的固有层和肺组织粘膜下的血管数量增加。因此，在这项研究中，通过在卵清蛋白（OVA）诱导的哮喘大鼠模型中抑制血管生成，采用了一种新策略来治疗呼吸系统疾病。 8周龄雄性Wistar白化大鼠21只，随机分为三组（每组n =7），包括（1）对照组、（2）OVA治疗组、（3）OVA+Bmab组。贝伐珠单抗药物）。第1天和第8天，第2组和第3组大鼠腹腔注射1 mg OVA和氢氧化铝的无菌磷酸盐缓冲盐水（PBS）。对照组仅在第1天和第8天腹腔注射盐水。最后一次注射后一周，大鼠（第 2 组和第 3 组）从第 15 天到第 25 天，每隔 2 天接受 OVA 吸入 30 分钟。在用 OVA 致敏和攻击后，OVA + Bmab 组（第 3 组）用 5 mg/kg 贝伐珠单抗药物治疗。分别通过实时PCR和免疫组织化学评估肺组织中IL-1β和TNF-α的基因和蛋白表达以及血管内皮生长因子（VEGF）蛋白的表达。 OVA 暴露增加了肺组织中的粘膜分泌和炎症细胞群以及血清中的 OVA 特异性 IgE 水平。此外，OVA 诱导的哮喘模型中 VEGF 和细胞因子表达显着升高（ p ≤ 0.05）。然而，OVA + Bmab 组大鼠的 VEGF、IL-1β 和 TNF-α 基因以及蛋白质显着下降（ p ≤ 0.05）。 结果表明，贝伐珠单抗通过下调 VEGF 表达，进而减少炎症细胞数量和细胞因子，有效减轻支气管炎症。诱发哮喘大鼠的血管生成抑制不仅可以通过阻断 VEGF 表达来抑制炎症过程，还可以抑制新血管的发育和哮喘发作的进展。