Huwait Etimad A, Al-Ghamdi Maryam A, Ghattas Maivel H, Hinnis Adel R, El-Maaty Dalia A Abo, Abo-Elmatty Dina M, Abdel-Hamed Asmaa R
Department of Biochemistry, Science College, King Abdulaziz University, Saudi Arabia.
Department of Medical Biochemistry, Faculty of Medicine, Port Said University, Port Said, Egypt.
Int J Health Sci (Qassim). 2021 Jan-Feb;15(1):22-28.
Among tropical diseases, schistosomiasis caused by is the second major cause of morbidity and mortality worldwide. Inflammation was considered as an adverse event that contributes to the pathology associated with schistosomiasis. Heme oxygenase-1 (HO-1) and vascular endothelial growth factor (VEGF) have been implicated in the process of angiogenesis. The current study aimed to evaluate the effect of infection on HO-1 gene expression, IL-4, IL-12, and VEGF to address the role of these factors in the pathogenesis of schistosomiasis.
Thirty mice divided equally into three groups comprised a non-infected control group and two -infected groups. Infected animals were studied at 8 and 12 weeks post-infection. Serum IL-4, IL-12, and VEGF were measured. HO-1 mRNA was detected by RT-PCR of liver homogenates and HO activity was assessed as percentage of carboxy hemoglobin.
-infected mice showed a progressive increase in serum IL-4 and VEGF and decrease in IL-12 levels. In addition, HO-1 expression and activity were increased in infected mice compared to control group with the maximum increase at egg deposition stage.
Our results suggested that the body response to acute stage of infection by elevating the expression of the stress gene HO-1 and that VEGF may serve as a new indicator of progression of . associated angiogenesis which regulates granuloma and/or fibrosis development in the liver of infected mice. Understanding the role of HO-1 and VEGF in pathogenesis of may provide a new pharmacological target.
在热带疾病中，由[病原体名称未给出]引起的血吸虫病是全球发病和死亡的第二大主要原因。炎症被认为是导致血吸虫病相关病理变化的不良事件。血红素加氧酶-1（HO-1）和血管内皮生长因子（VEGF）与血管生成过程有关。本研究旨在评估[病原体名称未给出]感染对HO-1基因表达、白细胞介素-4（IL-4）、白细胞介素-12（IL-12）和VEGF的影响，以探讨这些因素在血吸虫病发病机制中的作用。
30只小鼠平均分为三组，包括一个未感染对照组和两个[病原体名称未给出]感染组。对感染动物在感染后8周和12周进行研究。检测血清IL-4、IL-12和VEGF。通过肝脏匀浆的逆转录聚合酶链反应（RT-PCR）检测HO-1 mRNA，并将HO活性评估为羧基血红蛋白的百分比。
[病原体名称未给出]感染小鼠的血清IL-4和VEGF呈逐渐升高趋势，IL-12水平降低。此外，与对照组相比，感染小鼠的HO-1表达和活性增加，在虫卵沉积阶段增加最多。
我们的结果表明，机体通过提高应激基因HO-1的表达来应对[病原体名称未给出]感染的急性期，并且VEGF可能作为[病原体名称未给出]相关血管生成进展的新指标，该血管生成调节感染小鼠肝脏中的肉芽肿和/或纤维化发展。了解HO-1和VEGF在[病原体名称未给出]发病机制中的作用可能提供一个新的药理学靶点。
