Zaki Moushira, Orban Hisham A, Shahba Mohamed A, Moustafa Rehab S I, Adel Ahmed, Fadel Fatina I, Selim Abeer, El-Bassyouni Hala T, Youness Eman R
Biological Anthropology Department, Medical Research and Clinical Studies Institute, National Research Centre, Cairo, Egypt.
Medical Biochemistry Department, Medical Research and Clinical Studies Institute, National Research Centre, Cairo, Egypt.
BMC Pediatr. 2025 Jan 24;25(1):56. doi: 10.1186/s12887-025-05412-2.
Chronic inflammation and its control are crucial to the responses of glomerular and renal tubular cells. This contributes to the pathogenic mechanisms and advancement of the disease in Alport syndrome. The study aimed to elucidate the role of cyclooxygenase-2, Interleukin 4, Plasminogen activating inhibitor 1, and Prostaglandin E2 in the development and course of Alport syndrome.
In our study inflammatory markers were evaluated in 26 Alport syndrome patients, 15 males and 11 females and 24 controls.
Their age ranged from 4 to 16 years (mean ± SD was 8.50 ± 2.877) and 24 were normal controls matching age and sex. The serum levels of cyclooxygenase-2, Prostaglandin E2, Interleukin 4, and Plasminogen activating inhibitor 1 were evaluated in all patients. The serum level of cyclooxygenase-2, Prostaglandin E2, Interleukin 4, and Plasminogen activating inhibitor 1 were all increased significantly in the Alport syndrome patients compared to control (588.68 ± 73.08, 42.57 ± 4.18, 42.32 ± 3.49, and 846.47 ± 45.433, respectively versus controls (369.12 ± 50.28, 25.52 ± 4.98, 28.89 ± 3.19, and 312.79 ± 40.53 respectively).
The role of inflammatory markers cyclooxygenase-2, Prostaglandin E2, Interleukin 4, and Plasminogen activating inhibitor 1 in Alport syndrome that are causally connected and have a role in the development and course of Alport disease was delineated. This may highlight and speculate an innovative strategy for targeting the creation of safe and efficient anti-inflammatory treatments to inhibit disease progression in Alport syndrome.
慢性炎症及其控制对于肾小球和肾小管细胞的反应至关重要。这有助于阐明奥尔波特综合征的发病机制和疾病进展。本研究旨在阐明环氧合酶-2、白细胞介素4、纤溶酶原激活抑制剂1和前列腺素E2在奥尔波特综合征的发生发展过程中的作用。
在我们的研究中,对26例奥尔波特综合征患者(15例男性和11例女性)和24例对照者进行了炎症标志物评估。
他们的年龄在4至16岁之间(平均±标准差为8.50±2.877),24例为年龄和性别匹配的正常对照者。对所有患者的血清环氧合酶-2、前列腺素E2、白细胞介素4和纤溶酶原激活抑制剂1水平进行了评估。与对照组相比,奥尔波特综合征患者的血清环氧合酶-2、前列腺素E2、白细胞介素4和纤溶酶原激活抑制剂1水平均显著升高(分别为588.68±73.08、42.57±4.18、42.32±3.49和846.47±45.433,而对照组分别为369.12±50.28、25.52±4.98、28.89±3.19和312.79±40.53)。
炎症标志物环氧合酶-2、前列腺素E2、白细胞介素4和纤溶酶原激活抑制剂1在奥尔波特综合征中的作用已被阐明,它们之间存在因果关系,并在奥尔波特病的发生发展过程中发挥作用。这可能突出并推测出一种创新策略,即针对开发安全有效的抗炎治疗方法以抑制奥尔波特综合征的疾病进展。