Abd-El-Fatah Samaa Salah, Fathy Maha A, Alabiad Mohamed Ali, Aljafil Raja, Gobran Mai Ahmed, Ahmad Enssaf A, Alsharidah Ashwag S, Alorini Mohammed, Alnasser Sulaiman Mohammed, Awadh Sara A, Morgan Enas N
Department of Anatomy and Embryology, College of Medicine, Zagazig University, Al-Sharquia, Egypt.
Department of Medical Physiology, College of Medicine, Zagazig University, Al-Sharquia, Egypt.
Iran J Med Sci. 2024 Dec 1;49(12):794-807. doi: 10.30476/ijms.2024.99442.3152. eCollection 2024 Dec.
The risk of cardiovascular disease (CVD) in patients with chronic kidney disease (CKD) is estimated to be far greater than that in the general population. Adropin regulates endothelial function and may play a role in the pathogenesis of CVD. Angiotensin-converting enzyme inhibitor (ACEI) treatment was reported to have a protective effect on both renal and cardiovascular function. This study investigated whether adropin is associated with renal and cardiovascular outcomes after using ACEI treatment in CKD rats.
In 2021, in Zagazig, Egypt, rats were assigned to: GI, control group (n=8); GII, CKD group (n=8), and GIII, CKD+captopril group (n=8), in which CKD rats received 100 mg/Kg/day captopril orally. Adropin levels, renal function, blood pressure, and various CVD risk factors were measured. Renal, cardiac, and aortic tissues were examined histologically and immunohistochemically to detect the expression of vascular endothelial growth factor receptor-2 (VEGFR-2). To analyze data, ANOVA and Pearson's correlation tests were used (SPSS version 18, P<0.05 is significant).
Adropin was significantly lower in GII than in GI and GIII (P<0.001). Adropin in GII and GIII was negatively correlated with atherogenic index (P=0.019 and P=0.001, respectively), atherogenic co-efficient (P=0.012 and P=0.013, respectively), troponin I (P=0.021 and P=0.043, respectively), and nitric oxide (P=0.025 and P=0.038, respectively). VEGFR-2 expression decreased in GII and was elevated in GIII (P<0.001).
Adropin levels were significantly correlated with most CVD risk factors in CKD and captopril-treated CKD rats, indicating a role for adropin in the pathogenesis of CVD in CKD. It also refers to its implication in the ameliorative effect of ACEI treatment, possibly by affecting VEGFR-2 and nitric oxide release.
据估计,慢性肾脏病(CKD)患者发生心血管疾病(CVD)的风险远高于普通人群。内脂素可调节内皮功能,可能在CVD的发病机制中起作用。据报道,血管紧张素转换酶抑制剂(ACEI)治疗对肾脏和心血管功能均有保护作用。本研究调查了在CKD大鼠中使用ACEI治疗后,内脂素是否与肾脏和心血管结局相关。
2021年,在埃及扎加齐格,将大鼠分为:GI,对照组(n = 8);GII,CKD组(n = 8);以及GIII,CKD + 卡托普利组(n = 8),其中CKD大鼠口服100 mg/Kg/天的卡托普利。测量内脂素水平、肾功能、血压和各种CVD危险因素。对肾脏、心脏和主动脉组织进行组织学和免疫组织化学检查,以检测血管内皮生长因子受体-2(VEGFR-2)的表达。使用方差分析和Pearson相关检验分析数据(SPSS 18版,P < 0.05具有统计学意义)。
GII组的内脂素水平显著低于GI组和GIII组(P < 0.001)。GII组和GIII组的内脂素与致动脉粥样硬化指数(分别为P = 0.019和P = 0.001)、致动脉粥样硬化系数(分别为P = 0.012和P = 0.013)、肌钙蛋白I(分别为P = 0.021和P = 0.043)以及一氧化氮(分别为P = 0.025和P = 0.038)呈负相关。GII组VEGFR-2表达降低,GIII组升高(P < 0.001)。
内脂素水平与CKD及卡托普利治疗的CKD大鼠中的大多数CVD危险因素显著相关,表明内脂素在CKD患者CVD的发病机制中起作用。这也提示其可能通过影响VEGFR-2和一氧化氮释放,参与ACEI治疗的改善作用。