Ahmadi Saeedeh, Nahavandi Samin, Dehghani Aghdas, Sobhani Seyed Alireza, Abbasi Tuba
Endocrinology and Metabolism Research Center, Health institute, Hormozgan University of Medical Sciences, Jomhouri Boulevard, Bandar Abbas, Bandar Abbas, Iran.
Student Research Committee, Faculty of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
BMC Nephrol. 2025 Jul 12;26(1):380. doi: 10.1186/s12882-025-04323-9.
Pulmonary complications following renal ischemia-reperfusion injury (IRI) occur in a gender-dependent manner. Moreover, an imbalance in the renin-angiotensin system (RAS) exacerbates both renal and pulmonary diseases. Overactivation of the classical RAS component the angiotensin type 1 receptor (AT1R) and angiotensin II may worsen renal IRI and remote organ damage, with gender-specific differences. This study aims to investigate the effect of renal IR on lung injury across genders.
Sixty Wistar rats (30 females, 30 males) were randomly assigned to three groups within each gender: Sham, IR (Isch), and IR with losartan (AT1R antagonist; Isch). Bilateral renal ischemia was induced for 45 min in all groups except the sham group. After 24 h of reperfusion, blood samples were collected for serum analysis, and kidney and lung tissues were harvested for histopathological examination, as well as assessment of malondialdehyde (MDA), and nitrite levels. The left lung was also weighed to evaluate pulmonary edema.
Renal IR led to notable increases in plasma creatinine, blood urea nitrogen (BUN), MDA levels, and the extent of damage to the kidney and lung tissues in both genders. In female rats, losartan significantly decreased serum BUN (56.87 ± 13.1 vs. 112.9 ± 8.9 in groups Isch L and Isch), attenuated kidney scores (7.6 ± 1.3 vs. 12.8 ± 1.2 in groups Isch L and Isch), and increased renal (0.18 ± 0.02 vs. 0.10 ± 0.01 in groups Isch L and sham) and pulmonary nitrite concentrations (0.37 ± 0.07 vs. 0.22 ± 0.009 in groups Isch L and sham) following IR. On the other hand, serum MDA levels increased significantly in males treated with losartan (2.6 ± 0.11 vs. 3.9 ± 0.4 in groups sham and Isch L). Furthermore, losartan mitigated IR-induced lung injury in females (6.5 ± 0.6 vs. 8.3 ± 0.3 in groups Isch L and Isch), whereas it had no significant effect in males.
Our findings suggest that AT1R blockade with losartan confers a gender-dependent protective effect. Specifically, losartan may mitigate IR-induced renal and pulmonary damage in females, potentially through modulation of the nitric oxide pathway and attenuation of oxidative stress.
肾缺血再灌注损伤(IRI)后的肺部并发症存在性别差异。此外,肾素-血管紧张素系统(RAS)失衡会加重肾脏和肺部疾病。经典RAS成分血管紧张素1型受体(AT1R)和血管紧张素II的过度激活可能会加重肾IRI和远处器官损伤,且存在性别差异。本研究旨在探讨肾IR对不同性别的肺损伤的影响。
60只Wistar大鼠(30只雌性,30只雄性)在每个性别内随机分为三组:假手术组、IR(缺血)组和IR加氯沙坦(AT1R拮抗剂;缺血加氯沙坦组)。除假手术组外,所有组均诱导双侧肾缺血45分钟。再灌注24小时后,采集血样进行血清分析,并获取肾脏和肺组织进行组织病理学检查,以及评估丙二醛(MDA)和亚硝酸盐水平。还称量左肺重量以评估肺水肿情况。
肾IR导致两性的血浆肌酐、血尿素氮(BUN)、MDA水平以及肾脏和肺组织损伤程度显著增加。在雌性大鼠中,氯沙坦显著降低血清BUN(缺血加氯沙坦组和缺血组分别为56.87±13.1和112.9±8.9),减轻肾脏评分(缺血加氯沙坦组和缺血组分别为7.6±1.3和12.8±1.2),并增加IR后肾脏(缺血加氯沙坦组和假手术组分别为0.18±0.02和0.10±0.01)和肺部亚硝酸盐浓度(缺血加氯沙坦组和假手术组分别为0.37±0.07和0.22±0.009)。另一方面,氯沙坦治疗的雄性大鼠血清MDA水平显著升高(假手术组和缺血加氯沙坦组分别为2.6±0.11和3.9±0.4)。此外,氯沙坦减轻了IR诱导的雌性肺损伤(缺血加氯沙坦组和缺血组分别为6.5±0.6和8.3±0.3),而对雄性则无显著影响。
我们的研究结果表明,用氯沙坦阻断AT1R具有性别依赖性保护作用。具体而言,氯沙坦可能通过调节一氧化氮途径和减轻氧化应激来减轻IR诱导的雌性肾脏和肺部损伤。