Nitric oxide : biology and chemistry · 2025
Therapeutic potential of S-nitroso-l-cysteine in improving cardiorenal function in eNOS-KO CKD mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Wu Xiaofan, Zhao Jiahe, Xu Zhengqi, Jiang Feng, Wang Moran, Tao Jingwen, Zhang Cuntai, Lin Li, Li Sheng
Аннотация
OBJECTIVE: Patients with chronic kidney disease (CKD) usually exhibit high incidence and mortality rates of cardiovascular disease (CVD). Patients with CKD typically exhibit endothelial dysfunction, which represents one of the risk factors for CVD. As a signaling molecule, S-nitroso-l-cysteine (CSNO) plays a pivotal role in endothelial function. In this study, we explored the therapeutic value of CSNO on eNOS-KO CKD mice.
METHODS: Male eNOS-KO mice were randomly assigned to one of three groups: control, adenine-induced CKD, and CKD with CSNO nebulization (88 ppm, 20 min/day for 6 weeks). Cardiac function was assessed via Doppler echocardiography. Fibrosis, hypertrophy, lipid accumulation, ROS production, and apoptosis were evaluated by HE, Masson, WGA, Oil Red O, DHE, and TUNEL staining, respectively.
RESULTS: CSNO treatment significantly increased the kidney-to-body weight ratio compared to the eNOS-KO CKD group, and urinary creatinine levels exhibited an increasing trend, although this change was not statistically significant. Furthermore, CSNO markedly attenuated renal lipid accumulation. Echocardiography revealed that CSNO significantly enhanced left ventricular ejection fraction (LVEF) and tissue Doppler E'/A' ratio. The E/A ratio also increased in the CSNO treatment group, but this change was not statistically significant. Moreover, CSNO alleviated cardiac hypertrophy, decreased ROS production, apoptosis, and lipid accumulation compared to the eNOS-KO CKD group.
CONCLUSION: Collectively, the findings of the present study demonstrated that CSNO improved cardiorenal function in eNOS-KO CKD mice, thereby affording a novel therapeutic approach to treat CKD patients with endothelial dysfunction.
METHODS: Male eNOS-KO mice were randomly assigned to one of three groups: control, adenine-induced CKD, and CKD with CSNO nebulization (88 ppm, 20 min/day for 6 weeks). Cardiac function was assessed via Doppler echocardiography. Fibrosis, hypertrophy, lipid accumulation, ROS production, and apoptosis were evaluated by HE, Masson, WGA, Oil Red O, DHE, and TUNEL staining, respectively.
RESULTS: CSNO treatment significantly increased the kidney-to-body weight ratio compared to the eNOS-KO CKD group, and urinary creatinine levels exhibited an increasing trend, although this change was not statistically significant. Furthermore, CSNO markedly attenuated renal lipid accumulation. Echocardiography revealed that CSNO significantly enhanced left ventricular ejection fraction (LVEF) and tissue Doppler E'/A' ratio. The E/A ratio also increased in the CSNO treatment group, but this change was not statistically significant. Moreover, CSNO alleviated cardiac hypertrophy, decreased ROS production, apoptosis, and lipid accumulation compared to the eNOS-KO CKD group.
CONCLUSION: Collectively, the findings of the present study demonstrated that CSNO improved cardiorenal function in eNOS-KO CKD mice, thereby affording a novel therapeutic approach to treat CKD patients with endothelial dysfunction.