Turkish journal of medical sciences · 2025
Benzyl alcohol improves Ang II-induced vascular and renal injury.
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Gu Zhenyu, Hua Qi
Аннотация
BACKGROUND/AIM: The etiology of hypertension in pediatric populations is complex and multifactorial, with metabolic abnormalities playing a fundamental role in the pathogenesis of the condition. This study investigates the therapeutic effects of Benzyl alcohol (BA), identified through metabolomics analysis of pediatric hypertension serum, on Angiotensin II (Ang II)-induced vascular and renal injury in murine models.
MATERIALS AND METHODS: Male C57BL/6 mice were used to establish a vascular remodeling model by continuous 4-week Ang II infusion using a subcutaneous osmotic pump. Bioinformatics was used to identify target metabolites. The tail artery, common carotid artery diastolic, and systolic pressures in mice were determined with a blood pressure monitor. Vascular structure changes were assessed with HE and Masson staining, while kidney pathology was examined using HE. Serum urea nitrogen, creatinine, and cystatin C levels were measured with ELISA kit.
RESULTS: Metabolomics analysis identified metabolite BA as a potential target for hypertension management. Compared to the Ang II group, BA reduced systolic blood pressure by 11.58% and diastolic blood pressure by 14.62% in the fourth week. After sodium nitroprusside treatment, the Ang II group showed reduced vasodilation reactivity versus the control. BA significantly restored this reactivity, unlike acetylcholine. Furthermore, BA was observed to attenuate Ang II-induced vascular mediator thickening, the mediator-to-lumen ratio, and collagen deposition. Ang II administration resulted in renal structural damage and increased concentrations of urea nitrogen, creatinine, and serum cystatin C, which was reversed by BA treatment.
CONCLUSION: BA exhibits potential in enhancing the vasodilatory response, vascular remodeling, and renal injury associated with Ang II.
MATERIALS AND METHODS: Male C57BL/6 mice were used to establish a vascular remodeling model by continuous 4-week Ang II infusion using a subcutaneous osmotic pump. Bioinformatics was used to identify target metabolites. The tail artery, common carotid artery diastolic, and systolic pressures in mice were determined with a blood pressure monitor. Vascular structure changes were assessed with HE and Masson staining, while kidney pathology was examined using HE. Serum urea nitrogen, creatinine, and cystatin C levels were measured with ELISA kit.
RESULTS: Metabolomics analysis identified metabolite BA as a potential target for hypertension management. Compared to the Ang II group, BA reduced systolic blood pressure by 11.58% and diastolic blood pressure by 14.62% in the fourth week. After sodium nitroprusside treatment, the Ang II group showed reduced vasodilation reactivity versus the control. BA significantly restored this reactivity, unlike acetylcholine. Furthermore, BA was observed to attenuate Ang II-induced vascular mediator thickening, the mediator-to-lumen ratio, and collagen deposition. Ang II administration resulted in renal structural damage and increased concentrations of urea nitrogen, creatinine, and serum cystatin C, which was reversed by BA treatment.
CONCLUSION: BA exhibits potential in enhancing the vasodilatory response, vascular remodeling, and renal injury associated with Ang II.