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Published on: October 26, 2020
C-Phycoerythrin Prevents Chronic Kidney Disease-Induced Systemic Arterial Hypertension, Avoiding Oxidative Stress and
Oscar Iván Florencio-Santiago1, Vanesa Blas-Valdivia2, José Iván Serrano-Contreras3
1Laboratorio de Metabolismo I, Departamento de Fisiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Ciudad de México 07738, Mexico.
Insights
C-phycoerythrin (CPE) prevents chronic kidney disease (CKD) progression to systemic arterial hypertension (SAH) by reducing oxidative stress and vascular dysfunction. This bioactive compound offers potential therapeutic benefits for kidney disease complications.
Area of Science:
- Nephrology
- Pharmacology
- Biochemistry
Background:
- Chronic kidney disease (CKD) is a significant health burden, particularly in low- and middle-income countries.
- Systemic arterial hypertension (SAH) is a major complication of CKD, often diagnosed late.
- C-phycoerythrin (CPE), a compound from *Phormidium persicinum*, exhibits anti-inflammatory, antioxidant, and in vivo nephroprotective effects.
Purpose of the Study:
- To investigate the antihypertensive effects of C-phycoerythrin (CPE) in a rat model of chronic kidney disease (CKD).
- To evaluate CPE's impact on hemodynamic parameters, renal function, oxidative stress, and vascular dysfunction markers in CKD.
Main Methods:
- A 5/6 nephrectomy model was used in Wistar rats, divided into sham, sham + CPE, nephrectomized (NFx), and NFx + CPE groups.
- Hemodynamic evaluations were performed weekly for five weeks post-surgery.
- Renal function, oxidative stress markers, and the expression of the renin-angiotensin system (RAS) and related signaling pathways (AT1R, AT2R, Mas1/p-Akt/p-eNOS) were assessed.
Main Results:
- CKD induced hyperfiltration and systemic arterial hypertension (SAH) by the third week.
- Nephrectomized rats showed AT1R upregulation and AT2R downregulation, alongside alterations in the Mas1/p-Akt/p-eNOS axis.
- CPE treatment mitigated renal damage, preserved renal function, and prevented SAH development.
- CPE modulated the vasodilative AT1R, AT2R, and Mas1/p-Akt/p-eNOS axis, reducing oxidative stress and vascular dysfunction.
Conclusions:
- C-phycoerythrin (CPE) demonstrates significant antihypertensive effects in a preclinical model of chronic kidney disease (CKD).
- CPE prevents the progression of CKD to systemic arterial hypertension (SAH) by mitigating oxidative stress and vascular dysfunction.
- The findings suggest CPE's potential as a therapeutic agent for managing CKD complications.
Abstract:
Chronic kidney disease (CKD) is a burden in low- and middle-income countries, and a late diagnosis with systemic arterial hypertension (SAH) is the major complication of CKD. C-phycoerythrin (CPE) is a bioactive compound derived from Phormidium persicinum that presents anti-inflammatory and antioxidant effects in vitro and nephroprotective effects in vivo. In the current study, we determine the antihypertensive effect of CPE in a 5/6 nephrectomy-induced CKD model using twenty normotensives male Wistar rats, grouped into four groups (n = 5): sham; sham + CPE; 5/6 nephrectomy (NFx); and NFx + CPE. Treatment started a week post-surgery and continued for five weeks, with weekly hemodynamic evaluations. Following treatment, renal function, oxidative stress, and the expression of vascular dysfunction markers were assessed. The renal function analysis revealed CKD hyperfiltration, and the hemodynamic evaluation showed that SAH developed at the third week. AT1R upregulation and AT2R downregulation together with Mas1/p-Akt/p-eNOS axis were also observed. CPE treatment mitigated renal damage, preserved renal function, and prevented SAH with the modulation of the vasodilative AT1R, AT2R, and Mas1/pAKT/peNOS axis. This result reveals that CPE prevented CKD progression to SAH by avoiding oxidative stress and vascular dysfunction in the kidneys.
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