Antioxidant and anti-inflammatory effects of allicin in the kidney of an experimental model of metabolic syndrome

Author:

Arellano Buendia Abraham Said12,Juárez Rojas Juan Gabriel3,García-Arroyo Fernando2,Aparicio Trejo Omar Emiliano2,Sánchez-Muñoz Fausto4ORCID,Argüello-García Raúl5,Sánchez-Lozada Laura Gabriela2,Bojalil Rafael6ORCID,Osorio-Alonso Horacio2ORCID

Affiliation:

1. Doctorado en Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana, Mexico, Xochimilco, Mexico

2. Fisiopatología Cardio-Renal, Instituto Nacional de Cardiología Ignacio Chávez, Mexico, Tlalpan, México

3. Endocrinología, Instituto Nacional de Cardiología Ignacio Chávez, Mexico, Tlalpan, México

4. Inmunología, Instituto Nacional de Cardiología Ignacio Chávez, Mexico, Tlalpan, México

5. Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados del IPN, México, Gustavo A. Madero, México

6. Atención a la Salud, Universidad Autónoma Metropolitana, Mexico, Xochimilco, México

Abstract

Background Recent studies have suggested that metabolic syndrome (MS) encompasses a group of risk factors for developing chronic kidney disease (CKD). This work aimed to evaluate the antioxidant and anti-inflammatory effects of allicin in the kidney from an experimental model of MS. Methods Male Wistar rats (220–250 g) were used, and three experimental groups (n = 6) were formed: control (C), metabolic syndrome (MS), and MS treated with allicin (16 mg/Kg/day, gastric gavage) (MS+A). MS was considered when an increase of 20% in at least three parameters (body weight, systolic blood pressure (SBP), fasting blood glucose (FBG), or dyslipidemia) was observed compared to the C group. After the MS diagnosis, allicin was administered for 30 days. Results Before the treatment with allicin, the MS group showed more significant body weight gain, increased SBP, and FBG, glucose intolerance, and dyslipidemia. In addition, increased markers of kidney damage in urine and blood. Moreover, the MS increased oxidative stress and inflammation in the kidney compared to group C. The allicin treatment prevented further weight gain, reduced SBP, FBG, glucose intolerance, and dyslipidemia. Also, markers of kidney damage in urine and blood were decreased. Further, the oxidative stress and inflammation were decreased in the renal cortex of the MS+A compared to the MS group. Conclusion Allicin exerts its beneficial effects on the metabolic syndrome by considerably reducing systemic and renal inflammation as well as the oxidative stress. These effects were mediated through the Nrf2 pathway. The results suggest allicin may be a therapeutic alternative for treating kidney injury induced by the metabolic syndrome risk factors.

Funder

Instituto Nacional de Cardiología Ignacio Chávez

Publisher

PeerJ

Subject

General Agricultural and Biological Sciences,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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