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

PeerJ. 2023 Sep 27:11:e16132. doi: 10.7717/peerj.16132. eCollection 2023.

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.

Keywords: Allicin; Chronic kidney disease; Hypertension; Inflammation; Metabolic syndrome; Oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Antioxidants / pharmacology
  • Body Weight
  • Glucose Intolerance* / drug therapy
  • Inflammation / drug therapy
  • Kidney
  • Male
  • Metabolic Syndrome* / drug therapy
  • Models, Theoretical
  • Rats
  • Rats, Wistar
  • Renal Insufficiency, Chronic* / drug therapy

Substances

  • Antioxidants
  • allicin
  • Anti-Inflammatory Agents

Grants and funding

The financing for this research as well as the publishing in open access were covered by the Instituto Nacional de Cardiología Ignacio Chávez. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.