Abstract
Recent studies suggest that allicin may play a role in chronic kidney disease (CKD), reducing hypertension and oxidative stress and improving renal dysfunction. In the present study, CKD was induced by 5/6 nephrectomy and the animals were divided into four treatment groups as follows: control (C), CKD, CKD+allicin (40 mg/kg pathway oral) (CKDA), and CKD+Losartan (20 mg/kg) (CKDL). After CKD induction, the rats developed hypertension from week 3 to the end of the study. This was associated with increased creatinine and blood urea nitrogen (BUN) levels in serum, increased albuminuria, increased urinary excretion of N-acetyl-β-d-glucosaminidase (NAG), increased nephrin expression, and incrased histological alterations in the cortex. The levels of angiotensin receptors and endothelial nitric oxide synthase (eNOS) were decreased in the renal cortex from the CKD group. Otherwise, lipid and protein oxidation were higher in the CKD group than in the control group. A disturbance was observed in the expression levels of the nuclear factor erythroid 2-related factor 2/Kelch ECH associating protein 1 system (Nrf2/keap1) and the antioxidant enzymes catalase, superoxide dismutase, and heme oxygenase-1. Allicin or losartan treatments relieved renal dysfunction, hypertension, and oxidative stress. In addition, both treatments showed the same efficacy on the expression of angiotensin receptors, the nephrin, Nrf2/keap1 pathway, and eNOS. Further in silico analyses suggest that allicin and losartan could have a common mechanism involving interaction with AT1 receptors. Allicin showed antihypertensive, antioxidant, and nephroprotective effects. The beneficial effects showed by allicin are similar, or even better, than those of losartan. In fact, the effect of allicin on blood pressure and renal function is comparable to reductions seen with losartan, a prescription drug commonly used as a first-line therapy.
Highlights
Hypertension is the leading cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD), contributing to the disease itself or, most commonly, contributing to its progression
We recently reported that allicin treatment in rats with subtotal nephrectomy improves cardiac function and ameliorates oxidative stress and hypertension [18], supporting the hypothesis that allicin could be important as a complementary and/or alternative therapy to reduce the progression of CKD and decrease the risk of cardiovascular disease
As expected in this experimental model of CKD, the subtotal nephrectomy resulted in a renal dysfunction status at six weeks of follow-up, which was evidenced by the significant increase in creatinine and blood urea nitrogen (BUN) levels in serum, as well as the reduction in creatinine clearance (Table 1)
Summary
Hypertension is the leading cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD), contributing to the disease itself or, most commonly, contributing to its progression. Hypertension is reported as a consequence of kidney injury [1]. In the United States, approximately 30% of incident ESRD cases are attributed to hypertension [2]. Hypertension is highly prevalent in patients with CKD, playing a role in the high cardiovascular morbidity and mortality of this particular population. The risk of cardiovascular death in this patient group is greater than the risk of progression to ESRD. CKD is the most common form of secondary hypertension, and mounting evidence suggests that it is an independent risk factor for cardiovascular morbidity and mortality [3,4,5]
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