Cinnamon: an aromatic condiment applicable to chronic kidney disease

Abstract

Cinnamon, a member of the Lauraceae family, has been widely used as a spice and traditional herbal medicine for centuries and has shown beneficial effects in cardiovascular disease, obesity, and diabetes. However, its effectiveness as a therapeutic intervention for chronic kidney disease (CKD) remains unproven. The bioactive compounds within cinnamon, such as cinnamaldehyde, cinnamic acid, and cinnamate, can mitigate oxidative stress, inflammation, hyperglycemia, gut dysbiosis, and dyslipidemia, which are common complications in patients with CKD. In this narrative review, we assess the mechanisms by which cinnamon may alleviate complications observed in CKD and the possible role of this spice as an additional nutritional strategy for this patient group.

Keywords: Chronic renal insufficiency; Cinnamomum zeylanicum; Inflammation; Oxidative stress; Spices.

Figure 1.. Antioxidant and anti-inflammatory actions of cinnamon in cells.

Bioactive compounds from cinnamon may activate the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), leading to the synthesis of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), heme oxygenase 1 (HO-1), glutathione peroxidase 1 (GPx-1), and NAD(P)H dehydrogenase [quinone] 1 (NQO-1). Also, these compounds can inhibit nuclear factor kappa B (NF-κB), activator protein 1 (AP-1), and NLR family pyrin domain containing 3 (NLRP3), reducing inflammatory cytokine production. TLR-4, toll-like receptor 4; ERK, extracellular signal-regulated kinase; AKT, protein kinase B; Keap1, Kelch-like ECH-associated protein 1; TNF-α, tumor necrosis factor alpha; CRP, C-reactive protein; IL, interleukin.

Figure 2.. The potential benefits of cinnamon to patients with diabetes, obesity, or CVDs.

Cinnamon can provide physiological benefits by mimicking insulin action through insulin receptor autophosphorylation of the β-subunit of tyrosine and promoting glucose transporter (GLUT) translocation via the 5' adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. Cinnamaldehyde has antidiabetic activity through upregulation of the insulin signaling pathway, induction of peroxisome proliferator-activated receptors (PPARs), and inhibition of α-glucosidase and pancreatic α-amylase. Cinnamon may increase the expression of uncoupling protein 1 (UCP-1), promoting thermogenesis. It can also reduce hepatic expression of sterol regulatory element-binding protein-1c (SREBP-1c) and nuclear factor kappa B (NF-κB) and upregulate PPAR-α, fatty acid synthase, carnitine palmitoyltransferase I (CPT-1), and nuclear factor erythroid 2-related factor 2 (Nrf-2) to promote cytoprotective effects and reduce inflammation. Cinnamaldehyde might act as a natural agonist of transient receptor-ankyrin receptor 1 (TRPA1), reducing ghrelin secretion and food intake. Cinnamon may decrease SREBP-1 and cluster of differentiation 36 (CD36) expression and increase expression of PPAR-γ, reducing oxidative stress, inflammatory burden and, therefore, cardiovascular risk. LXR-α, liver X receptor alpha; CVD, cardiovascular disease.