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Review
.2022 Jan 20;19(1):6.
doi: 10.1186/s12986-021-00639-z.

A comprehensive insight into the molecular and cellular mechanisms of the effects of Propolis on preserving renal function: a systematic review

Affiliations
Review

A comprehensive insight into the molecular and cellular mechanisms of the effects of Propolis on preserving renal function: a systematic review

Paniz Anvarifard et al. Nutr Metab (Lond)..

Abstract

Background: The present systematic review is conducted, focusing on the existing evidence of Propolis's effects due to its various health benefits, mainly antioxidant and anti-inflammatory properties on preserving renal function.

Methods: A systematic search of PubMed, Scopus, Embase, ProQuest, and Google Scholar was undertaken for relevant papers published from the start until January 2021.

Results: This review revealed that Propolis affects fasting blood sugar (FBS), postprandial blood glucose, advanced glycation end products (AGEs) concentrations, malondialdehyde (MDA) levels, urinary concentrations of reactive oxygen metabolites (Tbars), total oxidant status (TOS), oxidative stress index (OSI), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) formation favorably. The findings on hemoglobin A1C (HbA1C), insulin, homeostasis model assessment of insulin resistance (HOMA-IR), β-cell function (HOMA-β), quantitative insulin sensitivity check index (QUICKI), and lipid profile were controversial. Moreover, a significant reduction in renal nuclear factor kappa B (NF-κB), serum immunoglobulins, renal ED-1+ cells, and urinary monocyte chemoattractant protein-1 (MCP-1) following Propolis supplementation has been reported, while the results on interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), nitric oxide (NO), nitric oxide synthetase (NOS), and high sensitivity C-reactive protein (hs-CRP) were controversial. Furthermore, included studies showed its anti- proteinuria and kidney restoring effects.

Conclusion: In this review, both human and animal studies provide us evidences that Propolis could potentially improve the glycemic status, oxidative stress, renal tissue damage, and renal function. Further studies are needed to determine the underlying mechanisms.

Keywords: AKI; Acute kidney injury; CKD; Chronic kidney disease; Kidney disease; Propolis; Renal function; Systematic review.

© 2022. The Author(s).

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
Flow diagram of the literature search and study selection process
Fig. 2
Fig. 2
The possible mechanisms for the effects of Propolis on hyperglycemia and hyperglycemia-induced renal damage. In diabetic patients, renal glucose uptake is increased in both the post-absorptive and postprandial states; however, muscle glucose uptake is either normal or reduced. Compensated increased glucose uptake in the kidney enhances ROS generation, eventually contributing to OS and pathogenetic pathways, which lead to renal tissue dysfunction. Propolis, by decreasing intestinal absorption of carbohydrate and expression of gluconeogenic genes in hepatocellular cells and elevating insulin production, cellular sensitivity to insulin, and the level of glycolysis in the liver, could alleviate hyperglycemia and prevent hyperglycemia-induced renal damage. Also, by its antioxidant properties, Propolis can reduce cellular dysfunction, inflammation, apoptosis, and fibrosis in kidney (Figure adapted from Fig. 2. in Ref. (6)). Abbreviations: ROS, reactive oxygen species; eNOS, endothelial nitric oxide synthase; PARP, poly ADP ribose polymerase; GAPDH, glyceraldehyde-3-dehydrogenase; AGE, advanced glycation end-product; DAG, diacylglycerol; DHAP, dihydroxyacetone phosphate; GFAT, glutamine fructose-6-phosphate amidotransferase; NF-κB, nuclear factor kappa B; PKC, protein kinase C; RAGE, receptor for AGE; UDP-GLcNAc, uridine diphosphate N-acetylglucosamine; PI3K, phosphatidylinositol 3-kinase; AMPK, 5'-adenosine monophosphate-activated protein kinase; GLUT 4, insulin-sensitive glucose transporter 4; IR, insulin receptor; Akt, serine/threonine protein kinase B; mTOR, mammalian target of rapamycin
Fig. 3
Fig. 3
The important suggested mechanisms for the effect of Propolis on dyslipidemia inA liver by inhibiting cholesterol and triglyceride synthesis and inducing ß-oxidation and cholesterol-bile acid turnover,B gastrointestinal system by inhibiting the absorption of triglyceride and probably cholesterol, andC adipose tissue by regulation of fat accumulation and lipolysis and dyslipidemia-induced renal damage. Abbreviations: CYP7A1, Cholesterol 7α-hydroxylase; SREBP, Sterol regulatory element-binding proteins; FAS, fatty acid synthase; ACAC-α, acetyl-CoA carboxylase α; HMGCS-1, 3-hydroxy-3-methylglutaryl-Coenzyme A synthase 1; HMGCR, 3-hydroxy-3-methylglutaryl-Coenzyme A reductase; SQLE, Squalene Epoxidase; PPAR, peroxisome proliferator-activated receptor; FA, fatty acid; TG, triglyceride; ROS, reactive oxygen species; NF-κB, nuclear factor kappa B; ECM, extracellular matrix
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