# Effects of Bee Bread (Perga) on Pro-Inflammatory Cytokine Levels and Histopathological Alterations in the Liver and Kidneys of Streptozotocin-Induced Diabetic Rats

**Authors:** Nur Akman, Turan Yaman, Ahmet Ufuk Kömüroğlu, Meryem Çalışır

PMC · DOI: 10.3390/biology15050380 · 2026-02-26

## TL;DR

This study shows that bee bread reduces inflammation and protects kidney tissue in diabetic rats more effectively than liver tissue.

## Contribution

The study reveals that bee bread has tissue-specific anti-inflammatory effects, particularly benefiting the kidneys in diabetic conditions.

## Key findings

- Bee bread significantly reduced inflammatory cytokines in the kidneys of diabetic rats.
- Kidney tissue structure improved with bee bread treatment, while liver recovery was limited.
- Bee bread's protective effects suggest it could be a natural modulator of inflammation in diabetes.

## Abstract

Diabetes is a chronic disease that leads to high blood sugar and persistent inflammation, which can progressively damage vital organs such as the liver and kidneys. Preventing inflammation-related organ injury is essential to reduce long-term complications. Bee bread, also known as perga, is a natural fermented bee product rich in biologically active compounds with potential anti-inflammatory properties. In this study, we examined whether bee bread could protect the liver and kidneys in rats with experimental diabetes. Diabetes caused significant increases in inflammatory markers and structural damage in both organs. Bee bread treatment markedly reduced inflammation and improved tissue structure in the kidneys. However, although some inflammatory markers decreased in the liver, structural recovery was limited. This difference between the two organs may be related to variations in local cellular signaling and immune regulation mechanisms. Overall, our findings suggest that bee bread exerts organ-specific protective effects, with a stronger benefit in the kidneys than in the liver. These results highlight the importance of understanding tissue-specific responses when evaluating natural products for diabetes-related complications.

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent systemic inflammation, which contributes to progressive multi-organ dysfunction, particularly in metabolically active tissues such as the liver and kidneys. Bee bread (Perga), a fermented bee pollen product rich in bioactive compounds, has been reported to exert anti-inflammatory and organ-protective effects; however, its tissue-specific influence on inflammatory responses under diabetic conditions remains incompletely defined. Thirty-two male Wistar Albino rats were randomly assigned to four groups: Control, DM, DM + Perga, and Perga. Diabetes was induced by streptozotocin (STZ; 55 mg/kg, i.p.). Perga was administered orally at a dose of 0.5 g/kg/day for 28 days. Pro-inflammatory cytokine levels (CRP, TNF-α, IL-1β, and IL-6) were quantified in liver and kidney tissues using ELISA. Histopathological alterations were evaluated by hematoxylin and eosin staining. DM significantly increased the IL-1β, IL-6, and CRP levels in hepatic tissue and elevated TNF-α, IL-1β, IL-6, and CRP levels in renal tissue. Perga administration attenuated these inflammatory responses, particularly reducing IL-1β and IL-6 levels in the liver and all measured cytokines in the kidney. Histopathological analyses revealed hepatocyte degeneration and necrosis, sinusoidal dilatation, tubular epithelial degeneration, and glomerular damage in diabetic rats, whereas Perga treatment partially improved hepatic alterations and improved renal structural integrity. These findings indicate that Perga exerts tissue-specific anti-inflammatory and protective effects in experimental diabetes, with a more pronounced impact on renal inflammation than on hepatic responses. Although its effects on hepatic TNF-α and CRP levels were limited, Perga may act as a natural modulator of cytokine-mediated inflammatory processes. Further studies are warranted to elucidate the underlying molecular mechanisms.

## Linked entities

- **Proteins:** CRP (C-reactive protein), TNF (tumor necrosis factor), IL1B (interleukin 1 beta), IL6 (interleukin 6)
- **Chemicals:** streptozotocin (PubChem CID 29327)
- **Diseases:** Diabetes (MONDO:0005015), Diabetes mellitus (MONDO:0005015)
- **Species:** Rattus norvegicus (taxon 10116), Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Crp (C-reactive protein) [NCBI Gene 25419] {aka Aa1249, Ab1-341, Ab2-196, Ac1-114, Ac1262, Ac2-069}, Il1b (interleukin 1 beta) [NCBI Gene 24494] {aka IL-1F2}, Tnf (tumor necrosis factor) [NCBI Gene 24835] {aka RATTNF, TNF-alpha, Tnfa}, Il6 (interleukin 6) [NCBI Gene 24498] {aka ILg6, Ifnb2}
- **Diseases:** Inflammatory (MESH:D007249), DM (MESH:D003920), multi-organ dysfunction (MESH:D009102), metabolic disorder (MESH:D008659), degeneration (MESH:D009410), glomerular damage (MESH:D007674), hepatic alterations (MESH:D056486), necrosis (MESH:D009336)
- **Chemicals:** STZ (MESH:D013311), Perga (-), hematoxylin (MESH:D006416), eosin (MESH:D004801)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12984150/full.md

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Source: https://tomesphere.com/paper/PMC12984150