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.

Although the endothelial dysfunction is related with tumor development, there is no consensus on the suppressive or supportive effect on tumor growth. The goal of the present study was to evaluate endothelial dysfunction related factors in animal breast cancer model that was developed by administrating endothelial nitric oxide synthase blocking agent, Nitro-L-arginine methyl ester hydrochloride (L-NAME). Endothelial dysfunction related main factors such as nitric oxide synthase, interleukin-6, vascular endothelial growth factor receptor-2 and vascular endothelial cadherin were investigated by immunohistochemically in tumor and carotid artery tissues. In tumor tissues apoptosis was determined by TUNEL assay. The level of endothelin-1 in blood was measured by ELISA. İntima-media thickness of carotid artery was evaluated with Doppler-USG measurements. As a result, in this study it was shown that vascular endothelial growth factor receptor-2, endothelin-1, endothelial nitric oxide synthase, interleukin-6, vascular endothelial cadherin and E-selectin molecules play a role in reducing breast tumor growth based on endothelial dysfunction.