Significance of propolis administration for homeostasis of CD4+CD25+ immunoregulatory T cells controlling hyperglycemia

Abstract

In the present study, we examined the effect of ethanolic soluble derivative of propolis (EEP) extract on immunological function in diabetic mouse models with the aim of highlighting the role of regulatory T cell, the change of cell surface molecule, and in vivo productions of IFN-γ. Murine models of diabetes mellitus (DM) were created by injecting normal mice with S961 peptide. Normal BALB/c mice were injected intraperitoneally with peptide S961 300 mg/kg body weight (BW) twice a day for eight days. On day 15, the spleen was isolated; then, cell surface molecules and regulatory T cells were analyzed using flow cytometry. The histopathological changes were monitored in the liver of treated and control mice. Afterward, we tested the ability of propolis as an immunomodulator that initiate normality metabolism and homeostasis. The propolis decreased blood sugar levels and increased the number of naïve T cells expressing CD62L molecule by suppressing the development of effector cells in diabetic mice. However, the propolis stimulated development of effector cells, which was indicated by increasing the number of CD4+CD25+ T cells in normal mice. Moreover, the propolis increased the production of IFN-γ in normal mice, whereas in mouse models of diabetes mellitus propolis tends to suppress the production of IFN-γ. The histological analysis of the liver shows that at a dose of 50–200 mg/kg BW propolis does not show a toxic effect so that the dose is categorized safe. Therefore, the ethanolic soluble derivative of propolis (EEP) extract warrant for further exploited as an antidiabetic agent that safe for human.

Antihyperglycemic effect of Sesbania grandiflora seed decoction on streptozotocin-induced diabetic mice: Inflammatory status and the role of interleukin-10

“…This finding contradicted previous research that found an increase of activated CD8 in diabetic mice compared to normal mice. 18 Possibly, our results showed a different tendency because we used an STZ injection method to induce the type 1 diabetic mouse model, while Rifa'i et al 18 used S961 peptide administration which resulted in type 2 diabetes. Furthermore, there is no explanation for the mechanism of how hyperglycemia could induce T-cell activation.…”

“…The supernatant was discarded, and the obtained pellet was subjected to intracellular staining with anti-mouse anti-IFN-γ, anti-mouse anti TNF-α and anti-mouse antiinterleukin-10 (IL-10) for 30 min. 18 …”

“…The single cell suspension containing around 2 3 × 10 6 cells was washed with PBS and stained with FITC-conjugated anti-mouse CD4, PE-conjugated anti-mouse CD8, PE-conjugated anti-mouse CD62L. 18 Intracellular cytokine staining was performed with a Cytofix/Cytoperm kit (BD-Biosciences Pharmingen) according to the protocol provided by the manufacturer. Pellets with approximately 2 3 × 10 6 cells were stained with FITC-conjugated anti-mouse CD4 for 30 min.…”

Detection of VipAlbumin® Effect in CD34 and SDF-1 Mobilization, in Streptozotocin-induced Diabetes Mellitus Mice

“…Highly reactive T cells could induce insulin resistance by its proinflammatory action, but T regulatory cells can prevent this effect by producing IL-10 and TGF-β. This cells can also prevents inflammatory condition being wide-spread, by reversing the activated memory T cells become naive type [45].…”

“…Another strategy also proposed to improve the healthy condition from diabetic patients with hyperglycemia by using propolis treatment [44]. This material is known to contain high-level of nutrient factor such as vitamins, polyphenols, and amino acids, that expected to improve insulin sensitvity and suppress the action of inflammatory molecules.…”