Effects of undenatured whey protein supplementation on CXCL12- and CCL21-mediated B and T cell chemotaxis in diabetic mice

Badr, Gamal; Mohany, Mohamed; Metwalli, Ali

doi:10.1186/1476-511x-10-203

Cited by 38 publications

(26 citation statements)

References 33 publications

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“…STZ and alloxan are used to induce diabetes in rodent lab animal models (Eleazu et al 2013). The pancreatic β-cells take up the STZ via the plasma membrane GLUT2 transporter2, resulting in inflates, and ultimately irreversible destroys the pancreatic β-cells (Eleazu et Camel milk has valuable therapeutic effects on treatment of wounds as it enhance wound healing and increase immune cell proliferation and chemotaxis state of experimental animals (Badr 2012 and2013;Badr et al 2011 and2012). Presence of peptides and proteins in camel's milk are the cause of its biological in digestion, absorption, growth and immunity (Korhonen and Pihlanto 2001).…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Camel Milk as Anti-Diabetic Supplement: Biochemical, Molecular and Immunohistochemical Study

Mansour

Nassan

Saleh

et al. 2017

Afr J Tradit Complement Altern Med

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Background: Diabetes is a serious disease affects human health. Diabetes in advanced stages is accompanied by general weakness and alteration in fats and carbohydrates metabolism. Recently there are some scientific trends about the usage of camel milk (CM) in the treatment of diabetes and its associated alterations. CM contains vital active particles with insulin like action that cure diabetes and its complications but how these effects occur, still unclear. Materials and Methods: Seventy-five adult male rats of the albino type divided into five equal groups. Group 1 served as a negative control (C). Group 2 was supplemented with camel milk (CM). Diabetes was induced in the remaining groups (3, 4 and 5). Group 3 served as positive diabetic control (D). Group 4 served as diabetic and administered metformin (D+MET). Group 5 served as diabetes and supplemented with camel milk (D+CM). Camel milk was supplemented for two consecutive months. Serum glucose, leptin, insulin, liver, kidney, antioxidants, MDA and lipid profiles were assayed. Tissues from liver and adipose tissues were examined using RT-PCR analysis for the changes in mRNA expression of genes of carbohydrates and lipid metabolism. Pancreas and liver were used for immunohistochemical examination using specific antibodies. Results: Camel milk supplementation ameliorated serum biochemical measurements that altered after diabetes induction. CM supplementation up-regulated mRNA expression of IRS-2, PK, and FASN genes, while down-regulated the expression of CPT-1 to control mRNA expression level. CM did not affect the expression of PEPCK gene. On the other hand, metformin failed to reduce the expression of CPT-1 compared to camel milk administered rats. Immunohistochemical findings revealed that CM administration restored the immunostaining reactivity of insulin and GLUT-4 in the pancreas of diabetic rats. Conclusion: CM administration is of medical importance and helps physicians in the treatment of diabetes mellitus.

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Section: Introductionmentioning

confidence: 99%

Protective Effect of Camel Milk as Anti-Diabetic Supplement: Biochemical, Molecular and Immunohistochemical Study

Mansour

Nassan

Saleh

et al. 2017

Afr J Tradit Complement Altern Med

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“…We previously reported that. CWP improves immunity during early life and protects against immune disorders during diabetes [29-31]. However, the effects of CWP on the diabetic immune system and its underlying mechanisms have not been studied.…”

Section: Introductionmentioning

confidence: 99%

Camel Whey Protein Protects B and T Cells from Apoptosis by Suppressing Activating Transcription Factor-3 (ATF-3)-Mediated Oxidative Stress and Enhancing Phosphorylation of AKT and IκB-α in Type I Diabetic Mice

Badr

Sayed

Omar

et al. 2017

Cell Physiol Biochem

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Background: Diabetes mellitus (DM) is associated with severe immune system complications. Camel whey protein (CWP) decreases free radicals (ROS) and modulates immune functions, but its effect on DM-impaired immune systems has not been studied. We investigated the impact of CWP on the immune system in a Type 1 diabetes mouse model. Methods: Three experimental groups were used: (1) non-diabetic control; (2) diabetic; and (3) CWP-treated diabetic mice. Results: Induction of diabetes by streptozotocin was associated with reduction of body weight and insulin level, increase in glucose level and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), and reduction in IL-2 and IL-4 levels. Upregulated ATF-3 expression was followed by a marked elevation in ROS levels. Lymphocytes from diabetic mice exhibited increased apoptosis through decreased phosphorylation of AKT and IκB-α, increased infiltration of T cells in the spleen and thymus, and decreased B cell numbers in the spleen. Supplementation with CWP decreased the levels of proinflammatory cytokines, ROS, and ATF-3 expression, and increased the levels of IL-4. Treatment with CWP decreased apoptosis by enhancing the phosphorylation of AKT and IκB-α as well as T-cell and B-cell distribution in the spleen and thymus. Conclusions: Our findings suggest the beneficial effects of CWP supplementation during diabetes on decreasing and orchestrating the redox status and subsequently rescuing the immune cells from exhaustion.

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“…We also use HL-60 cells as a model system because of their stable expression of CXCR4. It is likely that more widespread changes, perhaps affecting the cell migration apparatus, such as F-actin, 33 occur during chronic diabetic conditions that cannot be fully addressed by shortterm treatment with sRAGE. Nevertheless, we found that sRAGE also improved SDF-1-mediated migration of PBMCs isolated from Lepr db diabetic mice, suggesting that acutely administered sRAGE reverses, at least to some extent, the migration impairment that results from prior chronic exposure of the cells to the diabetic environment.…”

Section: Srage Improves Sdf-1 Activity In Diabetic Environmentsmentioning

confidence: 99%

Soluble Receptor for Advanced Glycation End Products Improves Stromal Cell–Derived Factor-1 Activity in Model Diabetic Environments

Olekson

Faulknor

Hsia

et al. 2016

Advances in Wound Care

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Objective: In diabetes, hyperglycemia causes the accumulation of advanced glycation end products (AGEs) that trigger reactive oxygen species (ROS) generation through binding the receptor for AGEs (RAGE). Because exogenous growth factors have had little success in enhancing chronic wound healing, we investigated whether hyperglycemia-induced AGEs interfere with cellular responses to extracellular signals. We used stromal cell-derived factor-1 (SDF-1), an angiogenic chemokine also known to promote stem cell recruitment in skin wounds. Approach: Human leukemia-60 (HL-60) cells and mouse peripheral blood mononuclear cells (PBMCs), which express the SDF-1 receptor CXCR-4, were incubated for 24 h in medium supplemented with 25 mM d-glucose. Soluble RAGE (sRAGE) was used to block RAGE activation. Response to SDF-1 was measured in cellular migration and ROS assays. A diabetic murine excisional wound model measured SDF-1 liposome and sRAGE activity in vivo. Results: Hyperglycemia led to significant accumulation of AGEs, decreased SDF-1-directed migration, and elevated baseline ROS levels; it suppressed the ROS spike normally triggered by SDF-1. sRAGE decreased the ROS baseline and restored both the SDF-1-mediated spike and cell migration. Topically applied sRAGE alone promoted healing and enhanced the effect of exogenous SDF-1 on diabetic murine wounds. Innovation: While there is interest in using growth factors to improve wound healing, this strategy is largely ineffective in diabetic wounds. We show that sRAGE may restore signaling, thus potentiating the effect of exogenously applied growth factors. Conclusion: Blocking RAGE with sRAGE restores SDF-1-mediated cellular responses in hyperglycemic environments and may potentiate the effectiveness of SDF-1 applied in vivo.

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Effects of undenatured whey protein supplementation on CXCL12- and CCL21-mediated B and T cell chemotaxis in diabetic mice

Cited by 38 publications

References 33 publications

Protective Effect of Camel Milk as Anti-Diabetic Supplement: Biochemical, Molecular and Immunohistochemical Study

Protective Effect of Camel Milk as Anti-Diabetic Supplement: Biochemical, Molecular and Immunohistochemical Study

Camel Whey Protein Protects B and T Cells from Apoptosis by Suppressing Activating Transcription Factor-3 (ATF-3)-Mediated Oxidative Stress and Enhancing Phosphorylation of AKT and IκB-α in Type I Diabetic Mice

Soluble Receptor for Advanced Glycation End Products Improves Stromal Cell–Derived Factor-1 Activity in Model Diabetic Environments

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