Limiting prolonged inflammation during proliferation and remodeling phases of wound healing in streptozotocin-induced diabetic rats supplemented with camel undenatured whey protein

Ebaid, Hossam; Ahmed, Osama M.; Mahmoud, Ayman M.; Ahmed, Rasha R.

doi:10.1186/1471-2172-14-31

Cited by 67 publications

(45 citation statements)

References 41 publications

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“…C (500 mg/kg) exerted significant improvement in liver and brain SOD activity in TAAtreated rats, while their combination maintained normal SOD activity in liver tissues. Current data is in accordance with other investigators who reported that whey proteins, including α-LAC, suppressed hepatic lipid peroxidation and stimulated the antioxidant defense system by increasing the level of glutathione and the activity of glutathione-S-transferase (GST), glutathione peroxidase (GPx) and superoxide dismutase (SOD) in wounded diabetic rats (Ebaid et al, 2013),α-LACattenuated the decrease in hepatic SOD activity in TAA-induced fibrosis and improved hepatic SOD activity in LPS-treated rats . In addition, vit.…”

Section: Resultssupporting

confidence: 92%

Antioxidant and Hypo-Ammonemic Activities of Alpha-Lactalbumin and Vitamin C in Thioacetamide-Induced Liver and Brain Damage in Rats

Mansour¹,

Nada²,

Elmahmoudy³

et al. 2015

J App Pharm Sci

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Hepatic encephalopathy (HE) is a syndrome resulting from acute or chronic liver failure. The main hypothesis suggests a state of hyperammonemia which is responsible for both direct and indirect alterations in cerebral metabolism with increased production of reactive oxygen and nitrogen species. The effect of milk-derived alphalactalbumin (α-LAC) and vitamin C (vit. C) was evaluated in thioacetamide (TAA)-induced HEmodel in the current study. Animals were treated with TAA (100 mg/kg, i.p.) or saline thrice weekly for six weeks to induce HE then treatment groups received orally α-LAC (100 or150 mg/kg) and /or vit. C (500 mg/kg)daily for two weeks. Twenty-four hours after last treatment sera, liver and brain samples were collected to assess serum ammonia level, activities of alanine transaminase (ALT), and aspartate transaminase (AST), brain and liver oxidative stress parameters as well as histopathological investigations.TAA rats experienced increases in serum activities of ALT and AST as well as serum levels of ammonia. Furthermore, TAA induced hepatic and brain oxidative damage as indicated by increase in lipid peroxidation (LP), decrease in reduced glutathione (GSH) and decrease in superoxide dismutase (SOD) activity as well as increased nitric oxide (NO) levels. TAA caused distortion of hepatic and brain architecture as shown by histopathological examination. Treatment with α-LAC either alone or combined with vit. C resulted in improved liver functions by decline in serum AST and ALT activities and reduction in serum ammonia level. Alpha-LAC and vit. C reduced LP and NO levels while increased GSH concentration and SOD activity in hepatic and brain tissues. Finally, α-LAC-vit. C combination improved the hepatic and brain histological picture. Alpha-LAC-vit. C combination may be a promising pharmacological tool in providing a natural source of branched-chain amino acids and powerful antioxidants to combat hepatic encephalopathy-associated hyperammonemia and its consequential oxidative damage in liver and brain.

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Section: Resultssupporting

confidence: 92%

Antioxidant and Hypo-Ammonemic Activities of Alpha-Lactalbumin and Vitamin C in Thioacetamide-Induced Liver and Brain Damage in Rats

Mansour¹,

Nada²,

Elmahmoudy³

et al. 2015

J App Pharm Sci

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“…Diverse physiological factors that contribute to wound-healing delay include but are not limited to impaired growth factor production, collagen accumulation, keratinocyte migration and proliferation and angiogenic response. A major determining factor for such a delay is a prolonged inflammatory phase that increases the time required for wound closure during diabetes (35). This step impedes the start of the next phase of wound healing, thereby causing a delay in granulation and proliferation.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of miRNAs during Delayed Wound Healing in Diabetes: Role of Dicer

Bhattacharya

Aggarwal

Singh

et al. 2015

Mol Med

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Delayed wound healing is a major complication associated with diabetes and is a result of a complex interplay among diverse deregulated cellular parameters. Although several genes and pathways have been identified to be mediating impaired wound closure, the role of microRNAs (miRNAs) in these events is not very well understood. Here, we identify an altered miRNA signature in the prolonged inflammatory phase in a wound during diabetes, with increased infiltration of inflammatory cells in the basal layer of the epidermis. Nineteen miRNAs were downregulated in diabetic rat wounds (as compared with normal rat wound, d 7 postwounding) together with inhibited levels of the central miRNA biosynthesis enzyme, Dicer, suggesting that in wounds of diabetic rats, the decreased levels of Dicer are presumably responsible for miRNA downregulation. Compared with unwounded skin, Dicer levels were significantly upregulated 12 d postwounding in normal rats, and this result was notably absent in diabetic rats that showed impaired wound closure. In a wound-healing specific quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) array, 10 genes were significantly altered in the diabetic rat wound and included growth factors and collagens. Network analyses demonstrated significant interactions and correlations between the miRNA predicted targets (regulators) and the 10 wound-healing specific genes, suggesting altered miRNAs might fine-tune the levels of these genes that determine wound closure. Dicer inhibition prevented HaCaT cell migration and affected wound closure. Altered levels of Dicer and miRNAs are critical during delayed wound closure and offer promising targets to address the issue of impaired wound healing.

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“…The impaired immune system in diabetic mice was associated with an increase in blood glucose levels, a decrease in insulin levels, and a decrease in body weight, which were partially reversed by CWP treatment. Likewise, CWP stimulated insulin release and lower blood glucose levels in type 1 diabetic rats [39, 40]. It also decreased elevated levels of IL-1β, IL-6, and TNF-α in diabetic mice.…”

Section: Discussionmentioning

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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Limiting prolonged inflammation during proliferation and remodeling phases of wound healing in streptozotocin-induced diabetic rats supplemented with camel undenatured whey protein

Cited by 67 publications

References 41 publications

Antioxidant and Hypo-Ammonemic Activities of Alpha-Lactalbumin and Vitamin C in Thioacetamide-Induced Liver and Brain Damage in Rats

Antioxidant and Hypo-Ammonemic Activities of Alpha-Lactalbumin and Vitamin C in Thioacetamide-Induced Liver and Brain Damage in Rats

Downregulation of miRNAs during Delayed Wound Healing in Diabetes: Role of Dicer

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

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