Stereological and gene expression examinations on the combined effects of photobiomodulation and curcumin on wound healing in type one diabetic rats

We examined the effects of photobiomodulation (PBM) independently and combined with curcumin on stereological parameters and basic fibroblast growth factor (bFGF), hypoxia-inducible factor-1α (HIF-1α), and stromal cell-derived factor-1α (SDF-1α) gene expressions in an excisional wound model of rats with type one diabetes mellitus (T1DM). T1DM was induced by an injection of streptozotocin (STZ) in each of the 90 male Wistar rats. One round excision was generated in the skin on the back of each of the 108 rats. The rats were divided into six groups (n = 18 per group): control (diabetic), untreated group; vehicle (diabetic) group, which received sesame oil; PBM (diabetic) group; curcumin (diabetic) group; PBM + curcumin (diabetic) group; and a healthy control group. On days 4, 7, and 15, we conducted both stereological and quantitative real-time PCR (qRT-PCR) analyses. The PBM and PBM + curcumin groups had significantly better inflammatory response modulation in terms of macrophages (P < .01), neutrophils (P < .001), and increased fibroblast values compared with the other groups at day 4 (P < .001), day 7 (P < .01), and day 15 (P < .001). PBM treatment resulted in increased bFGF gene expression on days 4 (P < .001) and 7 (P < .001), and SDF-1α gene expression on day 4 (P < .001). The curcumin group had increased bFGF (P < .001) expression on day 4. Both the PBM and PBM + curcumin groups significantly increased wound healing by modulation of the inflammatory response, and increased fibroblast values and angiogenesis. The PBM group increased bFGF and SDF-1α according to stereological and gene expression analyses compared with the other groups. The PBM and PBM + curcumin groups significantly increased the skin injury repair process to more rapidly reach the proliferation phase of the wound healing in T1DM rats.     

The effect of the glycolipoprotein extract (G‐90) from earthworm Eisenia foetida on the wound healing process in alloxan‐induced diabetic rats

Diabetes is now regarded as a major public health problem. The number of patients is estimated to increase to over 439 million cases by 2030. One of the major health clinical problems in patients with diabetes patients is impaired wound healing. Diabetic foot ulcer is a major complication of diabetes mellitus in 12 to 25% of patients, which increases the risk of damage in the limbs or amputation. The earthworm Eisenia foetida glycolipoprotein (as known G‐90) is a blend of macromolecules with some biological properties including mitogenicity, anticoagulation, fibrinolysis, bacteriostatic and antioxidatiaon. Given the biological properties of G‐90, this study was conducted to investigate the effect of extract obtained from the homogenate of Eisenia foetida (G‐90) on the wound healing process in alloxan‐induced diabetic rats. The results of the present study revealed that treatment by using G‐90 can speed up the wound healing process, which is exactly similar to the effect of D‐panthenol treatment in rats. These findings also demonstrated that G‐90 treatment decreases the risk of infection in the wound site compared with D‐panthenol treatment. In addition, histological analysis indicated that a better extracellular matrix formation with increased fibroblast proliferation, neovascularization, collagen synthesis and early epithelial layer formation was observed in G‐90 treated group. Therefore, the G‐90 could be considered as a new wound healing agent introducing promising therapeutic approaches in both human and veterinary medicine. Copyright © 2016 John Wiley & Sons, Ltd.     

Suppression of the PI3K-Akt pathway is involved in the decreased adhesion and migration of bone marrow-derived mesenchymal stem cells from non-obese diabetic mice

T1DM (type 1 diabetes mellitus) is an autoimmune disease characterized by T-cell-mediated damage of islet β-cells. The pathology of NOD (non-obese diabetic) mouse involves the insulitis induced by infiltration of T-cells, a similar pathogenic mechanism in T1DM patient. BM-MSCs (bone marrow mesenchymal stem cells) are multipotent progenitor cells that can be isolated from a number of sources. Recent studies have shown that transplantation of MSCs to the NOD mice could prevent the process and have the therapeutic effects on T1DM. In our studies, we have found that migration and adhesion of BM-MSCs from NOD mice were suppressed compared with the BM-MSCs from ICR (imprinting control region) mice, accompanying with the abnormal distribution of FAK (focal adhesion kinase) and F-actin (filamentous actin). Further, we have found that the activation of PI3K (phosphoinositide 3-kinase)-Akt pathway was suppressed in BM-MSCs from NOD mice. When the PI3K-Akt pathway was inhibited by LY294002, the adhesion and migration of BM-MSCs from ICR mice were suppressed as well. These results indicated that the suppression of PI3K-Akt pathway is involved in the decreased adhesion and migration of BM-MSCs from NOD mice.     

Polymorphic markers of the NO synthase genes and genetic predisposition to diabetic polyneuropathy in type 1 diabetes mellitus

The allele and genotype frequency distributions of polymorphic markers of the NOS1, NOS2, and NOS3 genes coding for three different NO synthases were compared for type 1 diabetes mellitus (T1DM) patients with or without diabetic polyneuropathy (DPN). The groups (total 180 patients, ethnic Russians or East Slavs from Moscow) had nonoverlapping (polar) phenotypes. Group DPN+ included patients with DPN and T1DM duration of no more than 5 years. Control group DPN- included patients without DPN and with T1DM duration of at least 10 years. No significant differences in allele and genotype frequency distributions were revealed for the polymorphic markers (CA) _n of gene NOS1 (CCTTT) _n of gene NOS2, and ecNOS4a/4b and Glu298Asp of gene NOS3, suggesting a lack of association between the polymorphic markers and DPN. In the case of the (CCTTT) _n polymorphic marker of the NOS2 gene, a tendency toward an association with DPN was observed for allele 14. Carriers of this allele have a lower risk of DPN in T1DM.__________Translated from Molekulyarnaya Biologiya, Vol. 39, No. 2, 2005, pp. 224–229.Original Russian Text Copyright © 2005 by Zotova, Voronko, Bursa, Galeev, Strokov, Nosikov.