Diabetic wound healing is a complicated procedure because hyperglycemia changes the various stages of wound healing. In type 2 diabetes mellitus (T2DM), oxidative stress is proven to be a critical factor in causing non-healing wounds and aggravating the inflammatory phase, resulting in the amputation of lower limbs in T2DM patients. This makes scientists figure out how to control oxidative stress and chronic inflammation at the molecular level. Nuclear factor erythroid 2- related factor 2 (Nrf2) releases antioxidant proteins to suppress reactive oxygen species (ROS) activation and inflammation. The current review discusses the role of Nrf2 in improving diabetic wound healing by reducing the production of ROS and thus reducing oxidative stress, as well as inhibiting nuclear factor kappa B (NF-kB) dissociation and nuclear translocation, which prevents the release of inflammatory mediators and increases antioxidant protein levels, thereby improving diabetic wound healing. As a result, the researcher will be able to find a more effective diabetic wound healing therapy.

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Background: Diabetes foot ulcers (DFU) are among the most common complications in diabetic patients, leading to amputation and psychological distress. This mini-review covers the general physiology of ulcer healing as well as the pathophysiology of DFU and its therapies. Only a few treatments have been sanctioned and numerous compounds from various pharmacological groups are now being tested at various stages for the prevention and treatment of DFUs. Objective: The main objective of this mini-review is to give concise information on how diabetes mellitus impairs the healing of chronic ulcers by disrupting numerous biological systems of the normal healing process, resulting in diabetic foot ulceration, and the current therapeutic approaches. Method: A review of accessible material from systemic searches in the PubMed/Medline, Scopus, Cochrane Database of Systematic Reviews, published review articles, and Clinical Trials databases (US National Library of Medicine) with no period of limitation was conducted. Result: The treatment of DFUs comprises wound dressings, use of matrix metalloproteinase inhibitors in wound dressing, antibiotics, skin substitutes, pressure off-loading growth factors and stem cells, gene therapy, topical oxygen therapy, etc. Conclusion: The majority of these treatments are aimed at treating diabetic foot ulcers and preventing diabetic wounds from becoming infected. Yet, there is no single therapy that can be advised for diabetic foot ulcer patients. Future treatment strategies should be considered an appropriate treatment option for persistent wounds.

Wound healing is a complicated organised process that includes numerous phases that connect diverse cellular events and activate several intracellular molecular pathways in injured cells and tissues. Delay in wound healing owing to high levels of oxidative stress is a major difficulty in various metabolic illnesses, including diabetes mellitus. Several therapeutic wound dressing materials and methods, such as hyperbaric oxygen treatment and negative pressure wound therapy, have been developed to speed up wound healing and restore cellular homeostasis. A significant advance has been made in locating transcriptional regulators involved in wound healing. The redox sensitive transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is the major regulator of antioxidant defense regulation, inducing the expression of cyto-protective genes and increasing the generation of antioxidants that scavenge free radicals.Activators of Nrf2 have been shown to reduce oxidative stress and improve wound healing in a variety of pathophysiological situations, including diabetes and its consequences such as diabetic foot ulcers, chronic kidney disease, and diabetic nephropathy. Several therapeutic chemicals have been discovered to alleviate oxidative stress and consequently increase cell proliferation. Angiogenesis results in tissue healing through activating the transcription factor Nrf2. This review focuses on role of Nrf2 mediated antioxidant gene expression for diabetic wound healing.

BACKGROUNDWith the increasing trend in the diabetic population and the diabetic nephropathy, it is necessary for us to look into the bone metabolism in the diabetics with CKD. This study aims to describe the bone metabolism and the bone turnover rates in diabetic kidney disease and to see if there is a difference between diabetic and non-diabetic CKD in the bone turnover rates. MATERIALS AND METHODSWe did a cross-sectional observational study between January and June 2016 at the Govt. Kilpauk Medical College with 90 CKD patients. Of them 44 were diabetics with a mean age of 56.18 +/-8.88 and 46 were non-diabetics with a mean age of 52.19 +/-14.55. Patients were analysed for various biochemical parameters. The data were analysed using SPSS (Statistical Package for Social Sciences) ver 16.01. RESULTS82% of our diabetic CKD patients have diabetic retinopathy. Diabetic retinopathy is not associated with abnormalities in bone turnover (odds ratio= 1). For the diabetic CKD (n= 44), the prevalence of hypoparathyroidism is 4.5%, hyperparathyroidism is 59%, hyperparathyroidism more than twice the upper limit of normal is 36.36%, hypocalcaemia is 15.9%, hypercalcaemia is 4.5%, hypophosphataemia is 20.45% and vitamin D deficiency is 95.45%. The most common bone turnover abnormality observed in diabetics in our study is the mixed turnover state (30%) followed by osteomalacia (21%), whereas in non-diabetics, high turnover state (26%) is the most common abnormality, but there is no statistically significant difference between the two (p= 0.81). Low turnover state in diabetics and non-diabetics in our study are 7% and 9% respectively. CONCLUSIONThus, we conclude that a mixed bone turnover state followed by osteomalacia is commoner in diabetic CKD than other patterns. Diabetic retinopathy is not predictive of the bone turnover state. Diabetic and non-diabetic CKD need not be considered as separate entities as far as bone metabolism is considered.