The Brain Extracellular Matrix (ECM) plays a crucial role in both the developing and adult brain by providing structural support and mediating cell-cell interactions. In this review, we focus on the major constituents of the ECM and how they function in both normal and injured brain, and summarize the changes in the composition of the ECM as well as how these changes either promote or inhibit recovery of function following Traumatic Brain Injury (TBI). Modulation of ECM composition to facilitates neuronal survival, regeneration and axonal outgrowth is a potential therapeutic target for TBI treatment.

Diabetes mellitus is a growing health problem worldwide and is associated with severe liver complications. The aim of the present study is to analyse the status of metabolic and free-radical-scavenging enzymes and second messengers in the liver of streptozotocin (STZ)-induced diabetic rats, and to determine the hepatoprotective role of vitamin D 3 . All studies were performed using the liver of adult male Wistar rats. Gene expression studies were carried out using real-time PCR with specific probes. Second messenger levels were determined using 3 H-labelled Biotrak assay kits, and glucose uptake assay with D-[ 14 C]glucose. The present results show that there was a decrease in hepatic glucose uptake, malate dehydrogenase activity, glycogen content, inositol triphosphate (IP 3 ) and cyclic GMP levels, and superoxide dismutase, glutathione peroxidase, phospholipase C, cyclic AMP-responsive element-binding protein, vitamin D receptor (VDR) and insulin receptor (INSR) gene expression in the diabetic rats when compared with the controls (all P,0·05), while cyclic AMP levels and GLUT2 expression were increased (P,0·05). Treatment of the diabetic rats with vitamin D 3 and insulin reversed the altered parameters to near control values. In conclusion, the data suggest a novel role of vitamin D 3 in restoring impaired liver metabolism in STZ-induced diabetic rats by regulating glucose uptake, storage and metabolism. We demonstrated that the restoring effect of vitamin D 3 is mediated through VDR modulation, thereby improving signal transduction and controlling free radicals in the liver of diabetic rats. These data suggest a potential role for vitamin D 3 in the treatment of diabetes-associated hepatic complications.Key words: Vitamin D: Diabetes: Liver: Oxidative stress: Metabolism: Insulin Diabetes-associated complications are major causes of morbidity and mortality. The liver plays a unique role in glucose homeostasis. Because of its anatomical location, it is ideally suited to control the systemic supply of absorbed nutrients, and it is one of only two organs that both consume and produce substantial amounts of glucose. The central role of the liver in the maintenance of blood glucose levels is assured by complex regulation by metabolic substrates, insulin and other hormones (1) . Diabetes-associated hyperglycaemia and hypoinsulinaemia lead to the impairment of hepatic glucose and lipid metabolism. Virtually, the entire spectrum of liver diseases is seen in patients with diabetes, including liver cirrhosis, a significant cause of death in diabetic patients, even more relevant than CVD (2) . Interest in the development of novel antidiabetic agents has been fuelled by the intense complications due to therapeutic treatment of diabetes and associated liver failure (2,3) . An increased prevalence of diabetes has been observed in vitamin D-deficient individuals (4) , and our previous study has shown that vitamin D 3 treatment restores blood glucose homeostasis in streptozotocin (STZ)-induced diabetic rats (5) . Bind...

Curcumin, an active principle component in rhizome of Curcuma longa, has proved its merit for diabetes through its anti-oxidative and anti-inflammatory properties. This study aims at evaluating the effect of curcumin in modulating the altered dopaminergic receptors, CREB and phospholipase C in the cerebral cortex and cerebellum of STZ induced diabetic rats. Radioreceptor binding assays and gene expression was done in the cerebral cortex and cerebellum of male Wistar rats using specific ligands and probes. Total dopaminergic receptor binding parameter, Bmax showed an increase in cerebral cortex and decrease in the cerebellum of diabetic rats. Gene expression studies using real time PCR showed an increased expression of dopamine D1 and D2 receptor in the cerebral cortex of diabetic rats. In cerebellum dopamine D1 receptor was down regulated and D2 receptor showed an up regulation. Transcription factor CREB and phospholipase C showed a significant down regulation in cerebral cortex and cerebellum of diabetic rats. We report that curcumin supplementation reduces diabetes induced alteration of dopamine D1, D2 receptors, transcription factor CREB and phospholipase C to near control. Our results indicate that curcumin has a potential to regulate diabetes induced malfunctions of dopaminergic signalling, CREB and Phospholipase C expression in cerebral cortex and cerebellum and thereby improving the cognitive and emotional functions associated with these regions. Furthermore, in line with these studies an interaction between curcumin and dopaminergic receptors, CREB and phospholipase C is suggested, which attenuates the cortical and cerebellar dysfunction in diabetes. These results suggest that curcumin holds promise as an agent to prevent or treat CNS complications in diabetes.

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Hypoglycemia is the major problem to blood glucose homeostasis in treatment of diabetes and is associated with severe irreversible consequences including seizures, coma and death. GABAergic inhibitory function in the cerebral cortex plays an important role in controlling the excitability and responsiveness of cortical neurons. Present study analysed effects of insulin induced hypoglycemia and streptozotocin induced diabetes on the cortical GABA receptor binding, GABA(Aά1), GABA(B) receptor subtype expression, GAD and GLUT3 expression. Diabetic rats showed decreased [(3)H] GABA binding in the cerebral cortex compared to control while hypoglycemia exacerbated the decrease. GABA receptor subunits; GABA(Aά1), GABA(B) and GAD expression significantly decreased in diabetic rats whereas hypoglycemia significanly decreased the expression compared to diabetic. GLUT3 expression significantly up regulated during both hypo and hyperglycemia. Our results showed that hypoglycemia and hyperglycemia decreased GABAergic neuroprotective function in the cerebral cortex, which account for the increased vulnerability of cerebral cortex to subsequent neuronal damage during hypo/hyperglycemia.

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Solvent effects in aqueous media for the fast heterogeneous catalytic reduction of p-nitrophenol were studied using two silver nanocatalysts. Binary and ternary silver nanocatalysts (BNC and TNC) utilize functionalized multiwalled carbon nanotubes (MWCNTs) and polythiophene-functionalized MWCNT nanocomposites as hosts for silver nanoparticles, respectively. The catalytic reduction kinetics were measured by UV–visible absorption spectroscopy by observing the decrease of the sodium nitrophenolate ion peak at 400 nm. The first-order rate constants (k) obtained to reduce p-nitrophenol (1.0 × 10–4 M) in an aqueous medium using TNC and BNC by taking optimum nanocatalytic concentrations were 0.0134 and 0.0364 s–1, with the activity factor 113.34 and 303.34 s–1 g–1, respectively. The role played by each component of BNC and TNC nanocomposites was determined using control experiments. UV–visible (UV–vis) absorption spectroscopy, powder X-ray diffraction studies, and X-ray photoelectron spectroscopy (XPS) analysis on recycled catalysts have revealed no substantial deactivation in catalytical activity or loss of silver nanoparticles for recycled TNC up to the fifth cycle and for recycled BNC up to the sixth cycle. Field emission scanning electron microscopy (FE-SEM) analysis manifested the crystalline byproducts of sodium metaborate hydrates which could also decelerate catalytic activity in higher cycles. The relative rates of catalytic hydrogenation in different solvent–water mixtures indicated that a 10% glycerol–water mixture is a green and nontoxic solvent combination for accelerating the catalytic reduction of p-nitrophenol. The quantity of catalyst and sodium borohydride was minimized by employing a 10% glycerol–water mixture. The highest activity factor of 936.50 s–1 g–1 was achieved using the BNC nanocatalyst (0.005 mg/mL) with the P-NP to NaBH4 molar ratio of 1:200. The catalytic reduction of p-nitrophenol in different solvent–water mixtures revealed that the reduction rate directly depends on the active hydrogen present in the solvent molecules. The industrial-scale reduction of concentrated p-nitrophenol (1.0 × 10–1 M) was achieved by the addition of NaBH4 (25 times higher molar equivalent to P-NP) using a relatively low catalyst concentration (BNC-0.18) in a reasonable reaction time of 1 h. The ternary nanocatalyst (TNC) has shown stable dispersion in water than BNC, which is suitable as an excellent antibacterial agent for Escherichia coli bacteria cultured in water-based nutrient broth at a low concentration (10 μg/mL).