Increasing evidence in both experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of both types of diabetes mellitus. Free radicals are formed disproportionately in diabetes by glucose oxidation, nonenzymatic glycation of proteins, and the subsequent oxidative degradation of glycated proteins. Abnormally high levels of free radicals and the simultaneous decline of antioxidant defense mechanisms can lead to damage of cellular organelles and enzymes, increased lipid peroxidation, and development of insulin resistance. These consequences of oxidative stress can promote the development of complications of diabetes mellitus. Changes in oxidative stress biomarkers, including superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, glutathione levels, vitamins, lipid peroxidation, nitrite concentration, nonenzymatic glycosylated proteins, and hyperglycemia in diabetes, and their consequences, are discussed in this review. In vivo studies of the effects of various conventional and alternative drugs on these biomarkers are surveyed. There is a need to continue to explore the relationship between free radicals, diabetes, and its complications, and to elucidate the mechanisms by which increased oxidative stress accelerates the development of diabetic complications, in an effort to expand treatment options.

Diabetes, oxidative stress, and antioxidants: a review

Connexins are ubiquitous channel forming proteins that assemble as plasma membrane hemichannels and as intercellular gap junction channels that directly connect cells. In the heart, gap junction channels electrically connect myocytes and specialized conductive tissues to coordinate the atrial and ventricular contraction/relaxation cycles and pump function. In blood vessels, these channels facilitate long-distance endothelial cell communication, synchronize smooth muscle cell contraction, and support endothelial-smooth muscle cell communication. In the central nervous system they form cellular syncytia and coordinate neural function. Gap junction channels are normally open and hemichannels are normally closed, but pathologic conditions may restrict gap junction communication and promote hemichannel opening, thereby disturbing a delicate cellular communication balance. Until recently, most connexin-targeting agents exhibited little specificity and several off-target effects. Recent work with peptide-based approaches has demonstrated improved specificity and opened avenues for a more rational approach toward independently modulating the function of gap junctions and hemichannels. We here review the role of connexins and their channels in cardiovascular and neurovascular health and disease, focusing on crucial regulatory aspects and identification of potential targets to modify their function. We conclude that peptide-based investigations have raised several new opportunities for interfering with connexins and their channels that may soon allow preservation of gap junction communication, inhibition of hemichannel opening, and mitigation of inflammatory signaling.

/pdf/connexins-in-cardiovascular-and-neurovascular-health-and-3kwefv693r.pdf

Connexins in Cardiovascular and Neurovascular Health and Disease: Pharmacological Implications

Hydrogen sulfide protects neurons against hypoxic injury via stimulation of ATP-sensitive potassium channel/protein kinase C/extracellular signal-regulated kinase/heat shock protein 90 pathway.

Oxidative stress is currently suggested to play a major role in the development of diabetes mellitus. There is an increasing demand of natural anti-diabetic agents, as continuous administration of existing drugs and insulin are associated with many side effects and toxicity. The present study was aimed to investigate the effect of Momordica charantia (MC) and Trigonella foenum graecum (TFG) extracts (aqueous) on antioxidant status and lipid peroxidation in heart tissue of normal and alloxan induced diabetic rats. In a 30 days treatment, rats were divided into six groups (I-VI) of five animals in each, experiments were repeated thrice. administration of MC (13.33 g pulp/kg body weight/day) and TFG (9 g seeds powder/kg body weight/day) extracts in diabetic rats has remarkably improved the elevated levels of fasting blood glucose. A signifi cant decrease in lipid peroxidation (p<0.001) and significant increase in the activities of key antioxidant enzymes such as superoxide dismutase (sOD), catalase (C aT), glutathione-s-transferase (G sT) and reduced glutathione (G sh) contents in heart tissue of diabetic rats were observed (group V and VI) upon MC and TFG treatment. Our studies demonstrate the anti-hyperglycemic and anti-oxidative potential of Momordica charantia and Trigonella foenum graecum, which could exert beneficial effects against the diabetes and associated free radicals complications in heart tissue.

/pdf/the-plant-extracts-of-momordica-charantia-and-trigonella-3xt6ivfvpq.pdf

The plant Extracts of Momordica Charantia and Trigonella Foenum Graecum Have Antioxidant and Anti-Hyperglycemic Properties for Cardiac Tissue During Diabetes Mellitus

Several lines of evidence indicate that a rapid loss of neuronal protein kinase C (PKC) activity is a characteristic feature of cerebral ischemia and is a necessary step in the NMDA-induced death of cultured neurons. Exposing embryonic day 18 primary rat cortical neurons to 50 microM NMDA or 50 microM glutamate for 10 min caused approximately 80% cell death over the next 24 h, but excitotoxic death was largely averted, i.e., by 70-80%, in cells pretreated with brain-derived neurotrophic factor (BDNF). An 8-h preexposure to BDNF (50-100 ng/ml) maximally protected cortical cells from the effects of NMDA and glutamate, although the transient application of BDNF between 8 and 4 h before NMDA was equally protective. These effects of BDNF were abolished at supralethal, i.e., >100 microM, NMDA concentrations. It is significant that BDNF pretreatment prevented the inactivation of PKC in cortical cells normally seen 30 min to 2 h following lethal NMDA or glutamate exposure. This BDNF effect did not arise from changes in NMDA channel activity because neither whole-cell NMDA current amplitudes nor increases in intracellular free Ca2+ concentration were altered by the 8-h BDNF pretreatment. Furthermore, BDNF offered no neuroprotection to cells treated with the PKC inhibitors staurosporine (10-20 nM), calphostin C (1-2.5 microM), or GF-109203X (100 nM) at the time of NMDA addition. These results underscore the importance of PKC inactivation in glutamate-induced neuronal death. They also suggest that BDNF neuroprotection arises, at least in part, via its ability to block the mechanism by which pathophysiological Ca2+ influx through the NMDA receptor causes membrane PKC inactivation.

Evidence that Brain‐Derived Neurotrophic Factor Neuroprotection Is Linked to Its Ability to Reverse the NMDA‐Induced Inactivation of Protein Kinase C in Cortical Neurons

Comparison of the changes in protein kinase c induced by glutamate in primary cortical neurons and by in vivo cerebral ischaemia

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Comparison of the changes in protein kinase c induced by glutamate in primary cortical neurons and by in vivo cerebral ischaemia