Nutritional strategies cause memory damage and alter biochemical parameters without causing neuroinflammation.

Obesity results from an energy imbalance and has been considered an epidemic due to its increasing rates worldwide. It is classified as a low-grade chronic inflammatory disease and has associated comorbidities. Different nutritional strategies are used for the purpose of weight loss, highlighting low-carbohydrate (LC) diets, ketogenic diets, and intermittent fasting (IF). These strategies can lead to metabolic and behavioral changes as they stimulate different biochemical pathways. Therefore, this study evaluated memory, energy metabolism, neuroinflammation, oxidative stress, and antioxidant defense parameters in mice subjected to an LC diet, ketogenic diet (KD), or IF. Eighty male Swiss mice, 60 days old, were divided into 4 groups: control, LC, KD, or IF. Body weight was measured weekly, and food intake every 48 h. After 15 days of nutritional interventions, the animals were subjected to the behavioral object recognition test and subsequently euthanized. Then, visceral fat was removed and weighed, and the brain was isolated for inflammatory and biochemical analysis. We concluded from this study that the LC and KD strategies could damage memory, IF improves the production of adenosine triphosphate (ATP), and the LC, KD, and IF strategies do not lead to neuroinflammatory damage but present damage at the level of oxidative stress.

Effects of aquatic high intensity interval training on parameters of functional autonomy, mental health, and oxidative dysfunction in elderly subjects with type 2 diabetes.

The present study investigated the effects of aquatic exercise on parameters of functional autonomy, mental health, and oxidative dysfunction in elderly patients with DM2. A total of 130 elderly were included in the longitudinal clinical study and were attributed to the non-diabetic group (n = 27) and diabetes the group (n = 22). Both groups participated in 24 sessions of Hydro-HIIT, 48 h before and after Hydro-HIIT, the GDLAM index, depression, and anxiety scores and markers of oxidative dysfunction were quantified. After intervention, GI decreased in both groups (non-diabetes group = -24%; diabetes group = -22%) (p < 0.05), markers of depression (-46%), anxiety (-60%), DCFH-DA (-55%), SOD (+59%), TNF-α (-37%) and IL-1 (-48%) in diabetes group (p < 0.05). The intervention with Hydro-HIIT improves aspects related to functional autonomy, mental health, and exerts consequently, a modulating effect on oxidative stress and inflammatory response in elderly people diagnosed with DM2.

High concentrations of fructose cause brain damage in mice.

Excessive fructose consumption is associated with the incidence of obesity and systemic inflammation, resulting in increased oxidative damage and failure to the function of brain structures. Thus, we hypothesized that fructose consumption will significantly increase inflammation, oxidative damage, and mitochondrial dysfunction in the mouse brain and, consequently, memory damage. The effects of different fructose concentrations on inflammatory and biochemical parameters in the mouse brain were evaluated. Male Swiss mice were randomized into four groups: control, with exclusive water intake, 5%, 10%, and 20% fructose group. The 10% and 20% fructose groups showed an increase in epididymal fat, in addition to higher food consumption. Inflammatory markers were increased in epididymal fat and in some brain structures. In the evaluation of oxidative damage, it was possible to observe significant increases in the hypothalamus, prefrontal cortex, and hippocampus. In the epididymal fat and in the prefrontal cortex, there was a decrease in the activity of the mitochondrial respiratory chain complexes and an increase in the striatum. Furthermore, short memory was impaired in the 10% and 20% groups but not long memory. In conclusion, excess fructose consumption can cause fat accumulation, inflammation, oxidative damage, and mitochondrial dysfunction, which can damage brain structures and consequently memory.

Bacterial cellulose membrane incorporated with silver nanoparticles for wound healing in animal model.

The bacterial cellulose membrane (CM) is a promising biomaterial due to its easy applicability and moist environment. Moreover, nanoscale silver compounds (AgNO3) are synthesized and incorporated into CMs to provide these biomaterials with antimicrobial activity for wound healing. This study aimed to evaluate the cell viability of CM incorporated with nanoscale silver compounds, determine the minimum inhibitory concentration (MIC) for Escherichia coli and Staphylococcus aureus, and its use on in vivo skin lesions. Wistar rats were divided according to treatment: untreated, CM (cellulose membrane), and AgCM (CM incorporated with silver nanoparticles). The euthanasia was performed on the 2nd, 7th, 14th, and 21st days to assess inflammation (myeloperoxidase-neutrophils, N-acetylglucosaminidase-macrophage, IL-1ß, IL-10), oxidative stress (NO-nitric oxide, DCF-H2O2), oxidative damage (carbonyl: membrane's damage; sulfhydryl: membrane's integrity), antioxidants (superoxide dismutase; glutathione), angiogenesis, tissue formation (collagen, TGF-ß1, smooth muscle α-actin, small decorin, and biglycan proteoglycans). The use of AgCM did not show toxicity, but antibacterial effect in vitro. Moreover, in vivo, AgCM provided balanced oxidative action, modulated the inflammatory profile due to the reduction of IL-1ß level and increase in IL-10 level, in addition to increased angiogenesis and collagen formation. The results suggest the use of silver nanoparticles (AgCM) enhanced the CM properties by providing antibacterial properties, modulation the inflammatory phase, and consequently promotes the healing of skin lesions, which can be used clinically to treat injuries.

Gold nanoparticles application to the treatment of brain dysfunctions related to metabolic diseases: evidence from experimental studies.

Nanotechnology is an emerging and expanding technology worldwide. The manipulation of materials on a nanometric scale generates new products with unique properties called nanomaterials. Due to its significant expansion, nanotechnology has been applied in several fields of study, including developing materials for biomedical applications, i.e., nanomedicine. The use of nanomaterials, including nanoparticles, in nanomedicine, is promising and has been associated with pharmacokinetics, bioavailability, and therapeutic advantages. In this regard, it is worth mentioning the Gold Nanoparticles (AuNPs). AuNPs' biomedical application is extensively investigated due to their high biocompatibility, simple preparation, catalytic, and redox properties. Experimental studies have pointed out critical therapeutic actions related to AuNPs in different pathophysiological contexts, mainly due to their anti-inflammatory and antioxidant effects. Thus, in this review, we will discuss the main experimental findings related to the therapeutic properties of AuNPs in metabolic, neurodegenerative diseases, and ultimately brain dysfunctions related to metabolic diseases.

Role of Oxidative Stress on Insulin Resistance in Diet-Induced Obesity Mice.

Insulin resistance is the link between obesity and type 2 diabetes mellitus. The molecular mechanism by which obese individuals develop insulin resistance has not yet been fully elucidated; however, inconclusive and contradictory studies have shown that oxidative stress may be involved in the process. Thus, this study aimed to evaluate the effect of reactive species on the mechanism of insulin resistance in diet-induced obese mice. Obese insulin-resistant mice were treated with N-acetylcysteine (NAC; 50 mg/kg per day, for 15 days) by means of oral gavage. Twenty-four hours after the last NAC administration, the animals were euthanized and their tissues were extracted for biochemical and molecular analyses. NAC supplementation induced improved insulin resistance and fasting glycemia, without modifications in food intake, body weight, and adiposity. Obese mice showed increased dichlorofluorescein (DCF) oxidation, reduced catalase (CAT) activity, and reduced glutathione levels (GSH). However, treatment with NAC increased GSH and CAT activity and reduced DCF oxidation. The gastrocnemius muscle of obese mice showed an increase in nuclear factor kappa B (NFκB) and protein tyrosine phosphatase (PTP1B) levels, as well as c-Jun N-terminal kinase (JNK) phosphorylation compared to the control group; however, NAC treatment reversed these changes. Considering the molecules involved in insulin signaling, there was a reduction in insulin receptor substrate (IRS) and protein kinase B (Akt) phosphorylation. However, NAC administration increased IRS and Akt phosphorylation and IRS/PI3k (phosphoinositide 3-kinase) association. The results demonstrated that oxidative stress-associated obesity could be a mechanism involved in insulin resistance, at least in this animal model.

Topical application of a TRPA1 antagonist reduced nociception and inflammation in a model of traumatic muscle injury in rats.

Musculoskeletal pain is a widely experienced public healthcare issue, especially after traumatic muscle injury. Besides, it is a common cause of disability, but this pain remains poorly managed. However, the pathophysiology of traumatic muscle injury-associated pain and inflammation has not been fully elucidated. In this regard, the transient receptor potential ankyrin 1 (TRPA1) has been studied in inflammatory and painful conditions. Thus, this study aimed to evaluate the antinociceptive and anti-inflammatory effect of the topical application of a TRPA1 antagonist in a model of traumatic muscle injury in rats. The mechanical trauma model was developed by a single blunt trauma impact on the right gastrocnemius muscle of Wistar male rats (250-350 g). The animals were divided into four groups (Sham/Vehicle; Sham/HC-030031 0.05%; Injury/Vehicle, and Injury/HC-030031 0.05%) and topically treated with a Lanette® N cream base containing a TRPA1 antagonist (HC-030031, 0.05%; 200 mg/muscle) or vehicle (Lanette® N cream base; 200 mg/muscle), which was applied at 2, 6, 12, 24, and 46 h after muscle injury. Furthermore, we evaluated the contribution of the TRPA1 channel on nociceptive, inflammatory, and oxidative parameters. The topical application of TRPA1 antagonist reduced biomarkers of muscle injury (lactate/glucose ratio), spontaneous nociception (rat grimace scale), inflammatory (inflammatory cell infiltration, cytokine levels, myeloperoxidase, and N-acetyl-ß-D-glucosaminidase activities) and oxidative (nitrite levels and dichlorofluorescein fluorescence) parameters, and mRNA Trpa1 levels in the muscle tissue. Thus, these results demonstrate that TRPA1 may be a promising anti-inflammatory and antinociceptive target in treating muscle pain after traumatic muscle injury.

Effects of Ethanolic Extract of Cynara cardunculus (Artichoke) Leaves on Neuroinflammatory and Neurochemical Parameters in a Diet-Induced Mice Obesity Model.

This study aimed to evaluate the effect of Cynara cardunculus leaf ethanol extract on inflammatory and oxidative stress parameters in the hypothalamus, prefrontal cortex, hippocampus, striatum, cerebral cortex and liver of high-fat diet-induced obese mice. Food intake, body weight, visceral fat weight, and liver weight were also evaluated. Male Swiss mice were divided into control (low-fat purified diet) and obese (high-fat purified diet) groups. After 6 weeks, mice were divided into control + saline, control + C. cardunculus leaf ethanol extract, obese + saline, obese + C. cardunculus leaf ethanol extract. Cynara cardunculus leaf ethanol extract (1600 mg/kg/day) or saline was administered orally for 4 weeks. Brain structures (hypothalamus, hippocampus, prefrontal cortex, striatum and cerebral cortex) and liver were removed. Treatment with C. cardunculus leaf ethanol extract did not affect body weight but did reduce visceral fat. Obesity can cause inflammation and oxidative stress and increase the activity of antioxidant enzymes in brain structures. Treatment with ethanolic extract of C. cardunculus leaves partially reversed the changes in inflammatory damage parameters and oxidative damage parameters and attenuated changes in the antioxidant defense. The C. cardunculus leaf ethanol extract benefited from the brains of obese animals by partially reversing the changes caused by the consumption of a high-fat diet and the consequent obesity. These results corroborate those of studies indicating that the C. cardunculus leaf ethanol extract can contribute to the treatment of obesity.

Effects of Zingiber officinale extract supplementation on metabolic and genotoxic parameters in diet-induced obesity in mice.

Obesity is an epidemic associated with many diseases. The nutraceutical Zingiber officinale (ZO) is a potential treatment for obesity; however, the molecular effects are unknown. Swiss male mice were fed a high-fat diet (59 % energy from fat) for 16 weeks to generate a diet-induced obesity (DIO) model and then divided into the following groups: standard diet + vehicle; standard diet + ZO; DIO + vehicle and DIO + ZO. Those in the ZO groups were supplemented with 400 mg/kg per d of ZO extract (oral administration) for 35 d. The animals were euthanised, and blood, quadriceps, epididymal fat pad and hepatic tissue were collected. DIO induced insulin resistance, proinflammatory cytokines, oxidative stress and DNA damage in different tissues. Treatment with ZO improved insulin sensitivity as well as decreased serum TAG, without changes in body weight or adiposity index. TNF-α and IL-1ß levels were lower in the liver and quadriceps in the DIO + ZO group compared with the DIO group. ZO treatment reduced the reactive species and oxidative damage to proteins, lipids and DNA in blood and liver in obese animals. The endogenous antioxidant activity was higher in the quadriceps of DIO + ZO. These results in the rat model of DIO may indicate ZO as an adjuvant on obesity treatment.

Effects of cryotherapy on the regeneration process and muscular mechanical properties after lacerative injury model.

Cryotherapy is a therapeutic modality widely used for the treatment of muscle injuries to control pain and inflammatory processes. This study aimed to investigate the effects of cryotherapy on the inflammatory and oxidative stress parameters and mechanical properties of, and pain in, the skeletal muscles of rats with lacerative muscle injury. The rats were anesthetized with 4% isoflurane and subjected to gastrocnemius muscle laceration injury. After injury, all animals in the intervention groups received cryotherapy treatment for 20 minutes using plastic bags containing crushed ice. The protocol comprised three daily applications at 3-hour intervals on the day of injury, with reapplication 24 hours later. Seventy-two male Wistar rats were divided into three groups: sham, muscle injury (MI), and MI + cryotherapy (MI + cryo). Muscle mechanical properties were analyzed by mechanical tensile testing on day 7 after injury. The MI + cryo group showed reduced TNF-α, IFN-γ, and IL1ß levels; elevated IL4, IL6, and IL10 levels; reduced oxidant production and carbonyl levels; and elevated sulfhydryl contents. Animals that underwent tissue cooling showed superoxide dismutase activity and glutathione levels close to those of the animals in the sham group. The MI and MI + cryo groups showed reduced values of the evaluated mechanical properties and lower mechanical thresholds compared to those of the animals from the sham group. Our results demonstrated that the proposed cryotherapy protocol reduced the inflammatory process and controlled oxidative stress but did not reverse the changes in the mechanical properties of muscle tissues or provide analgesic effects within the time frame analyzed.

Macrophages and Schwann cell TRPA1 mediate chronic allodynia in a mouse model of complex regional pain syndrome type I.

Complex regional pain syndrome type I (CRPS-I) is characterized by intractable chronic pain. Poor understanding of the underlying mechanisms of CRPS-I accounts for the current unsatisfactory treatment. Antioxidants and antagonists of the oxidative stress-sensitive channel, the transient receptor potential ankyrin 1 (TRPA1), have been found to attenuate acute nociception and delayed allodynia in models of CRPS-I, evoked by ischemia and reperfusion (I/R) of rodent hind limb (chronic post ischemia pain, CPIP). However, it is unknown how I/R may lead to chronic pain mediated by TRPA1. Here, we report that the prolonged (day 1-15) mechanical and cold allodynia in the hind limb of CPIP mice was attenuated permanently in Trpa1-/- mice and transiently after administration of TRPA1 antagonists (A-967079 and HC-030031) or an antioxidant (α-lipoic acid). Indomethacin treatment was, however, ineffective. We also found that I/R increased macrophage (F4/80+ cell) number and oxidative stress markers, including 4-hydroxynonenal (4-HNE), in the injured tibial nerve. Macrophage-deleted MaFIA (Macrophage Fas-Induced Apoptosis) mice did not show I/R-evoked endoneurial cell infiltration, increased 4-HNE and mechanical and cold allodynia. Furthermore, Trpa1-/- mice did not show any increase in macrophage number and 4-HNE in the injured nerve trunk. Notably, in mice with selective deletion of Schwann cell TRPA1 (Plp1-CreERT;Trpa1fl/fl mice), increases in macrophage infiltration, 4-HNE and mechanical and cold allodynia were attenuated. In the present mouse model of CRPS-I, we propose that the initial oxidative stress burst that follows reperfusion activates a feed forward mechanism that entails resident macrophages and Schwann cell TRPA1 of the injured tibial nerve to sustain chronic neuroinflammation and allodynia. Repeated treatment one hour before and for 3 days after I/R with a TRPA1 antagonist permanently protected CPIP mice against neuroinflammation and allodynia, indicating possible novel therapeutic strategies for CRPS-I.

Pulmonary oxidative stress in wild bats exposed to coal dust: A model to evaluate the impact of coal mining on health.

This study aimed to verify possible alterations involving histological and oxidative stress parameters in the lungs of wild bats in the Carboniferous Basin of Santa Catarina (CBSC) state, Southern Brazil, as a means to evaluate the impact of coal dust on the health of wildlife. Specimens of frugivorous bat species Artibeus lituratus and Sturnira lilium were collected from an area free of coal dust contamination and from coal mining areas. Chemical composition, histological parameters, synthesis of oxidants and antioxidant enzymes, and oxidative damage in the lungs of bats were analyzed. Levels of Na, Cl, Cu, and Br were higher in both species collected in the CBSC than in the controls. Levels of K and Rb were higher in A. lituratus, and levels of Si, Ca, and Fe were higher in S. lilium collected in the carboniferous basin. Both bat species inhabiting the CBSC areas exhibited an increase in the degree of pulmonary emphysema compared to their counterparts collected from control areas. Sturnira lilium showed increased reactive oxygen species (ROS) and 2',7'-dichlorofluorescein (DCF) levels, while A. lituratus showed a significant decrease in nitrite levels in the CBSC samples. Superoxide dismutase (SOD) activity did not change significantly; however, the activity of catalase (CAT) and levels of glutathione (GSH) decreased in the A. lituratus group from CBSC compared to those in the controls. There were no differences in NAD(P)H quinone dehydrogenase 1 protein (NQO1) abundance or nitrotyrosine expression among the different groups of bats. Total thiol levels showed a significant reduction in A. lituratus from CBSC, while the amount of malondialdehyde (MDA) was higher in both A. lituratus and S. lilium groups from coal mining areas. Our results suggested that bats, especially A. lituratus, living in the CBSC could be used as sentinel species for harmful effects of coal dust on the lungs.

Omega-3 polyunsaturated fatty acids have beneficial effects on visceral fat in diet-induced obesity model.

This study evaluated the effects of omega-3 polyunsaturated fatty acids (PUFAs) on oxidative stress and energy metabolism parameters in the visceral fat of a high-fat-diet induced obesity model. Energy intake, body mass, and visceral fat mass were also evaluated. Male Swiss mice received either a control diet (control group) or a high-fat diet (obese group) for 6 weeks. After this period, the groups were divided into control + saline, control + omega-3, obese + saline, and obese + omega-3, and to these groups 400 mg·(kg body mass)-1·day-1 of fish oil (or saline) was administered orally, for 4 weeks. Energy intake and body mass were monitored throughout the experiment. In the 10th week, the animals were euthanized and the visceral fat (mesenteric) was removed. Treatment with omega-3 PUFAs did not affect energy intake or body mass, but it did reduced visceral fat mass. In visceral fat, omega-3 PUFAs reduced oxidative damage and alleviated changes to the antioxidant defense system and the Krebs cycle. The mitochondrial respiratory chain was neither altered by obesity nor by omega-3 PUFAs. In conclusion, omega-3 PUFAs have beneficial effects on the visceral fat of obese mice because they mitigate changes caused by the consumption of a high-fat diet.

Cardioprotective effects of physical exercise on redox biology in mice exposed to hand-rolled cornhusk cigarette smoke.

The present study sought to evaluate the effects of physical training on histological parameters and oxidative stress in the myocardium of mice chronically exposed to hand-rolled cornhusk cigarette (HRCC) smoke. Male Swiss mice (60 days old, 30-35 g) were either exposed to ambient air or passively exposed to the smoke of 12 cigarettes daily over 3 sessions (4 cigarettes per session) for 60 consecutive days with or without physical training for 8 weeks. Forty-eight hours after the last training session, the heart was surgically removed for histological analysis and measurement of oxidative stress parameters. Histological imaging revealed cell disruption, with poorly defined nuclei, in the mice exposed to HRCC smoke, but not in the control group. However, mice exposed to HRCC smoke with physical training displayed signs of tissue repair and improved tissue integrity. Biochemical analysis revealed decreased production of superoxide, 2',7'-dichlorofluorescein (DCF), and nitrite, as well as decreased protein carbonylation, in the physical training groups, likely due to the exercise-induced increase in glutathione peroxidase (GPX) activity and glutathione (GSH) content. Taken together, our results suggest that physical exercise exerts cardioprotective effects by modulating the redox responses in animals exposed to HRCC smoke.

Vitamin D3 as adjuvant in the treatment of type 2 diabetes mellitus: modulation of genomic and biochemical instability.

Type 2 diabetes mellitus has undergone a worldwide growth in incidence in the world and has now acquired epidemic status. There is a strong link between type 2 diabetes and vitamin D deficiency. Because vitamin D has beneficial effects on glucose homeostasis, the aim of this study was to evaluate the influence of vitamin D3 supplementation on the modulation of glycaemic control and other metabolic effects, as well as modulation of genomic instability in patients with type 2 diabetes. We evaluated 75 patients with type 2 diabetes, registered in the Integrated Clinics of the University of Southern Santa Catarina. Participants received 4000 IU of vitamin D3 (25(OH)D) supplementation daily for 8 weeks. Blood samples were collected at the beginning and at the end of the supplementation, and 4 weeks after the end of supplementation. The glycidic and lipid profiles [total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein and triglycerides], oxidative stress, DNA damage and 25(OH)D levels were evaluated. Vitamin D3 supplementation for 8 weeks showed enough to significantly increase blood levels of 25(OH)D. A significant difference in lipid profile was observed only in non-HDL cholesterol. Significant changes were observed in glucose homeostasis (fasting glucose and serum insulin) and, in addition, a reduction in the parameters of oxidative stress and DNA damage. There was a significant reduction in the values of 25(OH)D 4 weeks after the end of the supplementation, but levels still remained above baseline. Use of vitamin D supplementation can be an ally in the health modulation of patients with type 2 diabetes mellitus.

Diet-induced obesity causes hypothalamic neurochemistry alterations in Swiss mice.

The aim of this study was to assess inflammatory parameters, oxidative stress and energy metabolism in the hypothalamus of diet-induced obese mice. Male Swiss mice were divided into two study groups: control group and obese group. The animals in the control group were fed a diet with adequate amounts of macronutrients (normal-lipid diet), whereas the animals in the obese group were fed a high-fat diet to induce obesity. Obesity induction lasted 10 weeks, at the end of this period the disease model was validated in animals. The animals in the obese group had higher calorie consumption, higher body weight and higher weight of mesenteric fat compared to control group. Obesity showed an increase in levels of interleukin 1ß and decreased levels of interleukin 10 in the hypothalamus. Furthermore, increased lipid peroxidation and protein carbonylation, and decreased level of glutathione in the hypothalamus of obese animals. However, there was no statistically significant difference in the activity of antioxidant enzymes, superoxide dismutase and catalase. The obese group had lower activity of complex I, II and IV of the mitochondrial respiratory chain, as well as lower activity of creatine kinase in the hypothalamus as compared to the control group. Thus, the results from this study showed changes in inflammatory markers, and dysregulation of metabolic enzymes in the pathophysiology of obesity.

Effect of aquatic exercise on mental health, functional autonomy, and oxidative dysfunction in hypertensive adults.

The aquatic exercise is an effective non-pharmacological therapy for prevention and control of hypertension. The objective of the present study was to investigate the effect of aquatic exercise on mental health, functional autonomy, and oxidative dysfunction in hypertensive adults. Methodologically 29 adults (mean age 53 ± 7.5 years) were included in the study, and were randomly grouped as hypertensive (n = 16) and non-hypertensive (n = 13). Both groups underwent low-intensity aquatic exercise program for 12 weeks. Outcomes were evaluated at week 0 and 12. The values for the following parameters decreased in the hypertensive group post training: anxiety (-6.2 ± 2 score; 60%), Timed Up and Go test (-7.4 ± 0.3 sec; 30%), protein carbonylation (-0.15 ± 0.03 nmol/mg protein; 50%), nitric oxide (12.4 ± 6 nmol/mg protein; 62%), interleukin-6 (-27.6 ± 5.7 pg/mg protein; 46%), and tissue necrosis factor-alpha (-52.4 ± 3.8 pg/mg protein; 40%); however, the values of the following parameters increased before training: Berg score (56 ± 2; 7.8%), flexibility (27 ± 1 cm; 71%); glutathione (3.1 ± 1.3 nmol/mg protein; 138%), and superoxide dismutase (1.6 ± 0.4 nmol/mg; 166%). In conclusion, we suggest that low-intensity aquatic exercise program improved anxiety, functional autonomy, and oxidative dysfunction in hypertensive adults.

Prior Exercise Training Prevent Hyperglycemia in STZ Mice by Increasing Hepatic Glycogen and Mitochondrial Function on Skeletal Muscle.

Diabetes mellitus is a metabolic disorder characterized by hyperglycemia. We investigated the effect of a prior 30 days voluntary exercise protocol on STZ-diabetic CF1 mice. Glycemia, and the liver and skeletal muscle glycogen, mitochondrial function, and redox status were analyzed up to 5 days after STZ injection. Animals were engaged in the following groups: Sedentary vehicle (Sed Veh), Sedentary STZ (Sed STZ), Exercise Vehicle (Ex Veh), and Exercise STZ (Ex STZ). Exercise prevented fasting hyperglycemia in the Ex STZ group. In the liver, there was decreased on glycogen level in Sed STZ group but not in EX STZ group. STZ groups showed decreased mitochondrial oxygen consumption compared to vehicle groups, whereas mitochondrial H2 O2 production was not different between groups. Addition of ADP to the medium did not decrease H2 O2 production in Sed STZ mice. Exercise increased GSH level. Sed STZ group increased nitrite levels compared to other groups. In quadriceps muscle, glycogen level was similar between groups. The Sed STZ group displayed decreased O2 consumption, and exercise prevented this reduction. The H2 O2 production was higher in Ex STZ when compared to other groups. Also, GSH level decreased whereas nitrite levels increased in the Sed STZ compared to other groups. The PGC1 α levels increased in Sed STZ, Ex Veh, and Ex STZ groups. In summary, prior exercise training prevents hyperglycemia in STZ-mice diabetic associated with increased liver glycogen storage, and oxygen consumption by the mitochondria of skeletal muscle implying in increased oxidative/biogenesis capacity, and improved redox status of both tissues. J. Cell. Biochem. 118: 678-685, 2017. © 2016 Wiley Periodicals, Inc.

IL-1ß Antagonist Receptor Peptide Associated with Photobiomodulation Accelerates Diabetic Wound Tissue Repair.

Chronic hyperglycemia caused by diabetes mellitus (DM) slows down the healing process due to prolonged inflammation which impedes the regeneration progression. Photobiomodulation (PBM) is considered a non-pharmacological intervention and has anti-inflammatory and biostimulatory effects that accelerate the healing process. Currently found IL-1ß inhibitors are difficult to implement due to their cytotoxic potential, excessive amounts, and invasive administration, and therefore, the application of this peptide in diabetic wounds represents a promising intervention to help resolve the inflammatory response. This study aimed to investigate the effect of an IL-1ß inhibitor molecule associated with PBM irradiation in a model of epithelial injury in diabetic mice. After the induction of the DM model with streptozotocin (STZ), the skin lesion model was implemented through surgical excision. Sixty C57BL/6 mice divided into five experimental groups (n = 12) were used: excisional wound (EW), DM + EW, DM + EW + DAP 1-2 (inhibitor peptide), DM + EW + PBM, and DM + EW + PBM + DAP 1-2. Treatment started 12 h after wound induction and was performed daily for 5 days. Twenty-four hours after the last application, the animals were euthanized and the outer edge of the wound was removed. The results obtained demonstrate that the DM + EW + PBM + DAP 1-2 group caused a reduction in the levels of pro-inflammatory cytokines, an increase in anti-inflammatory cytokines, and an increase in TGF-ß and maintenance of the cellular redox state with a consequent reduction in levels of inflammatory infiltrate and concomitant stimulation of type III collagen gene expression, as well as a decrease in the size of the wound in square centimeter 6 days after the injury. Only the combination of therapies was able to favor the process of tissue regeneration due to the development of an approach capable of acting at different stages of the regenerative process, through the mechanisms of action of interventions on the inflammatory process by avoiding its stagnation and stimulating progression of regeneration.