Lipid peroxidation and antioxidant status in rat: effect of food restriction and wheel running

Using the activity-based anorexia model, the aim of this investigation was to explore antioxidant enzyme activity (catalase, superoxide dismutase), total antioxidant status (TAS), and alpha-tocopherol in blood, liver, and gastrocnemius muscle associated with the food restriction and voluntary wheel running during 8 days. In addition, lipid peroxidation was measured by measurements of malondialdehyde (MDA). Wistars rats (n = 56) were randomly assigned to one of four groups: an ad lib sedentary group, a control wheel activity group, a food restriction-induced hyperactivity group (1 h/day ad lib food, 23 h/day ad lib wheel access), and a food-restricted sedentary group. The animals were killed when the rats in the food-restricted group had lost 25% of their free feeding weight. Antioxidant enzyme activities and TAS in blood, liver, and gastrocnemius muscle were unaffected by voluntary wheel running. A wheel activity effect (P < 0.05) was obtained for the MDA concentrations in plasma, with lower concentrations in trained animals. Food restriction effects were obtained for antioxidant capacity in liver, as well as for CAT activity in the gastrocnemius muscle and plasma MDA concentrations with lower values in the restricted animals. On the other hand, the food-restricted rats showed higher plasma TAS concentrations (P < 0.05) and higher alpha-tocopherol concentrations in the liver (P < 0.05) when compared to animals fed ad libitum. Our results also showed that food restriction coupled to wheel running decreased antioxidant parameters in liver, and plasmatic MDA concentrations and increased TAS plasma concentrations when compared to the ad libitum sedentary situation.     

Three months of moderate-intensity exercise reduced plasma 3-nitrotyrosine in rheumatoid arthritis patients

Purpose

Rheumatoid arthritis (RA) patients display high levels of oxidative stress. Transient exercise-induced increases in oxidative stress are thought to be adaptive in healthy populations. This study investigated the effect of exercise on markers of oxidative stress in RA, following acute exercise and a period of exercise training.

Methods

Acute exercise study: RA patients (N = 12, age: 56 ± 11) undertook a bout of exercise (30–40 min, 70 % VO_2MAX), and blood samples were taken before and after exercise to assess markers of oxidative stress. Training study: RA patients (N = 19, age: 56 ± 10) were randomised into either a control or exercise group, who undertook 3 exercise sessions per week (30–40 min @70 % VO_2MAX) for 3 months. Plasma markers of oxidative stress (protein carbonyls (PC), lipid hydroperoxides (LOOH), 3-nitrotyrosine (3-NT), total antioxidant capacity (TAC) and catalase (CAT) activity), inflammation (interleukin-8 (IL-8) and C-reactive protein (CRP)) and nitric oxide metabolites (NOx) were assessed before and after training.

Results

Acute exercise study: Protein carbonyls (PC) (+18 %) and NOx (+27 %) were significantly increased following exercise. Training study: 3-nitrotyrosine (3-NT) decreased (2.18 ± 1.78 to 1.10 ± 0.93 μM) in the exercise group only, alongside increases in aerobic fitness (24.45 ± 4.98 to 27.10 ± 4.51 ml/kg/min^?1) and reductions in disease activity score (DAS: 3.47 ± 1.17 to 2.88 ± 0.76). PC, LOOH, TAC, IL-8, CRP and NOx concentrations, and CAT activity were unchanged in both groups.

Conclusions

Aerobic exercise training did not increase markers of oxidative stress in RA patients. 3-Nitrotyrosine and disease activity were decreased following exercise training.     

The effects of two-stage carotid occlusion on spatial memory and pro-inflammatory markers in the hippocampus of rats

The purpose of this study was to evaluate the effects of cerebral hypoperfusion on cognitive ability, TNFα, IL1β and PGE2 levels in both hippocampi in a modified two-vessel occlusion model. Both common carotid arteries of adult male Wistar rats were permanently occluded with an interval of 1 week between occlusions. Learning and memory were significantly decreased after 1 month. This reduction was not significant after 2 months, which may be attributed to blood flow compensation. The TNFα level was significantly increased after 3 h and 1 day. IL1β was significantly increased after 1 day. After a week there was no significant difference in pro-inflammatory levels. Furthermore, there was no difference between right and left hippocampi. It is possible that TNFα and IL1β elevation initiates pathologic processes that contribute to memory impairment.     

Influence of acute exercise of varying intensity and duration on postprandial oxidative stress

Introduction

Aerobic exercise can reduce postprandial lipemia, and possibly oxidative stress, when performed prior to a lipid-rich meal.

Purpose

To compare the impact of acute exercise on postprandial oxidative stress.

Methods

We compared aerobic and anaerobic exercise bouts of different intensities and durations on postprandial blood triglycerides (TAG), oxidative stress biomarkers (malondialdehyde, hydrogen peroxide, advanced oxidation protein products), and antioxidant status (trolox equivalent antioxidant capacity, superoxide dismutase, catalase, glutathione peroxidase). Twelve trained men (21–35 years) underwent four conditions: (1) No exercise rest; (2) 60-min aerobic exercise at 70 % heart rate reserve; (3) five 60-s sprints at 100 % max capacity; and (4) ten 15-s sprints at 200 % max capacity. All exercise bouts were performed on a cycle ergometer. A high-fat meal was consumed 1 h after exercise cessation. Blood samples were collected pre-meal and 2 and 4 h post-meal and analyzed for TAG, oxidative stress biomarkers, and antioxidant status.

Results

No significant interaction or condition effects were noted for any variable (p > 0.05), with acute exercise having little to no effect on the magnitude of postprandial oxidative stress.

Conclusion

In a sample of healthy, well-trained men, neither aerobic nor anaerobic exercise attenuates postprandial oxidative stress in response to a high-fat meal.     

Acute exercises induce disorders of the gastrointestinal integrity in a murine model

Purpose

Many endurance athletes complain about gastrointestinal (GI) symptoms. It is assumed that exercise-induced shift of perfusion with consecutive hypoperfusion of the enteral vascular system leads to an increased GI permeability and tissue damage. Therefore, the aim of the study was to investigate permeability, apoptosis, electrogenic ion transport (Isc), and tissue conductance (Gt) of the small intestine in a murine exercise model.

Methods

After spirometry, male Swiss CD-1 mice were subjected to an intensive treadmill exercise (80 % VO_2max). Sedentary mice served as controls. The small intestine was removed at several time intervals post-exercise. Apoptotic cells were determined by the TUNEL method, while fluorescein isothiocyanate dextran permeation indicated intestinal permeability. The Gt and Isc measurements were carried out in a modified Ussing chamber.

Results

Apoptosis of epithelial cells increased continuously until 24 h post exercise (0.8 ± 0.42 versus 39.2 ± 26.0 %; p < 0.05). Compared with the control group the permeability increased 2 h after exercise (0.47 ± 0.07 versus 0.67 ± 0.14 FU/min; p < 0.05). Isc measurements of the ileum were augmented after 24 h (3.33 ± 0.56 versus 5.77 ± 1.16 μEq/h/cm²; p < 0.05). At this time the Gt increased as well (28.8 ± 3.37 versus 32.5 ± 2.59 mS/cm²; p < 0.05).

Conclusion

In the murine exercise model there is evidence that after intense endurance exercise repair processes occur in small intestinal epithelial cells, which affect permeability, Gt, and Isc. The formation of lamellipodia to close the “leaky” tight junctions caused by apoptosis might be an underlying mechanism.     

Resveratrol reduces light and electron microscopic changes in acetaminophen-induced hepatotoxicity in rats: Role of iNOS expression

Introduction: Hepatotoxicity is a major complication of acetaminophen (APAP), a widely used analgesic and antipyretic drug. Resveratrol (RSV) is a naturally occurring diphenol and it has anticancer, antioxidant, and anti-inflammatory properties. Objectives: In this study, the beneficial effects of RSV on APAP-induced hepatotoxicity was investigated in rats. Materials and methods: Group 1: Ethanol, Group 2: Saline, Group 3: RSV (10 mg/kg/ip), Group 4: APAP (1000 mg/kg/ip/single dose), Group 5: APAP+RSV (20 min after administration of APAP). The rats were sacrificed 24 h after administration of APAP. Light and electron microscopic changes were evaluated. Levels of malondialdehyde (MDA) and glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) activities were determined in liver tissue. Results: Rats of the ethanol, saline, and RSV groups did not present any histopathological alterations. In the APAP group, we observed vascular congestion, necrosis, inflammation, sinusoidal dilatation, and loss of glycogen content. In the APAP+RSV group, these changes were markedly reduced. iNOS immunostaining showed very weak positive stained hepatocytes the sections of control, saline, and RSV groups. However, in the APAP group, iNOS immunostaining was most evident in pericentral hepatocytes. In the same areas in APAP+RSV group, intensity of iNOS immunostaining decreased. A significant increase in MDA and decreases in GSH level, CAT, and SOD activity indicated that APAP-induced hepatotoxicity was mediated through oxidative stress. Significant beneficial changes were noted in tissue oxidative stress indicators in rats treated with RSV. Conclusion: These biochemical, histopathological, and ultrastructural findings revealed that RSV reduced the severity of APAP-induced alterations in liver.     

Activation of mitochondrial KATP channels mediates neuroprotection induced by chronic morphine preconditioning in hippocampal CA-1 neurons following cerebral ischemia

Purpose

Pharmacologic preconditioning, through activating several mechanisms and mediators, can increase the tolerance of different tissues against ischemia/reperfusion (I/R) injury. Recent studies have shown that morphine preconditioning has protective effects in different organs, especially in the heart. Nevertheless, its mechanisms are not well elucidated in the brain. The present study aimed to clarify whether the activation of mitochondrial KATP (mKATP) channels in chronic morphine (CM) preconditioning could decrease hippocampus damage following I/R injury.

Effects of high-intensity and blood flow-restricted low-intensity resistance training on carotid arterial compliance: role of blood pressure during training sessions

We examined the effects of high-intensity resistance training (HIT) and low-intensity blood flow-restricted (LI-BFR) resistance training on carotid arterial compliance. Nineteen young men were randomly divided into HIT (n = 9) or LI-BFR (n = 10) groups. The HIT and LI-BFR groups performed 75 and 30 %, respectively, of one-repetition maximum (1-RM) bench press exercise, 3 days per week for 6 weeks. During the training sessions, the LI-BFR group wore elastic cuffs around the most proximal region of both arms. Muscle cross-sectional area (CSA), 1-RM strength, and carotid arterial compliance were measured before and 3 days after the final training session. Acute changes in systolic arterial pressure (SAP), plasma endothelin-1 (ET-1), nitrite/nitrate (NOx), and noradrenalin concentrations were also measured during and after a bout of training session. The training led to significant increases (P < 0.01) in bench press 1-RM and arm and chest muscle CSA in the two training groups. Carotid arterial compliance decreased significantly (P < 0.05) in the HIT group, but not in the LI-BFR group. There was a significant correlation (r = ?0.533, P < 0.05) between the change in carotid arterial compliance and the acute change in SAP during training sessions; however, ET-1 and NOx did not correlate with carotid arterial compliance. Our results suggest that muscle CSA and strength increased following 6 weeks of both HIT and LI-BFR training. However, carotid arterial compliance decreased in only the HIT group, and the changes were correlated with SAP elevations during exercise sessions.     

Oxidative profile of sickle cell patients in a Cameroonian urban hospital

Background

Sickle cell disease (SCD) is a class of hemoglobinopathy resulting from a single mutation in the ß-globin chain inducing the substitution of valine for glutamic acid at the sixth amino acid position which leads to the production of abnormal haemoglobin (haemoglobin S [HbS]). Studies demonstrated the implication of oxidative stress in the development of the sickle cell disease.

Methods

The study aim was to determine the level of oxidative stress markers in a group of sickle cell homozygous patients (SS) in the Yaounde Central Hospital above 15 years of age. Hemolysates obtained from patients were used to investigate some oxidative stress markers including malondialdehyde (MDA), nitric oxide (NO), catalase (CAT), superoxide dismutase (SOD), peroxidase, total antioxidant capacity (TAC) and total protein concentration.

Results

Eighty four individuals, 42 males and 42 females participated (50 % each) with an age range of 15 to 55 years. The levels of markers were significantly higher in the healthy AA group than sickle (SS) (p?<?0.05), with the exception of MDA which was significantly high in sickle cell (SS) patients than healthy (p?=?0.037). With respect to the gender, both healthy and SS females showed a greater Total anti-oxidant capacity (65 μM) compared to the males (55 μM).

Conclusion

The increase in the oxidative stress level especially MDA in sickle cell homozygous patients compared to healthy AA individuals confirms that oxidative stress is involved in the pathogenesis of the sickle cell disease.

     

A study on the antioxidant defense system of psoriasis patients in the ethnic population of Kashmir-India

The study was designed to evaluate the role of antioxidant defense system in the etiology of psoriasis, a chronic skin disorder of complex etiology and pathology. Hospital-based case–control study was carried out in major referral hospital in Kashmir, North India. Cases (N?=?40) were composed of patients with psoriasis vulgaris, and controls (N?=?20) were healthy volunteers. Study included estimation in plasma of both patients and controls of glutathione (GSH) levels, superoxide dismutase (SOD) activity, and total antioxidant potential (AOP) as indices of antioxidant defense system and malondialdehyde (MDA) as a measure of lipid peroxidation (LP), an indicator of oxidative stress. The GSH levels, SOD activity, AOP, and malondialdehyde levels in plasma of psoriasis patients were 2.58?±?0.22 μM/l, 5.24?±?0.69 U/ml, 0.020?±?.011?nmol^?1/ml?h, and 0.88?±?0.20 nmol/ml and were 4.76?±?0.52 μM/l, 4.14?±?0.56U/ml, 0.042?±?0.018 nmol^?1/ml?h, and 0.53?±?0.16 nmol/ml in healthy voluntary controls, respectively. A significant decrease in GSH levels (p?<?0.005) and AOP (p?<?0.005) and significant increase in SOD activity (p?<?0.01) MDA levels (p?<?0.005) as an indicator of LP was observed.     

Low-volume exercise training attenuates oxidative stress and neutrophils activation in older adults

The purpose of this study was to investigate the effects of low-volume exercise training (100 min/week) on oxidative stress and neutrophils activation markers in older adults. Twenty-eight older adults (age range 65–78 years) were assigned into control (n = 14) or exercise (n = 14) groups. The exercise program consisted of walking 30–60 min/session, 2 days each week for 12 weeks. Blood samples were taken before starting the sessions (baseline) and when they ended. Fasting plasma and serum oxidative stress and inflammatory markers were measured using commercial kits. Cell surface expression of adhesion molecules on circulating leukocytes (CD66b and CD62L) was determined using flow cytometry. The concentrations of derivatives of reactive oxygen metabolites tended to be lower than the baseline values only in the exercise group (P = 0.05). The biological antioxidant potential, thioredoxin concentrations, and glutathione peroxidase activities significantly increased only in the exercise group (P < 0.05 for all). While CD66b expression tended to decrease only in the exercise group, CD62L expression significantly increased (P < 0.05). Our findings indicate that exercise training below the current recommended level of at least 150 min/week attenuates basal oxidative stress and neutrophil activation in older adults. Thus, our findings may encourage more people to incorporate a small amount of physical activity into their lives.     

Low level laser therapy before eccentric exercise reduces muscle damage markers in humans

The purpose of the present study was to determine the effect of low level laser therapy (LLLT) treatment before knee extensor eccentric exercise on indirect markers of muscle damage. Thirty-six healthy men were randomized in LLLT group (n = 18) and placebo group (n = 18). After LLLT or placebo treatment, subjects performed 75 maximal knee extensors eccentric contractions (five sets of 15 repetitions; velocity = 60° seg^?1; range of motion = 60°). Muscle soreness (visual analogue scale—VAS), lactate dehydrogenase (LDH) and creatine kinase (CK) levels were measured prior to exercise, and 24 and 48 h after exercise. Muscle function (maximal voluntary contraction—MVC) was measured before exercise, immediately after, and 24 and 48 h post-exercise. Groups had no difference on kineanthropometric characteristics and on eccentric exercise performance. They also presented similar baseline values of VAS (0.00 mm for LLLT and placebo groups), LDH (LLLT = 186 IU/l; placebo = 183 IU/l), CK (LLLT = 145 IU/l; placebo = 155 IU/l) and MVC (LLLT = 293 Nm; placebo = 284 Nm). VAS data did not show group by time interaction (P = 0.066). In the other outcomes, LLLT group presented (1) smaller increase on LDH values 48 h post-exercise (LLLT = 366 IU/l; placebo = 484 IU/l; P = 0.017); (2) smaller increase on CK values 24 h (LLLT = 272 IU/l; placebo = 498 IU/l; P = 0.020) and 48 h (LLLT = 436 IU/l; placebo = 1328 IU/l; P < 0.001) post-exercise; (3) smaller decrease on MVC immediately after exercise (LLLT = 189 Nm; placebo = 154 Nm; P = 0.011), and 24 h (LLLT = 249 Nm; placebo = 205 Nm; P = 0.004) and 48 h (LLLT = 267 Nm; placebo = 216 Nm; P = 0.001) post-exercise compared with the placebo group. In conclusion, LLLT treatment before eccentric exercise was effective in terms of attenuating the increase of muscle proteins in the blood serum and the decrease in muscle force.     

The effect of Ginkgo biloba extract on scopolamine-induced apoptosis in the hippocampus of rats

Apoptosis, known as programmed cell death, plays a crucial role in normal development and tissue homeostasis. Apoptosis is also involved in neurodegenerative diseases such as Alzheimer’s disease. Amnesia refers to the loss of memory and can also be a warning sign of neurodegenerative diseases. The antioxidant properties of Ginkgo biloba extract was known previously. Therefore, the aim of this study was to examine the effects of Ginkgo biloba extract on the rat’s hippocampal apoptotic neurons number after Scopolamine based amnesia. Thirty-six adult male Wistar rats were used. Rats were randomly divided into control, sham, protective and treatment groups. The rats in the sham group received only scopolamine hydrobromide (3 mg/kg) intraperitoneally. The rats in the protective and treatment groups received Ginkgo biloba extract (40, 80 mg/kg) for 7 days intraperitoneally before/after scopolamine injection. Then 48 h after the last injection, the brains of rats were withdrawn and fixed with paraformaldehyde, and then, after histological processing, the slices were stained with the TUNEL kit for apoptotic neurons. Data were compared by the ANOVA Post Hoc Tukey test; P < 0.05 was considered significant. Our results showed that Scopolamine (in the sham group) increased significantly the number of apoptotic neurons in all areas of the hippocampus compared with the control. Whereas, Ginkgo biloba extract reduce the neuronal apoptosis in the hippocampus before and/or after encounter with scopolamine. We concluded that pretreatment and treatment injection of Ginkgo biloba extract can have a protective effect for neurons and it can limit apoptosis in all area of the hippocampus.     

Neuromuscular function, hormonal and redox status and muscle damage of professional soccer players after a high-level competitive match

The main aim was to analyse the impact of an official match on hormonal and redox status, muscle damage and inflammation and neuromuscular function. Seven high-level male soccer players from the same team performed an official match and data were collected 72 h before, 24, 48 and 72 h post-match. Plasma testosterone/cortisol ratio (T/C), creatine kinase (CK), superoxide dismutase (SOD), glutathione peroxidase (GPX) and reductase (GR) activities, myoglobin (Mb), C-reactive protein (CRP), uric acid (UA), protein sulfhydryls (–SH), malondialdehyde (MDA) concentrations and total antioxidant status (TAS) were measured. Sprint, jump and change of direction performance, and maximal isokinetic knee extension and flexion were obtained as neuromuscular functional parameters. Cortisol increased and T/C decreased until 48 h recovery (P < 0.05). Mb, CRP and –SH (P < 0.05) increased at 24 h and CK, TAS, SOD and MDA (P < 0.05) increased up to 48 h recovery. GR increased and GPX decreased at 24 h recovery (P < 0.05). Jump performance decreased 24 h post-match (P < 0.05), but no significant alterations in sprint, change of direction and muscle strength were observed. In conclusion, an official match resulted in changes in plasma biomarkers until 48 h of recovery period, without major impact on performance.     

Protective Effects of Acupuncture in Cardiopulmonary Bypass-Induced Lung Injury in Rats

Acute lung injury caused by cardiopulmonary bypass (CPB) increases the mortality after cardiac surgery. Our previous clinical study suggested that electroacupuncture (EAc) has a protective effect during CPB, but the mechanism was unclear. So, we design this study to investigate the effects of EAc on CPB-induced lung injury and the underlying mechanism. Male Sprague Dawley rats were randomly divided into control, CPB, and CPB + EAc groups. A lung injury model was created by CPB surgery to serve as the CPB group, and EAc (2/100 Hz) was used before CPB in the CPB + EAc group. Lung tissue was collected at 0.5, 1, and 2 h after CPB. Pulmonary malondialdehyde (MDA) concentrations as well as superoxide dismutase (SOD), myeloperoxidase (MPO), and caspase-3 activity were determined. c-Jun N-terminal kinase (JNK), ERK, p38 and cleaved caspase 3 in the lung were analyzed by western blotting. A549 cells were treated by rat serum from the CPB and CPB + EAc groups, and cleaved caspase-3 activity was detected by fluorescent immunohistochemistry. CPB significantly increased the MPO activity, MDA content, apoptosis, caspase-3 activity, and phosphorylated p38 but decreased SOD activity compared with the control group. EAc significantly increased SOD activity at 0.5 and 2 h (p < 0.01 vs CPB) and reduced CPB-induced histological changes, MPO activity at 1 and 2 h (p < 0.05 vs CPB), MDA content at 2 h (p < 0.05 vs CPB), caspase-3 activity at 1 h (p < 0.05 vs CPB), and phosphorylated p38 and JNK at 0.5 h after CPB. The serum from the CPB group increased more positive staining cells of cleaved caspase-3 than that from the CPB + EAc group. EAc reversed the CPB-induced lung inflammation, oxidative damage, and apoptosis; the mechanism may involve decreased phosphorylation of p38 along with caspase-3 activity and activation.     

Hepatoprotective and antioxidant potential of ferulic acid against acetaminophen-induced liver damage in mice

In the present study, we aimed to investigate the hepatoprotective and antioxidant potential of ferulic acid against acetaminophen-induced liver damage in mice. Hepatotoxicity was induced in mice by single dose of acetaminophen (900 mg/kg body weight i.p.). Ferulic acid (80 mg/kg body weight i.p.) and silymarin (25 mg/kg/body weight i.p.) were administered 30 min after the injection of acetaminophen. After 4 h, the mice were killed; liver markers (aspartate transaminase, alanine transaminase, alkaline phosphatase, and total bilirubin) were estimated in serum, while the lipid peroxidation and antioxidant status (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and glutathione) were determined in liver homogenate. Liver markers (aspartate transaminase, alanine transaminase, alkaline phosphatase, and total bilirubin) and lipid peroxidation levels were found to be increased in mice exposed to acetaminophen, whereas the antioxidant status was found to be depleted compared to that of the control group. However, ferulic acid administration (80 mg/kg body weight i.p.) to acetaminophen-intoxicated mice significantly reverse (p?<?0.05) the above-mentioned changes similar to the positive drug silymarin as evidenced in liver histology. The results clearly exhibit that ferulic acid possesses promising hepatoprotective potential.     

Protective Effects of BML-111 on Cerulein-Induced Acute Pancreatitis-Associated Lung Injury via Activation of Nrf2/ARE Signaling Pathway

The aim of this study was to investigate whether BML-111 can exert protective effects on cerulein-induced acute pancreatitis-associated lung injury (APALI) via activation of nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant responsive element (ARE) signaling pathway. Severe acute pancreatitis (SAP) was established by intraperitoneal injection of cerulein (50 μg/kg) seven times at hourly intervals and Escherichia coli lipopolysaccharide (10 mg/kg) once after the last dose of cerulein immediately. BML-111 (1 mg/kg) was administered 1 h before the first injection of cerulein. Samples were taken at 3, 6, 12, and 24 h after the last injection. Pathologic lesions of the pancreas and lung tissues as well as the levels of serum amylase were analyzed; Myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), Nrf2, heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase-1 (NQO1) of lung tissue were determined. The findings revealed that the injuries of pancreas and lung were typically induced by cerulein. The administration of BML-111 reduced the levels of serum amylase, lung MPO, lung MDA, the wet-to-dry weight ratio, and the pathology injury scores of the lung and pancreas, which increased in the SAP group. The expressions of Nrf2, HO-1, NQO1, and activity of SOD in lung tissue increased in the BML-111 group compared with those in the SAP group. This study indicates that BML-111 may play a critical protective role in APALI induced by cerulein. The underlying mechanisms of protective role may be attributable to its antioxidant effects through the activation of Nrf2/ARE pathway.     

Circulating angiogenic and inflammatory cytokine responses to acute aerobic exercise in trained and sedentary young men

Purpose

Endurance exercise training can ameliorate many cardiovascular and metabolic disorders and attenuate responses to inflammatory stimuli. The purpose of this study was to determine whether the angiogenic and pro-inflammatory cytokine response to acute endurance exercise differs between endurance-trained and sedentary young men.

Methods

Ten endurance-trained and ten sedentary healthy young men performed 30 min of treadmill running at 75 % VO_2max with blood sampling before and after exercise. Plasma concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-8, IL-6, vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), placental growth factor (PlGF), and soluble VEGF receptor-1 (sFlt-1) were measured by multiplex ELISA.

Results

Acute exercise increased IL-6 by 165 % (P < 0.05), IL-8 by 32 % (P < 0.05), PlGF by ~16 % (P < 0.05), sFlt-1 by 36 % (P < 0.001), and tended to increase bFGF by ~25 % (P = 0.06) in main effects analyses. TNF-α and VEGF did not change significantly with exercise in either group. Contrary to our hypothesis, there were no significant differences in TNF-α, IL-6, VEGF, bFGF, PlGF, or sFlt-1 between groups before or after acute exercise; however, there was a tendency for IL-8 concentrations to be higher in endurance-trained subjects compared to sedentary subjects (P = 0.06).

Conclusions

These results indicate that 30 min of treadmill running at 75 % VO_2max produces a systemic angiogenic and inflammatory reaction, but endurance exercise training does not appear to significantly alter these responses in healthy young men.     

A single bout of downhill running transiently increases HOMA-IR without altering adipokine response in healthy adult women

Purpose

Eccentric exercise-induced muscle damage may cause marked alterations in insulin sensitivity. However, it is not entirely known whether such alterations are also related to changes in adipokine levels. The aim of this study was to investigate the effects of muscle damage due to downhill running on inflammation, insulin sensitivity and selected adipokines related to insulin regulation (adiponectin, visfatin, resistin).

Methods

Data were collected from 12 healthy adult women. Each subject participated in two trials, 4 weeks apart. The first trial was reserved for resting measurements only (control trial), while the second trial involved a 45-min exercise (?15 % slope, ~60 % of VO_2max) intervention (exercise trial). Insulin sensitivity (HOMA), creatine kinase activity (CK), delayed onset muscle soreness (DOMS), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), glucose, insulin, adiponectin, resistin, and visfatin were assessed pre-exercise and 1, 2, 3, and 4 days post-exercise and during the same time points in the control trial.

Results

Analyses revealed that CK, DOMS, TNF-α, IL-6, insulin and HOMA significantly increased (p < 0.05) throughout recovery (days 1–4). Adiponectin and visfatin remained unchanged, while resistin significantly increased (p < 0.05) only 2 days post-exercise. Visfatin was negatively correlated with HOMA at days 1 and 4 of recovery.

Conclusion

Although muscle damage due to downhill running caused a decline of insulin sensitivity, this response was not associated with the changes in adipokine levels.