PMID: 

J Affect Disord. 2020 Jan 10 ;265:59-62. Epub 2020 Jan 10. PMID: 31959584

Abstract Title: 

Sedentary behaviour is associated with depression symptoms: Compositional data analysis from a representative sample of 3233 US adults and older adults assessed with accelerometers.

Abstract: 

BACKGROUND: Evidence supporting the individual associations of sedentary behaviours with depression symptoms commonly ignores the inherent co-dependency between physical activity, sedentary behaviours and sleep in a given 24-hour period. Data analysis based on compositional methods effectively deals with this issue.AIM: To investigate the association between sedentary behaviour and depression symptoms synergistically using compositional analysis methods.METHODS: Participants were a representative sample of 3233 US adults and older adults from the 2005-2006 cycle of the NHANES with valid 24-hour lifestyle behaviours data (i.e., accelerometer-derived physical activity and sedentary behaviour and self-reported sleep) and available self-reported depression symptoms (PHQ-9). The association between sedentary behaviour and depression symptoms scoring was investigated using a compositional zero-inflated Poisson regression analysis. Subsequently, the model estimates were used to evaluate the effects on depression symptoms of replacing time spent in sitting activities with physical activity of different intensities and sleep.LIMITATIONS: The current study is limited by its cross-sectional design. Also, sleep time was self-reported, which could bias our estimations.RESULTS: Increased sedentary behaviour relative to other behaviours was statistically significantly associated with increased depression symptoms (p 

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PMID: 

J Nutr Health Aging. 2017 ;21(3):307-313. PMID: 28244571

Abstract Title: 

Efficacy and Therapeutic Potential of Curcumin Against Sepsis-Induced Chronic Lung Injury in Male Albino Rats.

Abstract: 

The present study investigates curcumin effect against sepsis-induced chronic lung injury (CLI) of male albino rats. Rats were grouped into four groups such rats undergoing a sham cecal ligature puncture (CLP), rats undergoing CLP, rats undergoing CLP and treated with saline and rats undergoing CLP and treated with curcumin (100 mg/kg bwt). After 45 days of treatment, bronchoalveolar fluid (BALF), blood and lung tissues were collected from the each animal. The total protein content, wet and dry (W/D) weight of lung tissues and some inflammatory cells in the BALF were measured. Histopathological analysis was carried out to investigate the alteration of the cellular architecture of lung tissues. Lipid peroxidation malondialdehyde (MDA), superoxide dismutase (SOD) and myeloperoxidase (MPO) levels were determined. Cytokines such as interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-a) and macrophage inhibitory factor (MIF) were measured in the BALF. Curcumin administration significantly reduced CLP-induced inflammation and pulmonary edema. Curcumin treatment is significantly reduced MPO activity, and inflammatory cell accumulation in the BALF and also protein level, MDA, SOD, and W/D ratio were significantly reduced in the lung tissues. Also, curcumin reduced the expression of IL-A, TNF-a and MIF levels in the lung tissues. Histopathological study revealed the significant reduction of CLP-induced CLI in the curcumin-treated male albino rats. Taking all these data together, it is concluded that curcumin can act as a suitable therapeutic agent against CLP-induced CLI of male albino rats.

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PMID: 

Arch Physiol Biochem. 2020 Jan 25:1-8. Epub 2020 Jan 25. PMID: 31983250

Abstract Title: 

Effect of combined calcium, magnesium, vitamin C and E supplementation on seminal parameters and serum oxidative stress markers in fructose-induced diabetic Wistar rats.

Abstract: 

Deleterious effects of diabetes on seminal quality, serum metals and antioxidants have been confirmed.This study evaluated the effect of combined calcium, magnesium, vitamin C and E supplementation on seminal parameters, serum total antioxidant capacity (TAC), nitric oxide (NO), malonyldialdehyde (MDA), calcium and magnesium in fructose-induced diabetic rats.Thirty rats were grouped into non-diabetic controls, diabetic controls, diabetic rats given vitamin E + C, calcium + magnesium and vitamin E + C + calcium + magnesium. The analytes were evaluated using standard methods. Statistical significance was set at 

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PMID: 

Int J Epidemiol. 2020 Jan 13. Epub 2020 Jan 13. PMID: 31930316

Abstract Title: 

Is mode of transport to work associated with mortality in the working-age population? Repeated census-cohort studies in New Zealand 1996, 2001 and 2006.

Abstract: 

BACKGROUND: Increasing active transport is proposed as a means to address both health and environmental issues. However, the associations between specific modes, such as cycling, walking and public transport, and health outcomes remain unclear. We examined the association between mode of travel to work and mortality.METHODS: Cohort studies of the entire New Zealand working population were created using 1996, 2001 and 2006 censuses linked to mortality data. Mode of travel to work was that reported on census day, and causes of death examined were ischaemic heart disease and injury. Main analyses were Poisson regression models adjusted for socio-demographics. Sensitivity analyses included: additional adjustment for smoking in the 1996 and 2006 cohorts, and bias analysis about non-differential misclassification of cycling vs car use.RESULTS: Walking (5%) and cycling (3%) to work were uncommon. Compared with people reporting using motor vehicles to travel to work, those cycling had a reduced all-cause mortality (ACM) in the socio-demographic adjusted models RR 0.87 (0.77-0.98). Those walking (0.97, 0.90-1.04) and taking public transport (0.96, 0.88-1.05) had no substantive difference in ACM. No mode of transport was associated with detectable statistically significant reductions in cause-specific mortality. Sensitivity analyses found weaker associations when adjusting for smoking and stronger associations correcting for likely non-differential misclassification of cycling.CONCLUSIONS: This large cohort study supports an association between cycling to work and reduced ACM, but found no association for walking or public-transport use and imprecise cause-specific mortality patterns.

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PMID: 

Blood Adv. 2020 Jan 28 ;4(2):312-321. PMID: 31978215

Abstract Title: 

N-acetylcysteine inhibits thrombosis in a murine model of myeloproliferative neoplasm.

Abstract: 

Thrombosis is a major cause of mortality in patients with myeloproliferative neoplasms (MPNs), though there is currently little to offer patients with MPN beyond aspirin and cytoreductive therapies such as hydroxyurea for primary prevention. Thrombogenesis in MPN involves multiple cellular mechanisms, including platelet activation and neutrophil-extracellular trap formation; therefore, an antithrombotic agent that targets one or more of these processes would be of therapeutic benefit in MPN. Here, we treated the JAK2V617F knockin mouse model of polycythemia vera with N-acetylcysteine (NAC), a sulfhydryl-containing compound with broad effects on glutathione replenishment, free radical scavenging, and reducing disulfide bonds, to investigate its antithrombotic effects in the context of MPN. Strikingly, NAC treatment extended the lifespan of JAK2V617F mice without impacting blood counts or splenomegaly. Using an acute pulmonary thrombosis model in vivo, we found that NAC reduced thrombus formation to a similar extent as the irreversible platelet inhibitor aspirin. In vitro analysis of platelet activation revealed that NAC reduced thrombin-induced platelet-leukocyte aggregate formation in JAK2V617F mice. Furthermore, NAC reduced neutrophil extracellular trap formation in primary human neutrophils from patients with MPN as well as healthy controls. These results provide evidence that N-acetylcysteine inhibits thrombosis in JAK2V617F mice and provide a pre-clinical rationale for investigating NAC as a therapeutic to reduce thrombotic risk in MPN.

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PMID: 

J Tradit Complement Med. 2020 Jan ;10(1):60-69. Epub 2019 Feb 27. PMID: 31956559

Abstract Title: 

Protective effects of luteolin on injury induced inflammation through reduction of tissue uric acid and pro-inflammatory cytokines in rats.

Abstract: 

Background and aim: Luteolin belongs to flavone group of flavonoids, present in many plants with potent antioxidant, anti-inflammatory and anti-proliferative effects. The objective of present study was to investigate protective effect of luteolin on injury induced inflammation via Monosodium urate (MSU) crystals induced and Acetaminophen (AMP) induced liver injury in rats.Experimental procedure: Protective effect of luteolin was observed by measurement of rat paw edema, lysosomal enzymes, antioxidants status and cytokine level. Measurement of uric acid level and neutrophil infiltration were done in AMP induced liver injury in rats. Luteolin was tested at 30 and 50 mg/kg doses and compare with colchicine.Results and conclusion: Luteolin significantly decreases paw edema in dose dependent manner compare to control group in MSU crystal-induced rats. Luteolin (50 mg/kg) was showed significant decrease in serum level of oxidative and lysosomal enzymes, proinflammatory cytokines i.e. tumor necrosis factor (TNF)-α (39.28 ± 3.17), interleukin (IL)-1β (12.07 ± 1.24), and IL-6 (24.72 ± 2.52) in MSU crystal-induced rats. In AMP induced liver injury, tissue uric acid level and myeloperoxidase were decreased significantly after treatment with luteolin as well as N-acetylcysteine. Serum level of liver enzymes was significantly reduced after treatment with luteolin. Histological observation of ankle joints and liver was support to protective effect of luteolin at both doses. In conclusion, luteolin showed anti-inflammatory effect through restoration of cytokine level, lysosomal enzymes level and antioxidants status. The reduction of liver tissue uric acid content may be one of the mechanisms for protective effect of luteolin. It can contribute to reduce injury induced inflammation.

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PMID: 

Arch Biochem Biophys. 2019 Dec 12 ;680:108227. Epub 2019 Dec 12. PMID: 31838118

Abstract Title: 

Redox status, inflammation, necroptosis and inflammasome as indispensable contributors to high fat diet (HFD)-induced neurodegeneration; Effect of N-acetylcysteine (NAC).

Abstract: 

Adequate dietary intake has a crucial effect on brain health. High fat diet (HFD) rich in saturated fatty acids is linked to obesity and its complications as neurodegeneration via inducing oxidative stress and inflammation. The present study aimed to evaluate the effect of HFD on cerebral cortex in addition to shedding the light on the modulatory role of N-acetylcytsteine (NAC) and its possible underlying biochemical and molecular mechanisms. Twenty eight male Wistar rats were equally and randomly divided into four groups. Group III, and group IV were fed on HFD (45% kcal from fat) for 10 weeks. Group II and group IV were treated with NAC in a dose of 150 mg/kg body weight via intraperitoneal route. Body weight, blood glucose, serum insulin, insulin resistance index, cerebral cortex redox and inflammatory status were evaluated. Cerebral cortex receptor-interacting serine/threonine-protein kinase3 (RIPK3), mixed-lineage kinase domain-like protein (MLKL), nod like receptor protein 3 (NLRP3), interleukin (IL)-18 levels were determined by immunoassay. In addition, apoptosis-associated speck-like proteins (ASC) expression by real-time PCR; inducible nitric oxide synthase (iNOS), glial fibrillary activating protein (GFAP) and matrix metalloproteinase-9 (MMP-9) expression by immunohistochemistry were evaluated. NAC supplementation protected against HFD-induced gain of weights, hyperglycemia, and insulin resistance. Furthermore, NAC improved redox and inflammatory status; decreased levels of RIPK3, MLKL, NLRP3, IL-18; down-regulated ASC, iNOS,GFAP and MMP-9 expression; and decreased myeloperoxidase activity in cerebral cortex. NAC could protect against HFD-induced neurodegeneration via improving glycemic status and peripheral insulin resistance, disrupting oxidative stress/neuroinflammation/necroptosis/inflammasome activation axis in cerebral cortex. NAC may represent a promising strategy for conserving brain health against metabolic diseases-induced neurodegeneration.

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PMID: 

Medicine (Baltimore). 2018 Nov ;97(45):e13087. PMID: 30407312

Abstract Title: 

N-acetylcysteine improves oxidative stress and inflammatory response in patients with community acquired pneumonia: A randomized controlled trial.

Abstract: 

Oxidative stress is considered to be part of the pathogenic mechanism for community-acquired pneumonia (CAP) and is closely linked to inflammation. Attenuation of oxidative stress would be expected to reduce pulmonary damage. Antioxidants have been found to be effective in alleviating lung injury and protecting against damage of other organs.The aim of the study was to compare the effect of adding N-acetylcysteine (NAC) to conventional treatment versus conventional treatment on oxidative stress, inflammatory factors, and radiological changes in CAP patients.Eligible CAP patients at Weihai Municipal Hospital were stratified and randomly assigned to either NAC group or non-NAC group between August 2016 and March 2017. The NAC group received conventional treatment for pneumonia and NAC (1200 mg/d). Thenon-NAC group received conventional therapy. malondialdehyde (MDA), superoxide dismutase (SOD), total antioxidant capacity (TAOC), tumor necrosis factor-α (TNF-α), and computed tomography (CT) images were evaluated at baseline and after treatment. The primary endpoint indicators werethe changes in oxidative stress parameters (MDA, TAOC, SOD) and TNF-α after treatment in the NAC group compared with those in the non-NAC group. The secondary endpoint indicator was any difference in CT scores after treatment in the NAC group compared with the non-NAC group.Baseline levels of MDA,TAOC, SOD, and TNF-α were similar between the 2 groups before treatment. Plasma levels of MDA and TNF-α decreased more (P 

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PMID: 

Int J Radiat Biol. 2020 Jan 28:1-32. Epub 2020 Jan 28. PMID: 31990607

Abstract Title: 

Protective effect of N-acetyl cysteine against radiotherapy-induced cardiac damage.

Abstract: 

Although radiotherapy (RT) is an important component of cancer treatment, it induces adverse tissue reactions in the around of cancer tissue. Therefore, radioprotectives are needed to protect normal tissues. The aim of the present study was to investigate the radioprotective effect of N-acetylcysteine (NAC) on RT- induced cardiac damage in rats for the acute term.The animals were divided into four groups. The rats in control group were injected with saline for 7 days; the rats in NAC group were injected NAC at dose of 240 mg/kg day for 7 days; the rats in RT group were injected with saline for 7 days plus was irradiated 1 hour after the last injection and the rats in NAC + RT group were injected with NAC for 7 days and irradiated 1 hour after the last NAC dose. The electrocardiogram was recorded and evaluated PR interval, QRS duration, QT interval, T wave alterations and heart rate. Serum interleukin-4, interleukin-6, tumor necrosis factor-alpha, interleukin 1 beta, galectin-3 levels and creatine kinase and creatine kinase isoenzyme-MB activities were determined in all groups. Also, tissue malondialdehyde and nitric oxide levels, superoxide dismutase, catalase and glutathione peroxidase activities were determined. In addition, histological changes of heart were evaluated. All measurements were performed 24 hours after RT.In the RT group, findings supporting cardiac injury were observed in the electrocardiogram. Also, cytokine levels and oxidative stress were significantly increased. Pretreatment of rats with NAC ameliorated cardiac injury induced by RT.Our findings suggested that NAC may be a potential radioprotector which is capable of preventing cardiac damage.

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PMID: 

Hum Exp Toxicol. 2019 Dec 13:960327119892042. Epub 2019 Dec 13. PMID: 31835924

Abstract Title: 

Piperine, a functional food alkaloid, exhibits inhibitory potential against TNBS-induced colitis via the inhibition of IκB-α/NF-κB and induces tight junction protein (claudin-1, occludin, and ZO-1) signaling pathway in experimental mice.

Abstract: 

BACKGROUND: Inflammatory bowel disease is a chronic immunoinflammatory disease of the gastrointestinal tract. Piperine, an alkaloid, has been reported to possess antioxidant, anti-inflammatory, antiapoptotic, and antiulcer potential.AIM: To elucidate the plausible mechanisms of action of piperine on experimental trinitrobenzenesufonic acid (TNBS)-induced colitis by assessing various biochemical, molecular, histological, and ultrastructural modifications.METHODS: Colitis was induced in male Sprague-Dawley rats via intrarectal instillation of TNBS. Then, the rats were treated with piperine (10, 20, and 40 mg/kg, p.o.) for 14 days.RESULTS: TNBS induced significant (0.05) colonic damage, which was assessed by disease activity index, macroscopic score, and stool consistency. The administration of piperine (20 and 40 mg/kg) significantly inhibited (0.05) these damages. Treatments with piperine (20 and 40 mg/kg) notably inhibited (0.05) the TNBS-induced elevation of oxido-nitrosative stress (superoxide dismutase, glutathione, malondialdehyde, and nitric oxide), 5-hydroxytryptamine, and hydroxyproline content in the colon. Furthermore, colonic inducible nitric oxide synthase (iNOs), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, interferon-gamma, and cyclooxygenase-2 (COX-2) messenger RNA (mRNA) expressions were upregulated after TNBS instillation and piperine (20 and 40 mg/kg) significantly attenuated (0.05) these elevated mRNA expressions. TNBS decreased the expressions of tight junction (TJ) protein (claudin-1, occludin, and zonula occludens-1 (ZO-1)) and increased the expressions of proapoptotic (caspase-1) protein. These expressions were markedly inhibited (0.05) by piperine treatment. Histological and ultrastructural studies of transmission electron microscopy suggested that piperine significantly ameliorated (0.05) TNBS-induced colonic aberrations.CONCLUSION: Piperine ameliorated the progression of TNBS-induced colitis by modulating the nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha/nuclear factor-kappa B signaling pathway, thus inhibiting the overexpression of proinflammatory cytokines (TNF-α and IL's), COX-2, iNOs, oxido-nitrosative stress, and proapoptotic proteins (caspase-1) that may improve the expression of TJ protein (claudin-1, occludin, and ZO-1).

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