Changes in serum levels of asymmetric-dimethylarginine (ADMA) in a rat model of non-alcoholic steatohepatitis: Role of oxidative stress

2014 ◽  
Vol 46 ◽  
pp. e27-e28
Author(s):  
A. Ferrigno ◽  
L.G. Di Pasqua ◽  
V. Rizzo ◽  
A.C. Croce ◽  
G. Bottiroli ◽  
...  
2016 ◽  
Vol 24 (7) ◽  
pp. 1070
Author(s):  
Fan Gao ◽  
Jian Ju ◽  
Wei Wang ◽  
Fu-Yuan Yan ◽  
Xiao-Qing Wang

2018 ◽  
Vol 61 ◽  
pp. 92-99 ◽  
Author(s):  
Lihui Zhou ◽  
Lian Ouyang ◽  
Shuangzhi Lin ◽  
Song Chen ◽  
YingJie Liu ◽  
...  

Alcohol ◽  
2009 ◽  
Vol 43 (2) ◽  
pp. 163-172 ◽  
Author(s):  
Christopher B. Forsyth ◽  
Ashkan Farhadi ◽  
Shriram M. Jakate ◽  
Yueming Tang ◽  
Maliha Shaikh ◽  
...  

2012 ◽  
Vol 12 (4) ◽  
pp. 741-750 ◽  
Author(s):  
Kalaiselvi Velayutham Anand ◽  
Mohamed Sultan Mohamed Jaabir ◽  
Philip A Thomas ◽  
Pitchairaj Geraldine

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Gaurav Patki ◽  
Farida Allam ◽  
Ritu Bohat ◽  
Faizan Jafri ◽  
Mohammad Saleem ◽  
...  

2016 ◽  
Vol 157 (45) ◽  
pp. 1781-1785 ◽  
Author(s):  
Iván Péter ◽  
Anna Jagicza ◽  
Zénó Ajtay ◽  
István Kiss ◽  
Balázs Németh

Psoriasis is among the most common dermatological diseases worldwide. Its significance is emphasized by adverse effects on quality of life, caused by chronic pain, physical and psychical disability due to psoriatic plaques. Besides the development of psoriatic arthritis, which often causes permanent joint damage, former studies revealed an increased risk of inflammatory bowel disease, cardiovascular disease and certain types of cancer. Genetic predisposition and oxidative stress caused by exogenous and endogenous factors can contribute to abnormal differentiation and hyperproliferation of keratinocytes, accordingly the development and maintenance of psoriasis. Moreover, excessive oxidative stress can be responsible for the onset of psoriasis complications. After a brief pathophysiological summary the authors discuss the role of oxidative stress in the development of psoriasis and its complications through several well studied biomarkers (asymmetric dimethylarginine, malondialdehyde, superoxide dismutase, catalase). Orv. Hetil., 2016, 157(45), 1781–1785.


2021 ◽  
Vol ahead-of-print (ahead-of-print) ◽  
Author(s):  
Jaber Jafarzadeh ◽  
Laleh Payahoo ◽  
Mohammad Yousefi ◽  
Ali Barzegar

Purpose This paper aims to depict the mechanistic role of vitamin D on dementia prevention, relief of the severity and the complication of the disease. All papers indexed in scientific databases, including Scopus, Elsevier, PubMed, Embase and Google Scholar between 2000 and 2021 were extracted and discussed. To present the mechanistic role of vitamin D in declining the severity of dementia, keywords including dementia, vitamin D, oxidative stress, inflammation, amyloid beta-Peptides were used. Design/methodology/approach Dementia is a prevalent cognitive disorder worldwide, especially in elderly people, which is accompanied by serious disabilities. Besides genetic, biological and lifestyle factors are involved in the incidence of dementia. An unhealthy diet along with micronutrient deficiencies are among modifiable factors. Vitamin D is one of the important micronutrients in brain health. Besides the involvement in gene expression, bone mineralization, apoptosis, inflammation, skeletal maturation, neurotropic action and hemostasis of phosphate and calcium, vitamin D also exerts neuroprotective effects via genomic and non-genomic pathways. Findings Vitamin D up-regulates the expression of various genes involved in dementia incidence via various mechanisms. Decreasing oxidative stress and the neuro-inflammatory cytokines levels, regulation of the expression of alternated Proteins including Tau and Amyloid-ß, calcium homeostasis in the central nervous system and also vascular are considered main mechanisms. Originality/value Considering the importance of diet in preventing dementia, adherence to a healthy diet that provides essential nutrients to brain function seems to be urgent. Controlling serum levels of vitamin D periodically and providing vitamin D by related sources or supplements, if there is a deficiency, is recommended. Future studies are needed to clarify other related mechanisms.


2021 ◽  
Vol 66 (3) ◽  
pp. 233-243
Author(s):  
Haiqin Wang ◽  
Li Nian ◽  
Zhonghua Li ◽  
Changhui Lu

Hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome is a life-threatening pregnancy complication. Though there are several medications widely used to treat HELLP syndrome, delivery is the only efficient treatment. The goal of the present study was to investigate the effects of platelet-derived growth factor-D (PDGF-D), a newly identified PDGF, in a rat model of HELLP syndrome which was accomplished by sFlt-1 and sEng injection. The expression levels of PDGF-D in pregnant women diagnosed with HELLP syndrome was determined. A HELLP rat model was established and the PDGF-D expression level in the plasma and the placenta tissue was evaluated. To evaluate the effects of PDGF-D in HELLP syndrome model, siPDGF-D was injected into the rats and the HELLP syndrome-related parameters were measured. The levels of inflammatory cytokines and PDGF-D were determined by ELISA. The oxidative stress activities in the plasma were also determined. Furthermore, the expression of PDGF-D/PDGFR-β/nuclear factor κB (NF-κB) p65 in placenta tissues was evaluated by Western blotting. Compared to the normal pregnant (NP) group, the levels of PDGF-D were augmented regardless of species. Knockdown of PDGF-D can result in the alleviation of HELLP syndrome development and progression in the HELLP rat model. Importantly, as a result of PDGF-D knockdown, the serum levels of inflammatory cytokines and oxidative stress activities were modulated, and the phosphorylation of PDGFR-β and NF-κB p65 in placenta tissue was inhibited. Taking together, our findings indicate that targeting PDGF-D could be used as a novel strategy to treat patients with HELLP syndrome.


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