Apelin-13 attenuates injury following ischemic stroke by targeting matrix metalloproteinases (MMP), endothelin- B receptor, occludin/claudin-5 and oxidative stress

2021 ◽  
Vol 118 ◽  
pp. 102015
Author(s):  
Raheleh Gholamzadeh ◽  
Fatemeh Ramezani ◽  
Pooya M. Tehrani ◽  
Nahid Aboutaleb
Stroke ◽  
2001 ◽  
Vol 32 (1) ◽  
pp. 275-278 ◽  
Author(s):  
Maria Cristina Polidori ◽  
Antonio Cherubini ◽  
Umberto Senin ◽  
Patrizia Mecocci

2008 ◽  
Vol 30 (4) ◽  
pp. 389-393 ◽  
Author(s):  
Lianbi Xue ◽  
Qiuhong Yu ◽  
Hongxia Zhang ◽  
Yaling Liu ◽  
Chunjuan Wang ◽  
...  

2019 ◽  
Author(s):  
Mingchao Zhang ◽  
Yujia Li ◽  
Jiucun Wang ◽  
Huiru Tang ◽  
Zhong Yang ◽  
...  

AbstractIt is critical to discover biomarkers for non-invasive evaluation of the levels of inflammation and oxidative stress in human body - two key pathological factors in numerous diseases. Our study has indicated keratin 1-based epidermal autofluorescence (AF) as a biomarker of this type: Inducers of both inflammation and oxidative stress dose-dependently increased epidermal green AF with polyhedral structure in mice, with the AF intensity being highly associated with the dosages of the inducers. Lung cancer also induced increased epidermal green AF of mice, which was mediated by inflammation. Significant and asymmetrical increases in green AF intensity with polyhedral structure were found in the Dorsal Index Fingers’ skin of acute ischemic stroke (AIS) patients. While the AF intensity of the subjects with high risk for developing AIS, ischemic stroke patients in recovery phase and lung cancer patients was significantly higher than that of healthy controls, both AF intensity and AF asymmetry of these four groups were markedly lower than those of the AIS patients, which have shown promise for AIS diagnosis. Several lines of evidence have indicated K1 as an origin of the AF, e.g., K1 siRNA administration attenuated the oxidative stress-induced AF increase of mice. Collectively, our study has indicated K1-based epidermal AF as a biomarker for non-invasive evaluation of the levels of inflammation and oxidative stress in the body. These findings have established a basis for novel keratin’s AF-based biomedical imaging technology for non-invasive, efficient and economic diagnosis and screening of such inflammation- and oxidative stress-associated diseases as AIS.


2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Zhongjun Chen ◽  
Tieping Fan ◽  
Xusheng Zhao ◽  
Zhichen Zhang

Abstract Objectives Studies have widely explored in the filed of ischemic stroke (IS) with their focus on transcription factors. However, few studies have pivoted on sex determining region Y-box 2 (SOX2) in IS. Thus, this study is launched to figure out the mechanisms of SOX2 in IS. Methods Rat middle cerebral artery occlusion (MCAO) was established as a stroke model. MCAO rats were injected with depleted SOX2 or long non-coding RNA plasmacytoma variant translocation 1 (PVT1) to explore their roles in neurological deficits, cerebral water content, neuron survival, apoptosis and oxidative stress. The relationship among SOX2, PVT1, microRNA (miR)-24-3p and signal transducer and activator of transcription 3 (STAT3) was verified by a series of experiments. Results SOX2, PVT1 and STAT3 were highly expressed while miR-24-3p was poorly expressed in cerebral cortex tissues of MCAO rats. Depleted SOX2 or PVT1 alleviated brain injury in MCAO rats as reflected by neuronal apoptosis and oxidative stress restriction, brain water content reduction, and neurological deficit and neuron survival improvements. Overexpression of PVT1 functioned oppositely. Restored miR-24-3p abolished PVT1 overexpression-induced brain injury in MCAO rats. SOX2 directly promoted PVT1 expression and further increased STAT3 by sponging miR-24-3p. Conclusion This study presents that depleting SOX2 improves IS via PVT1/miR-24-3p/STAT3 axis which may broaden our knowledge about the mechanisms of SOX2/PVT1/miR-24-3p/STAT3 axis and provide a reference of therapy for IS.


2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Xiaoguang Liu ◽  
Weihua Xiao ◽  
Lifang Zhen ◽  
Yongzhan Zhou ◽  
Jian Shou

Objective Skeletal muscle contusion is one of the most common muscle injury in sports medicine and traumatology. Bone marrow mesenchymal stem cells (BMSCs) transplantation is a promising strategy for muscle regeneration. However, the roles of BMSCs, especially the mechanisms involved, in the regeneration of contused skeletal muscle are still not fully recognized. The aim of the study is to evaluate the potential of BMSCs transplantation for muscle regeneration and mechanisms involved after contusion. Methods Ninety-nine C57BL/6J mice were divided into three groups: control group (n=11), muscle contusion and BMSCs treated group (n=44), muscle contusion and sham treated group (n=44). BMSCs were immediately transplanted into gastrocnemius muscles (GMs) following direct contusion. At different time points (3, 6, 12 and 24 days) post-injury, the animals were killed and then GMs were harvested. Morphological and gene expression analyses were used to elevate the effect of BMSCs transplantation and mechanisms involved. Results The results indicate that BMSCs transplantation impairs muscle regeneration, as well as more fibrotic scar formation after skeletal muscle contusion. Furthermore, macrophages, inflammatory cytokines, chemokines, matrix metalloproteinases and oxidative stress related enzymes were significantly increased after BMSCs transplantation. These results suggest that BMSCs transplantation impairs skeletal muscle regeneration and that macrophages, inflammatory cytokines, chemokines, matrix metalloproteinases and oxidative stress related enzymes may be involved in the process. Conclusions BMSCs transplantation aggravates inflammation, oxidative stress and fibrosis, and impairs skeletal muscle regeneration, which shed new light on the role of BMSCs in regenerative medicine and cautions the application of BMSCs for muscle injury.


2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Yuan Zhou ◽  
Shanshan Zhang ◽  
Xiang Fan

Stroke is the second most common cause of death globally and the leading cause of death in China. The pathogenesis of cerebral ischemia injury is complex, and oxidative stress plays an important role in the fundamental pathologic progression of cerebral damage in ischemic stroke. Previous studies have preliminarily confirmed that oxidative stress should be a potential therapeutic target and antioxidant as a treatment strategy for ischemic stroke. Emerging experimental studies have demonstrated that polyphenols exert the antioxidant potential to play the neuroprotection role after ischemic stroke. This comprehensive review summarizes antioxidant effects of some polyphenols, which have the most inhibition effects on reactive oxygen species generation and oxidative stress after ischemic stroke.


Author(s):  
Dragana Stanisic ◽  
Radmila Obradovic ◽  
Sanja Vujovic ◽  
Milica Jovanovic ◽  
Vladimir Zivkovic

Abstract Diabetes mellitus, a chronic disease considered by the World Health Organization to be an epidemic, is now recognized as one of the factors behind the onset of periodontal disease. The connection between periodontal disease, which is an irreversible inflammatory disease of the supporting tissue of the teeth, and systemic diseases is reflected in the existence of common risk factors, subgingival dental biofilm, as a constant source of proinflamma-tory cytokines synthesized intensely in inflammatory periodontium. Diabetes mellitus leads to increased oxidative stress in periodontal tissues causing worsening of the disease and periodontopathy exacerbates deficiency of pancreatic β-cells. The most important role in primary inflammatory response in the pathogenesis of periodontopathy is played by neutrophils. Neutrophils cause periodontium destruction by the release of enzymes (matrix metalloproteinases), cytotoxic substances (free radicals, reactive oxygen and nitrogen species) and the expression of membrane receptors. Matrix metalloproteinases within the “protease network” are critical to many physiological and pathological processes, including immunity, inflammation, bone resorption and wound healing. Matrix metalloproteinases levels are elevated in patients with metabolic syndrome and diabetes mellitus, which may contribute to more frequent complications. In this paper, the review of available literature data shows the correlation between periodontal disease and diabetes mellitus, as well as the role of matrix metalloproteinases and oxidative stress in these. In this regard, determining the value of matrix metalloproteinases may be helpful in the diagnosis of periodontal disease complicated by diabetes mellitus. Also, the parameters of oxidative stress could help to clarify the mechanisms of pathogenesis and etiology of periodontal disease, or indicate the potential benefit of antioxidant supplementation in these individuals. As the role of matrix metalloproteinases has not been fully clarified in the pathogenesis of periodontopathy, additional studies will be needed to indicate their importance.


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