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Grzegorz Machnik

Researcher at Medical University of Silesia

Publications -  62
Citations -  814

Grzegorz Machnik is an academic researcher from Medical University of Silesia. The author has contributed to research in topics: Superoxide dismutase & Oxidative stress. The author has an hindex of 17, co-authored 55 publications receiving 674 citations. Previous affiliations of Grzegorz Machnik include University of Silesia in Katowice.

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Metformin affects macrophages' phenotype and improves the activity of glutathione peroxidase, superoxide dismutase, catalase and decreases malondialdehyde concentration in a partially AMPK-independent manner in LPS-stimulated human monocytes/macrophages.

TL;DR: It is believed that metformin-based therapy, a cornerstone in diabetes therapy, not only improves the prognosis of diabetics by reducing blood glucose but also by reducing oxidative stress, inflammatory cytokine production and the shift toward alternative activation of macrophages.
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Gene expression and activity of antioxidant enzymes in the blood cells of workers who were occupationally exposed to lead.

TL;DR: It is concluded that lead has a significant influence not only on the activities of antioxidant enzymes but also on the dose-dependent expression in their genes.
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Immunolocalization and expression of kinin B1R and B2R receptors in human inflammatory bowel disease

TL;DR: Increased B(1)R gene and protein expression in active IBD provides a structural basis of the important role of bradykinin in chronic inflammation.
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Exenatide (a GLP-1 agonist) expresses anti-inflammatory properties in cultured human monocytes/macrophages in a protein kinase A and B/Akt manner

TL;DR: It is shown that exenatide skewed the macrophages phenotype toward anti-inflammatory phenotype and this effect is predominantly attributable to protein kinase A and to a less extent to B/Akt activation.
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Exenatide and metformin express their anti-inflammatory effects on human monocytes/macrophages by the attenuation of MAPKs and NFκB signaling

TL;DR: It is reported that metformin and exenatide inhibit the proinflammatory phenotype of human monocytes/macrophages via influence on MAPK, C/EBP beta, and NFκB.