Abstract
The interaction of reactive oxygen species (ROS) with lipids, proteins, nucleic acids and hydrocarbonates promotes acute and chronic tissue damage, mediates immunomodulation and triggers autoimmunity in systemic lupus erythematous (SLE) patients. The aim of the study was to determine the pathophysiological mechanisms of the oxidative stress-related damage and molecular mechanisms to counteract oxidative stimuli in lupus nephritis. Our study included 38 SLE patients with lupus nephritis (LN group), 44 SLE patients without renal impairment (non-LN group) and 40 healthy volunteers as control group. In the present paper, we evaluated serum lipid peroxidation, DNA oxidation, oxidized proteins, carbohydrate oxidation, and endogenous protective systems. We detected defective DNA repair mechanisms via 8-oxoguanine-DNA-glycosylase (OGG1), the reduced regulatory effect of soluble receptor for advanced glycation end products (sRAGE) in the activation of AGE-RAGE axis, low levels of thiols, disulphide bonds formation and high nitrotyrosination in lupus nephritis. All these data help us to identify more molecular mechanisms to counteract oxidative stress in LN that could permit a more precise assessment of disease prognosis, as well as developing new therapeutic targets.
Highlights
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with complex pathogenesis, characterized by formation of autoantibodies against normal structures of the body such as skin, joints, blood elements, kidney, and central nervous system, with a heterogeneity of clinical manifestations
Leucocytes and Hemoglobin were statistically significantly lower in SLE groups compared with the control group (p < 0.05), but without statistical variation between LN and non-LN subjects (p > 0.05)
Albumin was statistically significantly lower in SLE groups, when compared with control (p < 0.05) and in LN compared with non-LN group (p < 0.05)
Summary
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with complex pathogenesis, characterized by formation of autoantibodies against normal structures of the body such as skin, joints, blood elements, kidney, and central nervous system, with a heterogeneity of clinical manifestations. Keratinocyte activation induces chemokines synthesis (CXCL5, CXCL8, CXCL20), production of adhesion molecules, apoptosis, keratinocyte photodistruction, release of nuclear and cytoplasmic antigens, and immune response initiation. These pathogenic events are processed by dermic and epidermic macrophages and presented to dermal naïve T lymphocytes. In SLE-related skin lesions, vacuolar and hydropic degeneration of keratinocytes and lymphocytic infiltration in papillary dermis could be found
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