Abstract

context: Early interpretation of the toxic effect of free radicals leading to cardiovascular diseases (CVDs) in autoimmune disorders is a quenching thirst for therapeutic intervention and personal identification. aim: The study aims to evaluate the expression of Nrf2, NQO-1, and LpPLA2 genes along with markers of endothelial dysfunction and oxi-inflammatory stress in active RA patients and to enlighten the assessment of study group markers in the personal identification of RA patients for their early therapeutic intervention and prevention of vascular complications. materials & method: 64 active RA patients between 35-55 years and 64 healthy controls were recruited from North India region. Using specific primers, mRNA expression of Nrf2, NQO-1 & LpPLA2 genes were evaluated in blood by qPCR. 2 –ΔΔCT method was used to determine the fold change. Brachial artery flow mediated diameter (FMD), total antioxidant activity, malondialdehyde, TNF-α, IL-6 & hs-CRP levels were estimated by using standard methods followed by appropriate statistical analysis of data. results: Increased expression of NQO-1, Nrf2 and LpPLA2 was observed in RA patients along with marked altered levels (p<0.05; significant) of oxiinflammatory markers which may be due to compensatory activation of antioxidant defense mechanism. Remarkably, FMD% was significantly low (p<0.05) and inversely associated with the expression of NQO-1, Nrf2 and LpPLA2, which highlighted the culprit effect of oxi-inflammatory stress in inducing altered vascular homeostasis. conclusions: Thus, combinational analysis of molecular diagnostic signatures associated with toxic free radicals along with FMD measurement exhibits a great promise in personal identification of RA patients for early therapeutic intervention, mainly, by targeting the oxi-inflammatory stress mediated cytoprotective pathway, and thereby, reducing the burden of CVD morbidity and mortality in RA patients.

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