A study on correlation between oxidative stress parameters and inflammatory markers in type 2 diabetic patients with kidney dysfunction in north Indian population

Abstract

Background Research reports support the statement that oxidative stress and inflammation are well‐known risk factors for chronic kidney disease (CKD) in patients with diabetes. This study was designed to ascertain the associated role of oxidative stress parameters and inflammatory markers in diabetes and related CKD among the north Indian population. Methods The study was divided into three groups as healthy subjects (group 1), patients with diabetes without complication (group 2), and with CKD (group 3). Serum levels of malondialdehyde (MDA) and nitric oxide (NO), superoxide dismutase (SOD), catalase (CAT), and glutathione reductase (GR) content were estimated in all individuals. Inflammatory cytokines interleukin‐6 (IL‐6) and tumor necrosis factor‐α (TNF‐α)‐α were determined by enzyme‐linked immuno‐sorbent assay. Results MDA, protein carbonyl, and NO were significantly elevated in patients with type 2 diabetes as compared with healthy subjects (P ≤ 0.05). Total thiols content were found to be significantly decreased in patients with diabetes with CKD. The activity of antioxidant enzymes SOD, CAT, and GR showed a significant suppression in patients with type 2 diabetes with or without CKD as compared with healthy subjects. Nevertheless, the levels of proinflammatory cytokines IL‐6 and TNF‐α were significantly upregulated ( P ≤ 0.05) as compared with healthy subjects. Conclusion Determination of antioxidant defense parameters and inflammatory markers contributes to understand the relationship between oxidative stress and inflammation on the development and prevention of chronic kidney disease in Indian patients with diabetes.

The Role of the Gut Microbiome in Diabetes and Obesity-Related Kidney Disease

“…Decreased levels of the beneficial gut microbes, their associated SCFAs, and increased levels of harmful microbes were associated with CKD development [125]. In the context of any form of CKD, there is increased permeability of the intestinal barrier leading to transfer of toxins into the blood circulation; the effect is self-perpetuating in CKD, given the context of impaired renal function, endotoxins accumulate in the blood contributing to persistent systemic inflammation, pro-inflammatory cytokine release, and oxidative stress [125][126][127][128][129][130]. Collectively, these data provide proof of concept for the potential role of microbiota in limiting renal fibrosis.…”

lncRNA ANRIL play an important role in renal injury induced by diabetes

“…In a diabetic state, the human body experiences high oxidative stress and strong inflammatory responses. Consequently, a significant number of oxygen radicals and inflammatory factors are generated and released, which leads to more severe ischemiareperfusion injury of visceral organs [15,16]. As indicated by research findings, activity of both CCK-8 and SOD declines after hypoxia reoxygenation of HK-2 in the presence of high glucose.…”

SETD8 cooperates with MZF1 to participate in hyperglycemia-induced endothelial inflammation via elevation of WNT5A levels in diabetic nephropathy

“…Fifth, IL-6 and TNFα mRNA levels in tissue of participants should be provided, instead of the serum IL-6 and TNFα levels used in this study. However, serum IL-6 and TNFα have been reported to be used as predictors of kidney disease progression in diabetic nephropathy [ 34 , 35 ]. Moreover, the variation tendency of levels of serum inflammatory factors in participants was similar to that of mRNA expression of inflammatory factors in in vivo and in vitro studies in the present study.…”