Astaxanthin ameliorates experimental diabetes-induced renal oxidative stress and fibronectin by upregulating connexin43 in glomerular mesangial cells and diabetic mice

Chen, Qing; Tao, Jun; Li, Guoping; Zheng, Dongxiao; Tan, Yongjun; Li, Ruibo; Tian, Li; Li, Zhanghao; Cheng, Hong; Xie, Xi

doi:10.1016/j.ejphar.2018.09.028

Cited by 27 publications

(13 citation statements)

References 41 publications

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“…The antioxidant, astaxanthin, significantly reduced extracellular ROS from neutrophils in alloxan treated rats at baseline, but not when stimulated with artificial ROS inducer Phorbol 12-myristate 13-acetate (PMA) (158). Astaxanthin also significantly lowered ROS in retinal and pancreatic cells in rats with STZ-induced diabetes and is currently undergoing clinical trials for treating diabetic retinopathy (NCT03702374) (166)(167)(168). A further antioxidant Captopril, an angiotensinconverting enzyme inhibitor, was shown to be effective in reducing ROS in human subjects with T2D and STZ-treated rats in vitro (155,169).…”

Section: Extracellular Ros Production and Oxidative Stressmentioning

confidence: 99%

A Bittersweet Response to Infection in Diabetes; Targeting Neutrophils to Modify Inflammation and Improve Host Immunity

et al. 2021

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Chronic and recurrent infections occur commonly in both type 1 and type 2 diabetes (T1D, T2D) and increase patient morbidity and mortality. Neutrophils are professional phagocytes of the innate immune system that are critical in pathogen handling. Neutrophil responses to infection are dysregulated in diabetes, predominantly mediated by persistent hyperglycaemia; the chief biochemical abnormality in T1D and T2D. Therapeutically enhancing host immunity in diabetes to improve infection resolution is an expanding area of research. Individuals with diabetes are also at an increased risk of severe coronavirus disease 2019 (COVID-19), highlighting the need for re-invigorated and urgent focus on this field. The aim of this review is to explore the breadth of previous literature investigating neutrophil function in both T1D and T2D, in order to understand the complex neutrophil phenotype present in this disease and also to focus on the development of new therapies to improve aberrant neutrophil function in diabetes. Existing literature illustrates a dual neutrophil dysfunction in diabetes. Key pathogen handling mechanisms of neutrophil recruitment, chemotaxis, phagocytosis and intracellular reactive oxygen species (ROS) production are decreased in diabetes, weakening the immune response to infection. However, pro-inflammatory neutrophil pathways, mainly neutrophil extracellular trap (NET) formation, extracellular ROS generation and pro-inflammatory cytokine generation, are significantly upregulated, causing damage to the host and perpetuating inflammation. Reducing these proinflammatory outputs therapeutically is emerging as a credible strategy to improve infection resolution in diabetes, and also more recently COVID-19. Future research needs to drive forward the exploration of novel treatments to improve infection resolution in T1D and T2D to improve patient morbidity and mortality.

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Section: Extracellular Ros Production and Oxidative Stressmentioning

confidence: 99%

A Bittersweet Response to Infection in Diabetes; Targeting Neutrophils to Modify Inflammation and Improve Host Immunity

et al. 2021

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“…The antidiabetic effect of ASX has been studied in different animal models with variable outcomes (Figure 2) though the underlying mechanisms have not been clearly elucidated. Oral administration of ASX significantly reduced fasting blood glucose in db/db mice, a well-known obese model for T2DM [66][67][68][69]. A long-term administration of ASX (35 mg/kg for 12 weeks) showed that hypoglycemic effect is linked with a lower malondialdehyde (MDA) content and enhanced SOD activity in serum [70].…”

Section: Antidiabetic Effects Of Astaxanthinmentioning

confidence: 99%

Impact of Astaxanthin on Diabetes Pathogenesis and Chronic Complications

et al. 2020

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Oxidative stress (OS) plays a pivotal role in diabetes mellitus (DM) onset, progression, and chronic complications. Hyperglycemia-induced reactive oxygen species (ROS) have been shown to reduce insulin secretion from pancreatic β-cells, to impair insulin sensitivity and signaling in insulin-responsive tissues, and to alter endothelial cells function in both type 1 and type 2 DM. As a powerful antioxidant without side effects, astaxanthin (ASX), a xanthophyll carotenoid, has been suggested to contribute to the prevention and treatment of DM-associated pathologies. ASX reduces inflammation, OS, and apoptosis by regulating different OS pathways though the exact mechanism remains elusive. Based on several studies conducted on type 1 and type 2 DM animal models, orally or parenterally administrated ASX improves insulin resistance and insulin secretion; reduces hyperglycemia; and exerts protective effects against retinopathy, nephropathy, and neuropathy. However, more experimental support is needed to define conditions for its use. Moreover, its efficacy in diabetic patients is poorly explored. In the present review, we aimed to identify the up-to-date biological effects and underlying mechanisms of ASX on the ROS-induced DM-associated metabolic disorders and subsequent complications. The development of an in-depth research to better understand the biological mechanisms involved and to identify the most effective ASX dosage and route of administration is deemed necessary.

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“…Oxidative stress is the major cause of renal fibrosis during the progression of diabetic nephropathy. In diabetic (db/db) mice, astaxanthin administration improved the development and acceleration of diabetic nephropathy [101]; it improved experimental diabetes-induced renal oxidative stress and prevented renal fibrosis by upregulating connexin43 and activating the antioxidant Nrf2- (NF-E2-related factor 2-) ARE (antioxidant responsive element) pathway in glomerular mesangial cells [102]. In streptozotocin-induced diabetic rats, 12 weeks of astaxanthin treatment ameliorated morphological changes in the kidney via decreasing the protein expression of fibronectin and collagen IV and through the activation of Nrf2-ARE signaling [103].…”

Section: The Metabolic Effects Of Astaxanthinmentioning

confidence: 99%

Astaxanthin: A Potential Mitochondrial-Targeted Antioxidant Treatment in Diseases and with Aging

Sztretye

Dienes

Gönczi

et al. 2019

Oxidative Medicine and Cellular Longevity

139

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Oxidative stress is characterized by an imbalance between prooxidant and antioxidant species, leading to macromolecular damage and disruption of redox signaling and cellular control. It is a hallmark of various diseases including metabolic syndrome, chronic fatigue syndrome, neurodegenerative, cardiovascular, inflammatory, and age-related diseases. Several mitochondrial defects have been considered to contribute to the development of oxidative stress and known as the major mediators of the aging process and subsequent age-associated diseases. Thus, mitochondrial-targeted antioxidants should prevent or slow down these processes and prolong longevity. This is the reason why antioxidant treatments are extensively studied and newer and newer compounds with such an effect appear. Astaxanthin, a xanthophyll carotenoid, is the most abundant carotenoid in marine organisms and is one of the most powerful natural compounds with remarkable antioxidant activity. Here, we summarize its antioxidant targets, effects, and benefits in diseases and with aging.

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Astaxanthin ameliorates experimental diabetes-induced renal oxidative stress and fibronectin by upregulating connexin43 in glomerular mesangial cells and diabetic mice

Cited by 27 publications

References 41 publications

A Bittersweet Response to Infection in Diabetes; Targeting Neutrophils to Modify Inflammation and Improve Host Immunity

A Bittersweet Response to Infection in Diabetes; Targeting Neutrophils to Modify Inflammation and Improve Host Immunity

Impact of Astaxanthin on Diabetes Pathogenesis and Chronic Complications

Astaxanthin: A Potential Mitochondrial-Targeted Antioxidant Treatment in Diseases and with Aging

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