Dihydroartemisinin attenuates lipopolysaccharide-induced acute kidney injury by inhibiting inflammation and oxidative stress

Liu, Xinhui; Lu, Jiandong; Liao, Yijiao; Liu, Siqi; Chen, Yijun; He, Riming; Men, Ling; Lu, Chunjian; Chen, Zhihong; Li, Shunmin; Xiong, Guoliang; Yang, Shudong

doi:10.1016/j.biopha.2019.109070

Cited by 72 publications

(58 citation statements)

References 40 publications

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“…In consistent with previous report [41], we found that glycine pre-administration reversed LPS-induced depletion of NRF2 and led to the increased protein level of genes implicated in cellular survival [42]. In a recent study, the authors showed that NRF2 is a repressor of NF-κB [43]. Our results indicated that the glycine-induced downregulation of NF-κB was mediated, at least partially, via NRF2 signaling.…”

Section: Discussionsupporting

confidence: 92%

Glycine Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Regulating NLRP3 Inflammasome and NRF2 Signaling

Zhang

Jiang

et al. 2020

Nutrients

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Glycine supplementation has been reported to alleviate lipopolysaccharide (LPS)-induced lung injury in mice. However, the underlying mechanisms responsible for this beneficial effect remain unknown. In the present study, male C57BL/6 mice were treated with aerosolized glycine (1000 mg in 5 mL of 0.9% saline) or vehicle (0.9% saline) once daily for 7 continuous days, and then were exposed to aerosolized LPS (5 mg in 5 mL of 0.9% saline) for 30 min to induce lung injury. Sera and lung tissues were collected 24 h post LPS challenge. Results showed that glycine pretreatment attenuated LPS-induced decreases of mucin at both protein and mRNA levels, reduced LPS-triggered upregulation of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interferons, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interleukins. Further study showed that glycine-reduced LPS challenge resulted in the upregulation of nuclear factor κB (NF-κB), nucleotide binding domain (NOD)-like receptor protein 3 (NLRP3) inflammasome. In addition, LPS exposure led to the downregulation of NRF2 and downstream targets, which were significantly improved by glycine administration in the lung tissues. Our findings indicated that glycine pretreatment prevented LPS-induced lung injury by regulating both NLRP3 inflammasome and NRF2 signaling.

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Section: Discussionsupporting

confidence: 92%

Glycine Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Regulating NLRP3 Inflammasome and NRF2 Signaling

Zhang

Jiang

et al. 2020

Nutrients

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“…A similar effect was observed in the nephritis and septic AKI models Wan and Li, 2017;Liu et al, 2019). Also, ARSs were reported to inhibit disease progression via downregulating renal monocyte chemoattractant protein 1 (MCP-1) expression in LN, IgAN, and septic AKI models (Mi et al, 2009;Jin et al, 2009;Ma et al, 2009;Liu et al, 2019). In addition, ARSs were proved to alleviate the tubule-interstitial inflammation and fibrosis by inhibiting NF-kB and mothers against decapentaplegic homolog (Smad) signaling pathway in SNx rats, Heymann nephritis rats and UUO models (Ma et al, 2010;Li et al, 2015;Wen et al, 2019).…”

Section: In Vivosupporting

confidence: 73%

“…For LN mice, it has been reported that treatment with ARSs could decrease interferon-gamma (IFN-g), tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6) in serum, and blocked intercellular adhesion molecule-1 (ICAM-1), fractalkine, NF-kB signaling pathway in renal (Dong et al, 2003;Li et al, 2006;Wang et al, 2010;You et al, 2014;Liang et al, 2018). A similar effect was observed in the nephritis and septic AKI models Wan and Li, 2017;Liu et al, 2019). Also, ARSs were reported to inhibit disease progression via downregulating renal monocyte chemoattractant protein 1 (MCP-1) expression in LN, IgAN, and septic AKI models (Mi et al, 2009;Jin et al, 2009;Ma et al, 2009;Liu et al, 2019).…”

Section: In Vivomentioning

confidence: 81%

“…Oxidative stress is an important mediator in the development and progression of CKD and AKI and its complications due to increased production of reactive oxygen species (ROS) and diminished antioxidant capacity (Ruiz et al, 2013). In the condition of a surplus of ROS, ARSs were reported to exhibit an antioxidant effect (Kim et al, 2014;Yang et al, 2018;Liu et al, 2019). In addition, according to the characteristics of ARSs, tumor cells are more vulnerable due to higher levels of iron (Robert et al, 2005) and are more susceptible to further ROS insults induced by ARSs (Hamacher-Brady et al, 2011;Efferth, 2017).…”

Section: Mechanism Of Arss In Kidney Oxidative Stress Regulation Of Amentioning

confidence: 99%

“…Pretreated DHA or ARS could ameliorate oxidative stress in AKI mice by restoring malonyl dialdehyde (MDA), nitric oxide (NO), glutathione peroxidase (GSH), catalase (CAT), and superoxide dismutase (SOD) activity in the kidney (An Y. et al, 2017;Liu et al, 2019). In addition, ARM was shown to reduce the serum H 2 O 2 level and elevated renal cortical PGC-1a expression, but it did not exert obvious effects on CAT and SOD expression in the renal cortex in DN (Han et al, 2019).…”

Section: In Vivomentioning

confidence: 99%

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The Therapeutic Effect of Artemisinin and Its Derivatives in Kidney Disease

Xia

Liu

et al. 2020

Front. Pharmacol.

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Artemisinin (ARS) and its derivatives (ARSs) are recommended as the first-line antimalarial drugs for the treatment of malaria. Besides antimalarial function, its potent antiinflammatory and immunoregulatory properties, as well as the ability to regulate oxidative stress have brought them to a prominent position. As researchers around the world are continually exploring the unknown biological activities of ARS derivatives, experimental studies have shown much progress in renal therapy. This review aims to give a brief overview of the current research on ARSs applications for kidney treatment with the evaluation of therapeutic properties and potential molecular mechanisms.

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Folic acid‐induced animal model of kidney disease

2021

Anim Models and Exp Med

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Kidney disease may be generally classified clinically into two categories: acute kidney injury (AKI) and chronic kidney disease (CKD), both of which are tightly interconnected. 1-3 AKI can often develop in clinical settings in critically ill patients, leading to increased morbidity and mortality. 4,5 AKI is manifested by a rapid decline in the glomerular filtration rates (GFRs) 6 and its pathogenesis is complex, involving ischemia, sepsis, drug toxicity, and trauma. 7 If left unmanaged, AKI can develop into CKD, which is characterized by a progressive decrease in GFR, culminating in a gradual loss of renal function. 8 The transition from AKI to CKD can also be hastened by numerous risk factors such as obesity, hypertension, diabetes, and chronic inflammation. 9-11 Currently, there are no effective treatments for either AKI or CKD, stressing a continual need to elucidate the underlying pathological mechanisms of AKI and CKD. In this regard, animal models of kidney disease have been invaluable in that utilization of these animal models not only facilitates our understanding of the

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Dihydroartemisinin attenuates lipopolysaccharide-induced acute kidney injury by inhibiting inflammation and oxidative stress

Cited by 72 publications

References 40 publications

Glycine Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Regulating NLRP3 Inflammasome and NRF2 Signaling

Glycine Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Regulating NLRP3 Inflammasome and NRF2 Signaling

The Therapeutic Effect of Artemisinin and Its Derivatives in Kidney Disease

Folic acid‐induced animal model of kidney disease

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