Amelioration of Acute Kidney Injury in Lipopolysaccharide-Induced Systemic Inflammatory Response Syndrome by an Aldose Reductase Inhibitor, Fidarestat

Takahashi, Kazunori; Mizukami, Hiroki; Kamata, Kosuke; Inaba, Wataru; Kato, Noriaki; Hibi, Chihiro; Yagihashi, Soroku

doi:10.1371/journal.pone.0030134

Cited by 48 publications

(31 citation statements)

References 41 publications

(57 reference statements)

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“…2, A and B). To note, the tubular damage observed in this study appeared more severe than that of previous studies (Wu et al, 2007;Takahashi et al, 2012). Although the cause of the severity is unclear, it may be related to the LPS dosage tested and the animal husbandry condition.…”

Section: Paclitaxel Reduces Kidney Injury and Renal Dysfunction In Lpcontrasting

confidence: 65%

Paclitaxel Ameliorates Lipopolysaccharide-Induced Kidney Injury by Binding Myeloid Differentiation Protein-2 to Block Toll-Like Receptor 4–Mediated Nuclear Factor-κB Activation and Cytokine Production

Zhang

Liu

et al. 2013

J Pharmacol Exp Ther

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Recent studies suggest that paclitaxel, an anticancer agent, may modulate the injury and inflammatory responses in normal tissues. However, the underlying mechanism is not fully understood. Here we have examined the effect of paclitaxel on lipopolysaccharide (LPS)-induced acute kidney injury (AKI) in mice and further studied the mechanism. At relatively low doses, paclitaxel protected against LPS-induced AKI and improved animal survival. The beneficial effects of paclitaxel were accompanied by the downregulation of tumor necrosis factor-a, interleukin-1, and interleukin-6 production. In cultured renal tubular HK-2 cells, paclitaxel decreased the DNA-binding activity of nuclear factor-kB (NF-kB) during LPS treatment, inhibited the degradation of the inhibitor of kB-a, and blocked the expression and activation of NF-kB p65. At the upstream level, paclitaxel reduced LPS-induced association of myeloid differentiation protein-2 (MD-2) with Toll-like receptor 4 (TLR4). In an in vitro assay, paclitaxel was shown to directly bind recombinant MD-2. The inhibitory effect of paclitaxel on NF-kB activation and cytokine expression disappeared in MD-2 knockdown cells, indicating that paclitaxel acts through MD-2. Collectively, these results suggest that paclitaxel may bind MD-2 to block MD-2/ TLR4 association during LPS treatment, resulting in the suppression of NF-kB activation and inhibition of proinflammatory cytokine production.

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Section: Paclitaxel Reduces Kidney Injury and Renal Dysfunction In Lpcontrasting

confidence: 65%

Paclitaxel Ameliorates Lipopolysaccharide-Induced Kidney Injury by Binding Myeloid Differentiation Protein-2 to Block Toll-Like Receptor 4–Mediated Nuclear Factor-κB Activation and Cytokine Production

Zhang

Liu

et al. 2013

J Pharmacol Exp Ther

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“…Geranylgeranylacetone (GGA), a drug used in the treatment of gastric ulcers, ameliorated ischemic AKI via induction of heat shock protein 70 (Hsp70) (Suzuki et al, 2005). In addition, Fidarestat, an aldose reductase (AR) inhibitor used for treating diabetic complications, protected against LPS-induced endotoxic AKI probably by suppressing the inflammatory response (Kazunori et al, 2012). …”

Section: Chemical Renoprotectantsmentioning

confidence: 99%

Renoprotective approaches and strategies in acute kidney injury

Yang

Song

et al. 2016

Pharmacology & Therapeutics

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Acute kidney injury (AKI) is a major renal disease associated with a high mortality rate and increasing prevalence. Decades of research has suggested numerous chemical and biological agents with beneficial effects in AKI. In addition, cell therapy and molecular targeting have been explored for reducing kidney tissue damage and promoting kidney repair or recovery from AKI. Mechanistically, these approaches may mitigate oxidative stress, inflammation, cell death, and mitochondrial and other organellar damage, or activate cytoprotective mechanisms such as autophagy and pro-survival factors. However, none of these findings has been successfully translated into clinical treatment of AKI. In this review, we analyze these findings and propose experimental strategies for the identification of renoprotective agents or methods with clinical potential. Moreover, we propose the consideration of combination therapy by targeting multiple targets in AKI.

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“…LPS, the major outer membrane component in Gram-negative bacteria, can activate monocytes/macrophages and induce a variety of immune responses to severe infections, such as septic shock and systemic inflammatory response syndrome (SIRS) [7,8]. The development of the inflammatory process involves the production of pro-inflammatory cytokines and inflammatory mediators, such as tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), nitric oxide (NO) and prostaglandin E2 (PGE2), which are the main factors that mediate the LPS-induced toxic effects [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

The effect of anti-inflammatory properties of ferritin light chain on lipopolysaccharide-induced inflammatory response in murine macrophages

Fan

Zhang

Cai

et al. 2014

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Ferritin light chain (FTL) reduces the free iron concentration by forming ferritin complexes with ferritin heavy chain (FTH). Thus, FTL competes with the Fenton reaction by acting as an antioxidant. In the present study, we determined that FTL influences the lipopolysaccharide (LPS)-induced inflammatory response. FTL protein expression was regulated by LPS stimulation in RAW264.7 cells. To investigate the role of FTL in LPS-activated murine macrophages, we established stable FTL-expressing cells and used shRNA to silence FTL expression in RAW264.7 cells. Overexpression of FTL significantly decreased the LPS-induced production of tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β), nitric oxide (NO) and prostaglandin E2 (PGE2). Additionally, overexpression of FTL decreased the LPS-induced increase of the intracellular labile iron pool (LIP) and reactive oxygen species (ROS). Moreover, FTL overexpression suppressed the LPS-induced activation of MAPKs and nuclear factor-κB (NF-κB). In contrast, knockdown of FTL by shRNA showed the reverse effects. Therefore, our results indicate that FTL plays an anti-inflammatory role in response to LPS in murine macrophages and may have therapeutic potential for treating inflammatory diseases.

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Amelioration of Acute Kidney Injury in Lipopolysaccharide-Induced Systemic Inflammatory Response Syndrome by an Aldose Reductase Inhibitor, Fidarestat

Cited by 48 publications

References 41 publications

Paclitaxel Ameliorates Lipopolysaccharide-Induced Kidney Injury by Binding Myeloid Differentiation Protein-2 to Block Toll-Like Receptor 4–Mediated Nuclear Factor-κB Activation and Cytokine Production

Paclitaxel Ameliorates Lipopolysaccharide-Induced Kidney Injury by Binding Myeloid Differentiation Protein-2 to Block Toll-Like Receptor 4–Mediated Nuclear Factor-κB Activation and Cytokine Production

Renoprotective approaches and strategies in acute kidney injury

The effect of anti-inflammatory properties of ferritin light chain on lipopolysaccharide-induced inflammatory response in murine macrophages

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