Protective Effects of Luteolin on Lipopolysaccharide-Induced Acute Renal Injury in Mice

Xin, Shaobin; H, Yan; Ma, Jing; Sun, Qiang; Shen, Li

doi:10.12659/msm.898177

Cited by 45 publications

(26 citation statements)

References 35 publications

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“…The expression of this cytokine matches well with the behavior of IL-1 and, although no studies have been reported covering the effects after exposures to carbon-based nanomaterials, lowered expression of this cytokine was observed in rheumatoid arthritis patients after the exposures to anti-rheumatic drugs 47 . A similar effect has been documented in mice, where the induction of acute renal injury was protected by the bioactive flavonoid Luteolin, showing anti-inflammatory and renal protection effects 48 .…”

Section: Discussionsupporting

confidence: 65%

Interactions of graphene oxide and graphene nanoplatelets with the in vitro Caco-2/HT29 model of intestinal barrier

Domenech

Hernández

Demir

et al. 2020

Sci Rep

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Carbon-based nanomaterials are being increasingly used, demanding strong information to support their safety in terms of human health. As ingestion is one of the most important exposure routes in humans, we have determined their potential risk by using an in vitro model simulating the human intestinal barrier and evaluated the effects of both graphene oxide (GO) and graphene nanoplatelets (GNPs). A coculture of differentiated Caco-2/HT29 cells presenting inherent intestinal epithelium characteristics (i.e. mucus secretion, brush border, tight junctions, etc.) were treated with GO or GNPs for 24 h. Different endpoints such as viability, membrane integrity, NPs localization, cytokines secretion, and genotoxic damage were evaluated to have a wide view of their potentially harmful effects. No cytotoxic effects were observed in the cells that constitute the barrier model. In the same way, no adverse effects were detected neither in the integrity of the barrier (TEER) nor in its permeability (LY). Nevertheless, a different bio-adhesion and biodistribution behavior was observed for GO and GNPs by confocal microscopy analysis, with a more relevant uptake of GNPs. No oxidative damage induction was detected, either by the DCFH-DA assay or the FPG enzyme in the comet assay. Conversely, both GO and GNPs were able to induce DNA breaks, as observed in the comet assay. Finally, low levels of anti-inflammatory cytokines were detected, suggesting a weak anti-inflammatory response. Our results show the moderate/severe risk posed by GO/GNPs exposures, given the observed genotoxic effects, suggesting that more extensive genotoxic evaluations must be done to properly assess the genotoxic hazard of these nanomaterials. Carbon-based nanomaterials are being increasingly used, due to their growing relevance in many fields. Their large surface area and their excellent electric conductivity offer many physicochemical advantages that are exploited in many industrial fields, including biomedical applications 1. Nevertheless, as it occurs with other nanomaterials, its wide use supposes an increased hazard for human health 2. One of the most recently discovered carbon-based nanomaterials is graphene. Since its first description in 2004 3 , different modifications have been done in their single-atom-thick sheet of planar sp 2-bound carbons, creating numerous graphene-based nanomaterials. According to the EU Graphene Flagship project, these materials can be classified according to three different characteristics: (i) the number of graphene layers, (ii) the average lateral size, and (iii) the carbon/oxygen ratio 4,5. Although a large amount of literature associated with graphene-based nanomaterials has been generated, only a few of them focus on toxicity aspects 2,6. Hence, this paper focuses on graphene oxide (GO) and graphene nanoplatelets (GNPs) exposure risk, two graphene-based nanomaterials that have shown great potential for biomedical and polymeric composites applications 7,8. GO is a highly-oxidized form of graphene, containing different ...

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Section: Discussionsupporting

confidence: 65%

Interactions of graphene oxide and graphene nanoplatelets with the in vitro Caco-2/HT29 model of intestinal barrier

Domenech

Hernández

Demir

et al. 2020

Sci Rep

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“…NF-κB activation associated with increased ROS generation is pivotal in the consequent expression of pro-inflammatory cytokines like TNF-α. These chemokines may then facilitate migration and infiltration of inflammatory cell and a secondary wave of ROS generation, and further amplify the inflammatory cascade and injury [62]. In another way, paricalcitol weakens renin and angiotensin II expression in VDR knockout mice [63], telling that paricalcitol inhibits renal inflammation by overwhelming the RAAS, as angiotensin II is a known pro-inflammatory stimulus.…”

Section: Discussionmentioning

confidence: 99%

Effects of enalapril and paricalcitol treatment on diabetic nephropathy and renal expressions of TNF-α, p53, caspase-3 and Bcl-2 in STZ-induced diabetic rats

et al. 2019

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This study aimed to assess the renopreventive effect of enalapril and/or paricalcitol on streptozotocin (STZ) diabetes-induced nephropathy and to elucidate their mechanisms of action through investigation of the effects on renal oxidative stress, antioxidant defense system and expressions of TNF-α, p53, caspase-3, and Bcl-2. Diabetes mellitus was induced in fasting male Wistar rats by single intraperitoneal injection of STZ (45 mg /kg b.w.) dissolved in citrate buffer (pH 4.5). Ten days after STZ injection, the diabetic rats were treated with enalapril (25 mg/l of drinking water) and/or paricalcitol (8 μg/kg b.w. per os) dissolved in 5% DMSO daily for 4 weeks. The obtained data revealed that the treatment of diabetic Wistar rats with enalapril and/or paricalcitol led to significant decreases in the elevated serum urea, uric acid, creatinine, sodium and potassium levels; thereby reflecting the improvement of the impaired kidney function. The deteriorated kidney lipid peroxidation, GSH content and GST and catalase activities in diabetic rats were significantly ameliorated as a result of treatment with enalapril and/or paricalcitol. The elevated fasting and post-prandial serum glucose levels and the lowered serum insulin and C-peptide levels were also improved. The treatment with enalapril and paricalcitol in combination was the most potent in decreasing the elevated serum glucose levels. Moreover, the treatment of diabetic rats successfully prevented the diabetes-induced histopathological deleterious changes of kidney and islets of Langerhans of pancreas. In association, the immunohistochemically detected pro-inflammatory cytokine, TNF-α, and apoptotic mediators, p53 and caspase-3, were remarkably decreased in kidney of diabetic rats as a result of treatment while the expression of anti-apoptotic protein Bcl-2 was increased. Based on these findings, it can be concluded that enalapril and paricalcitol alone or in combination can prevent STZ diabetes-induced nephropathy through amelioration of the glycemic state and antioxidant defense system together with the suppression of oxidative stress, inflammation and apoptosis. However, the treatment of diabetic rats with enalapril and paricalcitol in combination has no further significant improvement effects on renal function and damage when compared with enalapril or paclitaxel treated diabetic groups.

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“…NF-κB activation associated with increased ROS generation is pivotal in the consequent expression of proinflammatory cytokines like TNF-α. These chemokines may then facilitate migration and infiltration of inflammatory cell and a secondary wave of ROS generation, and further amplify the inflammatory cascade and injury [43]. In another way, paricalcitol weakens renin and angiotensin II expression in VDR knockout mice [44], telling that paricalcitol inhibits renal inflammation by overwhelming the RAAS, as angiotensin II is a known proinflammatory stimulus.…”

Section: Discussionmentioning

confidence: 99%

Effects of enalapril and paricalcitol treatment on diabetic nephropathy and renal expressions of TNF-α, P53, Caspase-3 and Bcl-2 in STZ-induced diabetic rats

Ahmed

Ali

Gaid

et al. 2019

Preprint

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21This study aimed to assess the renopreventive effect of the angiotensin converting 22 enzyme inhibitor (ACEI), enalapril, and/or vitamin D receptor (VDR) activator, paricalcitol, 23 on streptozotocin (STZ) diabetes-induced nephropathy and to elucidate the mechanisms of 24 action through investigation of the effects on renal oxidative stress, antioxidant defense 25 system and expressions of TNF-α, P53, caspase-3, and Bcl-2. Diabetes mellitus was induced 26 in fasting male Wistar rats by single intraperitoneal injection of STZ (45 mg /kg b.w.) 27 dissolved in citrate buffer pH 4.5. Ten days after STZ injection, the diabetic rats were treated 28 with enalapril (25 mg/l of drinking water) and/or paricalcitol (8 µg/kg b.w. per os) dissolved 29 in 5% DMSO daily for 4 weeks. The obtained data revealed that the treatment of diabetic 30 Wistar rats with enalapril and/or paricalcitol led to a significant decrease in the elevated 31 serum urea, uric acid, creatinine and sodium, potassium levels; thereby reflecting 32 improvement of the impaired kidney function. The deteriorated kidney lipid peroxidation, 33 GSH content and GST and catalase activities in diabetic rats were significantly ameliorated 34 as a result of treatment with enalapril and/or paricalcitol. The elevated fasting and post-35 prandial serum glucose levels and the lowered serum insulin and C-peptide levels were also 36improved. Moreover, the treatment of diabetic rats successfully prevented the diabetes-37 induced histopathological deleterious changes of kidney and islets of Langerhans of pancreas. 38In association, the immunohistochemically detected pro-inflammatory cytokine TNF-α and 39 apoptotic mediators P53 and caspase-3 were remarkably decreased in kidney of diabetic rats 40 as a result of treatment, while the expression of anti-apoptotic protein Bcl-2 was increased. 41Based on these findings, it can be concluded that enalapril and paricalcitol can prevent STZ 42 diabetes-induced nephropathy though amelioration of the glycemic state and antioxidant 43 defense system together with the suppression of oxidative stress, inflammation and apoptosis.44

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Protective Effects of Luteolin on Lipopolysaccharide-Induced Acute Renal Injury in Mice

Cited by 45 publications

References 35 publications

Interactions of graphene oxide and graphene nanoplatelets with the in vitro Caco-2/HT29 model of intestinal barrier

Interactions of graphene oxide and graphene nanoplatelets with the in vitro Caco-2/HT29 model of intestinal barrier

Effects of enalapril and paricalcitol treatment on diabetic nephropathy and renal expressions of TNF-α, p53, caspase-3 and Bcl-2 in STZ-induced diabetic rats

Effects of enalapril and paricalcitol treatment on diabetic nephropathy and renal expressions of TNF-α, P53, Caspase-3 and Bcl-2 in STZ-induced diabetic rats

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