Leveraging the Pathophysiological Alterations of Obstructive Nephropathy to Treat Renal Fibrosis by Cerium Oxide Nanoparticles

Saifi, Mohd Aslam; Peddakkulappagari, Chandra Sekhar; Ahmad, Altaf; Godugu, Chandraiah

doi:10.1021/acsbiomaterials.9b01944

Cited by 11 publications

(4 citation statements)

References 49 publications

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“…In recent years, their application potential in the field of nanomedicine has also received increasing attention. Ce 3+ can improve free radical-induced oxidative damage by binding reactive oxygen radicals and thus shows great clinical value in treating reactive oxygen-related diseases such as neurodegenerative diseases (ischemic stroke, Alzheimer’s disease) [ 1 , 2 ], cancer [ 3 ], chronic inflammation [ 4 ], gastric ulcers caused by ethanol or pressure [ 5 , 6 ], rheumatoid arthritis [ 7 ], and chronic kidney disease [ 8 ]. In addition, the properties of CeO 2 -NP mimics can be used in enzyme-linked immunosorbent reagents to detect a variety of tumor cells [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of nano-cerium dioxide on intestinal microflora in rats by oral subchronic exposure

Ye,

Jia,

et al. 2024

PLoS ONE

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Objective To investigate intestinal toxicity in rats and the effects of Nano-cerium dioxide on intestinal flora in rats after oral sub-chronic exposure. Method Forty healthy male SD rats were randomly divided into four groups: a control group (deionized water) and three groups treated with different doses of Nano-ceria (e.g., 20 mg/kg, 100 mg/kg, and 500 mg/kg), with 10 rats in each group. The rats were given intragastric administrations (every other day) for 90 days. After the last intragastric administration, fresh fecal samples were collected by pressing the abdomen, and the animals were sacrificed. Jejunum, ileum and cecum tissues were retained for pathological analysis by Hematoxylin-eosin staining. The stool samples of rats were sequenced by the Illumina NovaSeq sequencing platform, and the sequencing results were further analyzed by QIIME2 software. Results The histopathology results show that compared with the control group, in the middle- and high-dose groups, epithelial tissue was shed, lamina propria glandular structures were damaged or disappeared, and large numbers of inflammatory cells were distributed in the mucosa. The intestinal flora results show that there were no significant differences in the α-/β-diversities in each Nano-ceria-treated group compared with the control group (P>0.05). Compared with the control group, the intestinal pathogenic bacteria, Mucispirillum and Streptococcus increased significantly after Nano-cerium dioxide ingestion, while Weissella decreased. The abundances of Akkermansia in all Nano-ceria-treated groups were higher than those in the control group, but the abundances decreased with increasing dose. MetagenomesSeq analysis show that, compared with the control group, the abundances of S24-7, Lactobacillus and Clostridiales in all experimental groups significantly decreased. Conclusions The sub-chronic toxicity of Nano-cerium dioxide to rats can affect the structure and abundance of intestinal microflora, long-term exposure to high doses (>100 mg/kg) causes enteritis, but there was no significant difference in the diversity of gut microbiota. Therefore, we infer that the enteritis in rats may be associated with the relative ratios of the pathogenic bacteria and intestinal probiotics, and increased of the intestinal pathogenic bacteria can disrupted intestinal homeostasis.

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Section: Introductionmentioning

confidence: 99%

Effects of nano-cerium dioxide on intestinal microflora in rats by oral subchronic exposure

Ye,

Jia,

et al. 2024

PLoS ONE

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“…To analyze the pancreas protein expression, immunoblotting technique was used as described earlier 27 , 28 . Small portions of pancreatic tissues were homogenized in RIPA lysis buffer.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of discoidin domain receptors by imatinib prevented pancreatic fibrosis demonstrated in experimental chronic pancreatitis model

Bansod

Saifi

Godugu

2021

Sci Rep

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Discoidin domain receptors (DDR1 and DDR2) are the collagen receptors of the family tyrosine kinases, which play significant role in the diseases like inflammation, fibrosis and cancer. Chronic pancreatitis (CP) is a fibro-inflammatory disease in which recurrent pancreatic inflammation leads to pancreatic fibrosis. In the present study, we have investigated the role of DDR1 and DDR2 in CP. The induced expression of DDR1 and DDR2 was observed in primary pancreatic stellate cells (PSCs) and cerulein-induced CP. Subsequently, the protective effects of DDR1/DDR2 inhibitor, imatinib (IMT) were investigated. Pharmacological intervention with IMT effectively downregulated DDR1 and DDR2 expression. Further, IMT treatment reduced pancreatic injury, inflammation, extracellular matrix deposition and PSCs activation along with inhibition of TGF-β1/Smad signaling pathway. Taken together, these results suggest that inhibition of DDR1 and DDR2 controls pancreatic inflammation and fibrosis, which could represent an attractive and promising therapeutic strategy for the treatment of CP.

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“…To analyze the pancreas protein expression, immunoblotting technique was used as described earlier [25,26]. Small portion of pancreatic tissues were homogenized in RIPA lysis buffer.…”

Section: Immunoblottingmentioning

confidence: 99%

Inhibition of DDR1 and DDR2 receptors: The Potential Therapeutic Option to Treat Pancreatic Fibrosis Demonstrated in Experimental Chronic Pancreatitis Model

Bansod¹,

Saifi²,

Godugu³

2020

Preprint

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Discoidin domain receptors (DDR1 and DDR2) are the collagen receptors of the family tyrosine kinases, which play significant role in the diseases like inflammation, fibrosis and cancer. Chronic pancreatitis (CP) is a fibro-inflammatory disease in which recurrent pancreatic inflammation leads to pancreatic fibrosis.Methods: In the present study for the first time, we have investigated the role of DDR1 and DDR2 in cerulein-induced CP. Pancreatic DDR1 and DDR2 expression was examined by immunoblotting and immunostaining analysis. Subsequently, the protective effects of selective DDR1 and DDR2 inhibitor, imatinib (IMT) was investigated in CP mice as a therapeutic intervention.Results: Activated pancreatic stellate cells (PSCs) and CP mice showed significant upregulation of DDR1 and DDR2 expression. Pharmacological intervention with IMT effectively downregulated DDR1 and DDR2 expression. Further, we found that pancreatic injury, inflammation, extracellular matrix (ECM) deposition and PSCs activation were significantly inhibited by IMT. Further, we found a significant inhibition of TGF-β1/Smad signaling pathway by IMT and showed its protective effects against CP and associated fibrosis.Conclusions: Taken together, these results suggest that inhibition of DDR1 and DDR2 controls pancreatic inflammation and fibrosis, which could represent an attractive and promising therapeutic strategy for the treatment of CP.

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Leveraging the Pathophysiological Alterations of Obstructive Nephropathy to Treat Renal Fibrosis by Cerium Oxide Nanoparticles

Cited by 11 publications

References 49 publications

Effects of nano-cerium dioxide on intestinal microflora in rats by oral subchronic exposure

Effects of nano-cerium dioxide on intestinal microflora in rats by oral subchronic exposure

Inhibition of discoidin domain receptors by imatinib prevented pancreatic fibrosis demonstrated in experimental chronic pancreatitis model

Inhibition of DDR1 and DDR2 receptors: The Potential Therapeutic Option to Treat Pancreatic Fibrosis Demonstrated in Experimental Chronic Pancreatitis Model

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