Biological activity of Echinops spinosus on inhibition of paracetamol-induced renal inflammation

2019 ◽  
Vol 97 (2) ◽  
pp. 176-186 ◽  
Author(s):  
Marwa G.A. Hegazy ◽  
Manal A. Emam ◽  
Hemmat I. Khattab ◽  
Nesma M. Helal
Keyword(s):  
Nuclear Factor Κb ◽  
Albino Rats ◽  
Alcohol Extract ◽  
Protection Mechanism ◽  
Sterile Saline ◽  
Inflammatory Parameters ◽  
Total Antioxidant ◽  
Mrna Gene ◽  
Factor Α ◽  
Mrna Gene Expression

This study was designed to evaluate the possible mechanisms through which Echinops spinosus (ES) extract demonstrates nephroprotective effect on the paracetamol acetominophen (N-acetyl-p-aminophenol (APAP)) induced nephrotoxicity in rats. Twenty-four Swiss albino rats were divided into four groups (six rats each). The placebo group was orally administered sterile saline, the APAP group received APAP (200 mg·kg–1·day–1 i.p.) daily, the ES group was given ES extract orally (250 mg/kg), and the APAP + ES group received APAP as for the APAP group and administrated the ES extract as for the ES group. Pretreatment of methyl alcohol extract of ES reduced the protein expression of inflammatory parameters including cyclooxygenase-2 and nuclear factor κB in the kidney. It also reduced the mRNA gene expression of tumor necrosis factor-α and interleukin-1β. The ES extract compensated for deficits in the total antioxidant activity, suppressed lipid peroxidation, and amended the APAP-induced histopathological kidney alterations. Moreover, ES treatment restored the elevated levels of urea nitrogen in the blood and creatinine in the serum by APAP. The ES extract attenuated the APAP-induced elevations in renal nitric oxide levels. We clarified that the ES extract has the potential to defend the kidney from APAP-induced inflammation, and the protection mechanism might be through decreasing oxidative stress and regulating the inflammatory signaling pathway through modulating key signaling inflammatory biomarkers.

scholarly journals EFFECT OF LYCOPENE IN AMELIORATION OF TESTICULAR AND RENAL TOXICITY INDUCED BY BOLDENONE UNDECYLENATE IN MALE ALBINO RATS

2019 ◽  
Vol 3 (3) ◽  
Author(s):  
Samar S Ibrahim ◽  
Alshaimaa M Said
Keyword(s):  
Dna Fragmentation ◽  
Renal Toxicity ◽  
Histopathological Examination ◽  
Kidney Tissue ◽  
Serum Testosterone ◽  
Control Group ◽  
Albino Rats ◽  
Total Antioxidant ◽  
Factor Α ◽  
Necrosis Factor

Background: The present study was designed to evaluate the relative ameliorating efficacy of lycopene against the deleterious effects of boldenone, an androgenic steroid, on the rat testis and kidney.  Materials and Methods: 40 male albino rats were divided into four groups; control group received intramuscular (i.m) injection of olive oil once a week; lycopene (Lc) group received lycopene (10 mg/kg b.w p.o daily); boldenone (Bol) group received (5 mg/kg b.w i.m once a week); Bol + Lc group received boldenone (5 mg/kg b.w i.m once a week) and lycopene (10 mg/kg b.w p.o daily) all for four weeks. Results: intramuscular injection of boldenone significantly induced lipid peroxidation and DNA fragmentation as well as inhibited total antioxidant capacity (TAC) and catalase (CAT) activity in testis and kidney tissue. Additionally, up-regulation of Bax and down-regulation of Bcl-2 gene expression after Bol injection along with marked increase in serum inflammatory cytokines and decrease in serum testosterone. These alterations were confirmed by the histopathological examination of testis and kidney. On the other hand, lycopene oral administration attenuated the testicular and renal injuries induced by boldenone injection. Conclusion: administration of antioxidants as lycopene effectively ameliorated the adverse effects of boldenone on testis and kidney tissues. Key words: Boldenone undecylenate, lycopene, DNA fragmentation, interleukin-1β, tumor necrosis factor-α, apoptosis.

Vanillin mitigates the adverse impact of cisplatin and methotrexate on rat kidneys

2017 ◽  
Vol 37 (9) ◽  
pp. 937-943 ◽  
Author(s):  
AA Fouad ◽  
WN Al-Melhim
Keyword(s):  
Fas Ligand ◽  
Nitrosative Stress ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Nuclear Factor Κb ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Total Antioxidant ◽  
Factor Α ◽  
Neutrophil Gelatinase ◽  
Rat Kidneys

The present study investigated the probable protective effect of vanillin (VLN) against kidney injury induced by cisplatin (CSN) and methotrexate (MTX) in rats. The rats received a single injection of either CSN (7.5 mg/kg, i.p.) or MTX (20 mg/kg, i.p.). VLN treatment (150 mg/kg/day, i.p.) was started 1 day before administration of the nephrotoxic agents and continued for 7 days. Both CSN and MTX significantly increased serum creatinine, cystatin C, and neutrophil gelatinase–associated lipocalin and kidney tissue renal malondialdehyde, inducible nitric oxide synthase, tumor necrosis factor-α, interleukin-18, nuclear factor-κB p65, cytosolic cytochrome C, and caspase-3 and significantly decreased renal total antioxidant capacity and Bcl-2/Bax ratio in rats. VLN significantly ameliorated the changes of biochemical parameters induced by CSN and MTX. VLN also significantly reduced CSN- and MTX-induced histopathological injury and the expression of Fas ligand in rat kidneys. In conclusion, VLN significantly protected against CSN- and MTX-induced kidney injury in rats by inhibiting oxidative/nitrosative stress, inflammation, and apoptosis.

Molecular Mechanisms of Curcumin in Neuroinflammatory Disorders: A Mini Review of Current Evidences

2019 ◽  
Vol 19 (3) ◽  
pp. 247-258 ◽  
Author(s):  
Mahsa Hatami ◽  
Mina Abdolahi ◽  
Neda Soveyd ◽  
Mahmoud Djalali ◽  
Mansoureh Togha ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
English Language ◽  
Molecular Mechanisms ◽  
Randomized Clinical Trials ◽  
Mitochondrial Dynamics ◽  
Nuclear Factor Κb ◽  
General Term ◽  
Neuroinflammatory Disease ◽  
Tnf Α ◽  
Factor Α

Objective: Neuroinflammatory disease is a general term used to denote the progressive loss of neuronal function or structure. Many neuroinflammatory diseases, including Alzheimer’s, Parkinson’s, and multiple sclerosis (MS), occur due to neuroinflammation. Neuroinflammation increases nuclear factor-κB (NF-κB) levels, cyclooxygenase-2 enzymes and inducible nitric oxide synthase, resulting in the release of inflammatory cytokines, such as interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). It could also lead to cellular deterioration and symptoms of neuroinflammatory diseases. Recent studies have suggested that curcumin (the active ingredient in turmeric) could alleviate the process of neuroinflammatory disease. Thus, the present mini-review was conducted to summarize studies regarding cellular and molecular targets of curcumin relevant to neuroinflammatory disorders. Methods: A literature search strategy was conducted for all English-language literature. Studies that assessed the various properties of curcuminoids in respect of neuroinflammatory disorders were included in this review. Results: The studies have suggested that curcuminoids have significant anti- neuroinflammatory, antioxidant and neuroprotective properties that could attenuate the development and symptom of neuroinflammatory disorders. Curcumin can alleviate neurodegeneration and neuroinflammation through multiple mechanisms, by reducing inflammatory mediators (such as TNF-α, IL-1β, nitric oxide and NF-κB gene expression), and affect mitochondrial dynamics and even epigenetic changes. Conclusion: It is a promising subject of study in the prevention and management of the neuroinflammatory disease. However, controlled, randomized clinical trials are needed to fully evaluate its clinical potential.

A direct requirement of nuclear factor-κB for suppression of apoptosis in ventricular myocytes

2000 ◽  
Vol 279 (3) ◽  
pp. H939-H945 ◽  
Author(s):  
Shareef Mustapha ◽  
Alla Kirshner ◽  
Danielle De Moissac ◽  
Lorrie A. Kirshenbaum
Keyword(s):  
Dna Binding ◽  
Gene Transcription ◽  
Ventricular Myocytes ◽  
Vital Staining ◽  
Fold Increase ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Cytoplasmic Factor ◽  
Tnf Α ◽  
Factor Α

Nuclear factor-κB (NF-κB) is a ubiquitously expressed cellular factor regulated by the cytoplasmic factor inhibitor protein κBα (IκBα). Activation of NF-κB by cytokines, including tumor necrosis factor-α (TNF-α), requires the phosphorylation and degradation of IκBα. An anti-apoptotic role for NF-κB has recently been suggested. In the present study, we ascertained whether death-promoting signals and apoptosis mediated by TNF-α are suppressed by NF-κB in postnatal ventricular myocytes. Stimulation of myocytes with TNF-α resulted in a 12.1-fold increase ( P < 0.01) in NF-κB-dependent gene transcription and DNA binding compared with controls. This was accompanied by a corresponding increase in the NF-κB target protein A20 as determined by Western blot analysis. Vital staining revealed that TNF-α was not cytotoxic to myocytes and did not provoke apoptosis. Adenovirus-mediated delivery of a nonphosphorylatable form of IκBα to inactivate NF-κB prevented TNF-α-stimulated NF-κB-dependent gene transcription and nuclear NF-κB DNA binding. Importantly, myocytes stimulated with TNF-α and defective for NF-κB activation resulted in a 2.2-fold increase ( P < 0.001) in apoptosis. To our knowledge, the data provide the first indication that a functional NF-κB signaling pathway is crucial for suppressing death-promoting signals mediated by TNF-α in ventricular myocytes.

scholarly journals Quality of Dabai Pulp Oil Extracted by Supercritical Carbon Dioxide and Supplementation in Hypercholesterolemic Rat—A New Alternative Fat

Foods ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 262
Author(s):  
Noor Atiqah Aizan Abdul Kadir ◽  
Azrina Azlan ◽  
Faridah Abas ◽  
Intan Safinar Ismail
Keyword(s):  
Fatty Acid Content ◽  
Total Antioxidant Status ◽  
High Cholesterol Diet ◽  
Reactive Protein ◽  
Total Antioxidant ◽  
Canarium Odontophyllum ◽  
Coa Reductase ◽  
Factor Α ◽  
Necrosis Factor

Dabai pulp oil (DPO) is new oil extracted from the pulp of Canarium odontophyllum. The quality and efficacy of DPO are needed to promote its potential as a new alternative fat. Therefore, we investigate the quality of DPO, which includes moisture and volatile content (MVC), free fatty acid content (FFA), iodine value (IV), and peroxide value (PV). Furthermore, we evaluate the efficacy of DPO against hypercholesterolemia elicited by a high-cholesterol diet in rats. The MVC of DPO was <0.001 ± 0.00%. Next, the FFA in DPO was 2.57 ± 0.03%, and the IV of DPO was 53.74 ± 0.08 g iodine/100 g oil. Meanwhile, the PV of DPO was 4.97 ± 0.00 mEq/kg. Supplementation of DPO in hypercholesterolemic rats for 30 days revealed the hypocholesterolemic effect (significant reduction of total cholesterol, triglyceride, and 3-hydroxy-3-methylglutaryl-CoA reductase) accompanied by a significant reduction of inflammatory markers (C-reactive protein, interleukin-6 and tumour necrosis factor-α), and lipid peroxidation (MDA). We also observed a significant improvement of lipoprotein lipase (LPL) and antioxidant capacities (total antioxidant status, superoxide dismutase, glutathione peroxidase, and catalase) of the rats. The results on the quality and efficacy of locally made DPO suggest its potential use as a healthy alternative fat in the future.

Localized pancreatic NF-κB activation and inflammatory response in taurocholate-induced pancreatitis

2001 ◽  
Vol 280 (6) ◽  
pp. G1197-G1208 ◽  
Author(s):  
Eva Vaquero ◽  
Ilya Gukovsky ◽  
Vjekoslav Zaninovic ◽  
Anna S. Gukovskaya ◽  
Stephen J. Pandol
Keyword(s):  
Transcription Factor ◽  
Inflammatory Response ◽  
Pancreatic Head ◽  
Pancreatic Injury ◽  
Nuclear Factor Κb ◽  
Saline Infusion ◽  
Activator Protein 1 ◽  
Local Inflammatory Response ◽  
Monocyte Chemoattractant Protein 1 ◽  
Factor Α

Transcription factor nuclear factor-κB (NF-κB) is activated in cerulein pancreatitis and mediates cytokine expression. The role of transcription factor activation in other models of pancreatitis has not been established. Here we report upregulation of NF-κB and inflammatory molecules, and their correlation with local pancreatic injury, in a model of severe pancreatitis. Rats received intraductal infusion of taurocholate or saline, and the pancreatic head and tail were analyzed separately. NF-κB and activator protein-1 (AP-1) activation were assessed by gel shift assay, and mRNA expression of interleukin-6, tumor necrosis factor-α, KC, monocyte chemoattractant protein-1, and inducible nitric oxide synthase was assessed by semiquantitative RT-PCR. Morphological damage and trypsin activation were much greater in the pancreatic head than tail, in parallel with a stronger activation of NF-κB and cytokine mRNA. Saline infusion mildly affected these parameters. AP-1 was strongly activated in both pancreatic segments after either taurocholate or saline infusion. NF-κB inhibition with N-acetylcysteine ameliorated the local inflammatory response. Correlation between localized NF-κB activation, cytokine upregulation, and tissue damage suggests a key role for NF-κB in the development of the inflammatory response of acute pancreatitis.

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