Prophylactic role of coenzyme Q10 and Cynara scolymus L on doxorubicin-induced toxicity in rats: Biochemical and immunohistochemical study

Mustafa, Hesham N.; Awdan, Sally A. El; Hegazy, Gehan A.; Jaleel, Gehad A. Abdel

doi:10.4103/0253-7613.169588

Cited by 62 publications

(39 citation statements)

References 21 publications

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“…GSH depletion leads to increased lipid Peroxidation and necrosis of hepatocytes. Furthermore, a significant increase in the MPO which removes H 2 O 2 and catalyzes the formation of toxic hypochlorous acid that leads to neutrophil infiltration and oxidative damage has been reported by Mustafa et al [13]. The present data is consistent with the previous study reporting that in the hepatic Caco-2 intestinal cells, AA induced oxidative stress through depletion of GSH, overproduction of ROS, and induction of apoptosis biomarkers that resulted in cell death [14].…”

Section: Discussionsupporting

confidence: 93%

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Hepatoprotective effect of taurine and coenzyme Q10 and their combination against acrylamide-induced oxidative stress in rats

Saleh¹,

Shahin²,

Kelada³

2017

Trop. J. Pharm Res

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Section: Discussionsupporting

confidence: 93%

“…Studies have shown that the CoQ10 has free radical-scavenging activities, liver injuryreducing properties and endothelial dysfunction improving [8]. It also has anti-oxidants, antifibrosis and anti-inflammatory effects [9].…”

Section: Introductionmentioning

confidence: 99%

Hepatoprotective effect of taurine and coenzyme Q10 and their combination against acrylamide-induced oxidative stress in rats

Saleh¹,

Shahin²,

Kelada³

2017

Trop. J. Pharm Res

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“…IHC staining quantification was made using three non-overlapping fields per specimen, selected indiscriminately for analysis. Measurements were made with the use of NIS-Elements imaging software (Nikon, Brighton, MI) associated with an Nikon TE200U microscope and quantified using NIH ImageJ (v1.49) (http://rsb.info.nih.gov/ij) as previously described [20]. Briefly, the optical density (OD) of p-ALK immunostaining was evaluated with OD estimated using the following formula: OD = log (max intensity/mean intensity), where max intensity = 255 for 8-bit images [20].…”

Section: Methodsmentioning

confidence: 99%

Co-targeting ALK and EGFR parallel signaling in oral squamous cell carcinoma

et al. 2016

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Squamous cell carcinoma (SCC) comprises 90% of all head and neck cancers and has a poor survival rate due to late-stage disease that is refractive to traditional therapies. Epidermal growth factor receptor (EGFR) is over-expressed in greater than 80% of head and neck SCC (HNSCC). However, EGFR targeted therapies yielded little to no efficacy in clinical trials. This study investigated the efficacy of co-targeting EGFR and the anaplastic lymphoma kinase (ALK) whose promoter is hypomethylated in late-stage oral SCC (OSCC). We observed increased ALK activity in late-stage human OSCC tumors and invasive OSCC cell lines. We also found that while ALK inhibition alone had little effect on proliferation, co-targeting ALK and EGFR significantly reduced OSCC cell proliferation in vitro. Further analysis showed significant efficacy of combined treatment in HSC3-derived xenografts resulting in a 30% decrease in tumor volumes by 14 days (p < 0.001). Western blot analysis showed that co-targeting ALK and EGFR significantly reduced EGFR phosphorylation (Y1148) in HSC3 cells but not Cal27 cells. ALK and EGFR downstream signaling interactions are also demonstrated by Western blot analysis in which lone EGFR and ALK inhibitors attenuated AKT activity whereas co-targeting ALK and EGFR completely abolished AKT activation. No effects were observed on ERK1/2 activation. STAT3 activity was significantly induced by lone ALK inhibition in HSC3 cells and to a lower extent in Cal27 cells. Together, these data illustrate that ALK inhibitors enhance anti-tumor activity of EGFR inhibitors in susceptible tumors that display increased ALK expression, most likely through abolition of AKT activation.

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“…The optical density of Caspase 3 immunostaining was measured by using the NIH ImageJ (v1.50) program. 41 Optical density was calculated by the following formula:…”

Section: Morphometric Studymentioning

confidence: 99%

A study of the neurotoxic effects of tramadol and cannabis in adolescent male albino rats

et al. 2016

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Background: Adolescence is a critical period for cerebral development. Exposure to addictive substances during this phase leads to various alterations in brain functions that persist into adulthood. The present study was designed to study the neurotoxic effects of tramadol and cannabis, alone and in combination, in adolescent male albino rats by studying their behavioral, biochemical, and histopathological neurotoxic effects and their long–term consequences after withdrawal.Methods: For this purpose, 132 adolescent male albino rats were divided into 5 groups (22 rats/ group). Group I (negative control), received only regular diet and tap water to measure the basic parameters, Group II (positive control; IIA&IIB); IIA, gavaged with normal saline. IIB, gavaged with olive oil. Group III (tramadol), gavaged with tramadol (42, 84 and 168 mg/kg/day) in the first, second and third ten days of the study respectively. Group IV (cannabis), gavaged with hashish extract (92, 184 and 368 mg/kg/day) in the first, second and third ten days of the study respectively. Group V (tramadol+cannabis), gavaged with tramadol and hashish extract in the same doses as Group III&IV. By the end of the first month, the half number of rats was subjected to performing behavior tests. Specimens from the brain were taken for performing biochemical and histopathological studies. All remaining rats were held for another 4 weeks non–dosing spontaneous recovery period after withdrawal of the treatment and were evaluated again by the same previous parameters.Results: Abuse of tramadol or cannabis, alone and in combination, caused antidepressant effect (sucrose preference test), impaired spatial memory (Morris water maze), elevated serotonin levels in the cerebral cortex and hippocampus, induced oxidative stress (significantly elevated malondialdehyde level and reduced catalase activity) as well as deleteriously altered brain histopathology and marked increase in brain Caspase–3 expression. However, abuse of both tramadol and cannabis conferred more antidepressant effect but more neurotoxic effect. After withdrawal, the antidepressant effect was reversed, no improvement of the spatial memory, marked depletion of 5–HT, more improvement in antioxidants and apoptotic markers and incomplete regression of brain histopathological alteration resulted.Conclusions: Abuse of tramadol and cannabis, alone and in combination, induced neurotoxicity which proved behaviorally, biochemically and histopathologically.

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Prophylactic role of coenzyme Q10 and Cynara scolymus L on doxorubicin-induced toxicity in rats: Biochemical and immunohistochemical study

Cited by 62 publications

References 21 publications

Hepatoprotective effect of taurine and coenzyme Q10 and their combination against acrylamide-induced oxidative stress in rats

Hepatoprotective effect of taurine and coenzyme Q10 and their combination against acrylamide-induced oxidative stress in rats

Co-targeting ALK and EGFR parallel signaling in oral squamous cell carcinoma

A study of the neurotoxic effects of tramadol and cannabis in adolescent male albino rats

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