Amr Fouad
Suez Canal University, Tour Guidance, Faculty Member
Cisplatin (CP) and doxorubicin (DX) can cause testicular injury by inducing oxidative/nitrosative stress, inflammation, and apoptosis, Naringenin (NG) has antioxidant, antinitrative, anti-inflammatory, and anti-apoptotic effects. This... more
Cisplatin (CP) and doxorubicin (DX) can cause testicular injury by inducing oxidative/nitrosative stress, inflammation, and apoptosis, Naringenin (NG) has antioxidant, antinitrative, anti-inflammatory, and anti-apoptotic effects. This study investigated the potential ability of NG to block gonadotoxicity induced CP and DX in male rats. The rats received one injection of either CP (10 mg/kg, i.p.) or DX (15 mg/kg, i.p.), and treated with NG (50 mg/kg/day, p.o.) for 10 days beginning 6 days prior to CP and DX administration. NG significantly prevented the decreases of serum testosterone and inhibin B in rats received CP and DX. Additionally, NG significantly decreased the elevated testicular malondialdehyde, tumor necrosis factor-α/interleukin-10 ratio, and caspase-3 in CP- and DX-treated rats. NG also significantly raised the decreased testicular Bcl-2/Bax ratio, and total antioxidant status in CP- and DX-challenged rats. In addition, NG significantly increased P-glycoprotein level i...
Multiple sclerosis (MS) is a complex autoimmune disease with a heterogeneous presentation and diverse disease course. Recent studies indicate a rising prevalence of MS in the Middle East. To characterize the demographics and disease... more
Multiple sclerosis (MS) is a complex autoimmune disease with a heterogeneous presentation and diverse disease course. Recent studies indicate a rising prevalence of MS in the Middle East. To characterize the demographics and disease features of Egyptian patients attending four tertiary referral MS centers in Cairo. This was a retrospective, observational study on 1,581 patients between 2001 and 2015. Medical records were reviewed and data were identified and extracted in a standardized electronic registry. The mean age of disease onset was 26.6±7.8 years, with the majority being female (2.11:1). Relapsing-remitting MS was the most common type (75.1%). The main presenting symptom was motor weakness (43.9%), which was also the most frequent symptom during the disease course. Family history of MS was found in 2.28%. Higher initial Expanded Disability Status Scale score, black holes, and infratentorial lesions on initial magnetic resonance imaging were independent factors for disease pr...
Research Interests:
Epigallocatechin-3-gallate (EG), the main active flavonoid in green tea, has well-known anti-inflammatory, antioxidant, and anti-apoptotic activities. The EG protection against testicular injury induced by cisplatin was studied in... more
Epigallocatechin-3-gallate (EG), the main active flavonoid in green tea, has well-known anti-inflammatory, antioxidant, and anti-apoptotic activities. The EG protection against testicular injury induced by cisplatin was studied in Sprague-Dawley rats. Cisplatin (10 mg/kg, i.p) was given as a single injection to rats. EG was given at 40 and 80 mg/kg/day, i.p., for 5 days, starting the same day of cisplatin insult. Serum testosterone, and testicular malondialdehyde, total antioxidant status, nitric oxide, interleukin-6, interleukin-1β, cytochrome C, Bax/Bcl-2 ratio, and caspase-3 were measured. In addition, testicular histopathological examination and immunohistochemical expression of testicular tumour necrosis factor-α were evaluated. Cisplatin, compared to the control, significantly decreased serum testosterone (6.48 ± 0.7 vs. 50.8 ± 4.91 ng/10 mL), and testicular tissue antioxidant status (17.3 ± 1.21 vs. 64.12 ± 5.4 μmol/g), and significantly increased interleukin-6 (85.81 ± 6.11 ...
Research Interests:
The potential nephroprotection of punicalagin (PNG) against lipopolysaccharide (LPS)-induced acute kidney injury in rats was investigated. Rats received a single i.v. dose of LPS (5 mg/kg), and treated with PNG (50 mg/kg, i.p.), 1 h... more
The potential nephroprotection of punicalagin (PNG) against lipopolysaccharide (LPS)-induced acute kidney injury in rats was investigated. Rats received a single i.v. dose of LPS (5 mg/kg), and treated with PNG (50 mg/kg, i.p.), 1 h before, and 1 h following LPS administration. LPS caused significant increases of serum creatinine and neutrophil gelatinase-associated lipocalin. LPS also resulted in significant increases in interleukin-18, tumor necrosis factor-α, interleukin-6, malondialdehyde, nitric oxide, Bax/Bcl-2 ratio and myeloperoxidase, inducible nitric oxide synthase, caspases 3, 8 and 9 activities, and a significant decrease in total antioxidant capacity in kidney tissues. PNG significantly ameliorated the alterations in the measured parameters. Additionally, PNG attenuated the histopathological injury and reduced kidney injury molecule-1 expression in kidneys of rats that received LPS. It was concluded that PNG ameliorated endotoxemic acute kidney injury in rats by counteracting inflammation, oxidative/nitrative stress and apoptosis.
Research Interests:
Research Interests:
This study investigated the possible hepatoprotection of punicalagin in rats received cyclophosphamide (20mg/kg/day, i.p., for 7 days). Punicalagin given at two doses, 15 and 30mg/kg/day, p.o., for 7 days, starting the same day of... more
This study investigated the possible hepatoprotection of punicalagin in rats received cyclophosphamide (20mg/kg/day, i.p., for 7 days). Punicalagin given at two doses, 15 and 30mg/kg/day, p.o., for 7 days, starting the same day of cyclophosphamide administration. Punicalagin significantly and dose-dependently reduced the elevations of serum alanine aminotransferase, and liver nuclear factor-κB p65, tumor necrosis factor-α, interleukin-1β, malondialdehyde, nitric oxide, Bax/Bcl-2 ratio, inducible nitric oxide synthase, caspases 3 and 9 activities, and prevented the decrease of hepatic total antioxidant capacity. Punicalagin also attenuated the histopathological liver tissue damage, and decreased cyclooxygenase-2 expression in liver of rats received cyclophosphamide in a dose-dependent manner. It was concluded that punicalagin protected rat liver against cyclophosphamide toxicity by inhibiting oxidative/nitrosative stress, inflammation, and apoptosis.
Research Interests:
Lipopolysaccharide (LPS) induces acute lung injury (ALI) through oxidative stress and inflammation. Naringenin exerts antioxidant and anti-inflammatory effects. The possible protective effect of naringenin was investigated against ALI... more
Lipopolysaccharide (LPS) induces acute lung injury (ALI) through oxidative stress and inflammation. Naringenin exerts antioxidant and anti-inflammatory effects. The possible protective effect of naringenin was investigated against ALI induced by LPS in rats. Rats received a single injection of LPS (5 mg/kg, i.v.). Naringenin was given for 4 consecutive days, at 2 doses (50 and 100 mg/kg/day, p.o.), starting 3 days before LPS administration. LPS significantly increased wet/dry lung weight ratio, malondialdehyde, nitric oxide (NO), interleukin-6, and myeloperoxidase activity in the lung tissues. Naringenin, particularly the higher dose, significantly ameliorated the LPS-induced changes in the measured parameters. Also, naringenin markedly reduced the histopathological lung tissue injury that resulted from LPS. Naringenin significantly decreased the LPS-induced expression of nuclear factor-x03BA;B, inducible NO synthase, tumor necrosis factor-α, caspase-3, and significantly increased h...
Research Interests:
This works aim is to evaluate the efficacy of skin grafts and flaps in reconstruction of post-burn hand and wrist deformities. A prospective study of 57 burn contractures of the wrist and dorsum of the hand was performed. Flaps were used... more
This works aim is to evaluate the efficacy of skin grafts and flaps in reconstruction of post-burn hand and wrist deformities. A prospective study of 57 burn contractures of the wrist and dorsum of the hand was performed. Flaps were used only if there was a non-vascularized structure after contracture release, otherwise a skin graft was used. Active range of motion (ROM) was used to assess hand function. The extension deformity cohort uniformly underwent skin graft following contracture release with a mean improvement of 71 degrees (p<0.0001). The flexion deformity cohort was treated with either skin grafts (8 patients) or flaps (9 patients) with a mean improvement of 44 degrees (p<0.0001). Skin grafts suffice for dorsal hand contractures to restore functional wrist ROM. For flexion contractures, flaps were more likely for contractures >6 months. Early release of burn contracture is advisable to avoid deep structure contracture.
Research Interests:
Oxidative/nitrosative stress, inflammation, and apoptosis play a crucial role in the pathogenesis of arsenic-induced testicular injury. Telmisartan, the angiotensin II-receptor antagonist, possesses antioxidant and anti-inflammatory... more
Oxidative/nitrosative stress, inflammation, and apoptosis play a crucial role in the pathogenesis of arsenic-induced testicular injury. Telmisartan, the angiotensin II-receptor antagonist, possesses antioxidant and anti-inflammatory activities. The protective effect of telmisartan against arsenic-induced testicular damage was investigated in rats. Testicular damage was induced by sodium arsenite (10 mg kg
The possible protective effect of thymoquinone against eye lens changes in diabetic rats was investigated. Following diabetes induction by a single injection of streptozotocin (45 mg/kg, i.p.), thymoquinone was administered in three... more
The possible protective effect of thymoquinone against eye lens changes in diabetic rats was investigated. Following diabetes induction by a single injection of streptozotocin (45 mg/kg, i.p.), thymoquinone was administered in three different doses (20, 40, and 80 mg/kg/day, p.o.) for 12 weeks. Thymoquinone significantly and dose-dependently attenuated the hypoinsulinemia and hyperglycemia in diabetic rats. Also, thymoquinone (particularly 40 and 80 mg/kg) significantly decreased the elevations of malondialdehyde, nitric oxide, tumor necrosis factor-α, glycated proteins, aldose reductase activity, sorbitol level, and caspase-3 activity in the lens tissues of diabetic rats. In addition, thymoquinone (particularly 40 and 80 mg/kg) significantly ameliorated the diabetes-induced reductions of glutathione peroxidase, superoxide dismutase, and catalase activities, and total and soluble protein contents in the lens tissues. It was concluded that thymoquinone significantly protected the lens tissue against changes induced by diabetes in rats through its antioxidant, anti-inflammatory, and antidiabetic effects.
Research Interests:
Brachioplasty, commonly called an arm lift, is a surgical procedure to reshape and provide improved contour to the upper arms and connecting area of chest wall. With the ever-increasing number of patients undergoing surgical treatment for... more
Brachioplasty, commonly called an arm lift, is a surgical procedure to reshape and provide improved contour to the upper arms and connecting area of chest wall. With the ever-increasing number of patients undergoing surgical treatment for obesity, a growing number of patients are presenting for brachioplasty after massive weight loss. Many techniques have been described to correct upper arm laxity in massive weight loss patients. The aim of this prospective study was to compare the L shaped and T shaped brachioplasty as regard complication rates and patient’s satisfaction. The study conducted on 2 groups, each group of 30 patients with post bariatric massive weight loss and arm laxity, one group underwent T- brachioplasty and the others group underwent L-brachioplasty, and the results were analyzed. The results showed that The T-brachioplasty has less incidence rates of seroma, wound dehiscence ad hypertrophic scar; L-brachioplasty has less incidence rate of infection, scar contract...
Cadmium-induced testicular toxicity is mediated through oxidative stress and inflammation which eventually lead to cell death. Simvastatin, the antihyperlipidemic agent, exhibits additional antioxidant and anti-inflammatory activities.... more
Cadmium-induced testicular toxicity is mediated through oxidative stress and inflammation which eventually lead to cell death. Simvastatin, the antihyperlipidemic agent, exhibits additional antioxidant and anti-inflammatory activities. The aim of the present work was to investigate the protective effect of simvastatin against cadmium-induced testicular toxicity in rats. The rats received a single intraperitoneal (i.p.) injection of cadmium chloride (2 mg/kg). Simvastatin treatment (5 mg/kg/day, i.p.) was applied for three consecutive days, starting 1 day before cadmium administration. Cadmium significantly decreased serum testosterone, and testicular reduced glutathione and catalase activity, and significantly increased testicular malondialdehyde, nitric oxide, and cadmium ion levels. Simvastatin significantly ameliorated the biochemical changes induced by cadmium. Cadmium-induced testicular tissue injury observed by histopathological examination was attenuated by simvastatin. In addition, simvastatin significantly decreased the expression of inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-α, nuclear factor-κB, and caspase-3, and increased heme oxygenase-1 expression in testicular tissue of rats exposed to cadmium toxicity. It was concluded that simvastatin, through its antioxidant and anti-inflammatory activities, provided a significant protective effect against cadmium-induced testicular toxicity in rats. However, starting treatment with simvastatin before cadmium exposure, as done in the present work, is not clinically applicable. Therefore, other investigations are needed to assess the protective effect of simvastatin treatment following induction of cadmium testicular toxicity.
Research Interests:
The protective effect of thymoquinone was investigated against cadmium-induced testicular toxicity in rats. Testicular toxicity was induced by a single intraperitoneal (i.p.) injection of cadmium chloride (2 mg kg(-1) ). Thymoquinone... more
The protective effect of thymoquinone was investigated against cadmium-induced testicular toxicity in rats. Testicular toxicity was induced by a single intraperitoneal (i.p.) injection of cadmium chloride (2 mg kg(-1) ). Thymoquinone treatment (10 mg kg(-1) day(-1) , i.p.) was applied for five consecutive days, starting 3 days before cadmium administration. Thymoquinone significantly attenuated the cadmium-induced decreases in serum testosterone, and testicular reduced glutathione and superoxide dismutase activity and significantly decreased the elevations of testicular malondialdehyde, nitric oxide and cadmium ion levels resulted from cadmium chloride administration. Also, thymoquinone ameliorated the cadmium-induced testicular tissue injury observed by histopathological examination. In addition, thymoquinone significantly decreased the cadmium-induced expression of inducible nitric oxide synthase, tumour necrosis factor-α, cyclooxygenase-2, nuclear factor-κB and caspase-3 in testicular tissue. It was concluded that thymoquinone, through its antioxidant and anti-inflammatory activities, may represent a potential candidate to protect the testes against the detrimental effect of cadmium exposure.
Research Interests:
The protective effect of naringenin, a flavonoid compound isolated from citrus fruits, was investigated against nephrotoxicity induced by gentamicin (80mgkg(-1)/day, i.p., for eight days) in rats. Naringenin treatment (50mgkg(-1)/day,... more
The protective effect of naringenin, a flavonoid compound isolated from citrus fruits, was investigated against nephrotoxicity induced by gentamicin (80mgkg(-1)/day, i.p., for eight days) in rats. Naringenin treatment (50mgkg(-1)/day, p.o.) was administered for eight days, starting on the same day of gentamicin administration. Gentamicin caused significant elevations of serum creatinine, and kidney tissue levels of malondialdehyde, nitric oxide, and interleukin-8, and a significant decrease in renal glutathione peroxidase activity. Naringenin treatment significantly ameliorated the changes in the measured biochemical parameters resulted from gentamicin administration. Also, naringenin markedly attenuated the histopathological renal tissue injury observed with gentamicin. Immunohistochemical examinations showed that naringenin significantly reduced the gentamicin-induced expression of kidney injury molecule-1, vascular endothelial growth factor, inducible nitric oxide synthase, and caspase-9, and increased survivin expression in the kidney tissue. It was concluded that naringenin, through its antioxidant and anti-inflammatory effects, may represent a therapeutic option to protect against gentamicin nephrotoxicity.
Research Interests:
Research Interests:
Research Interests:
Research Interests:
The nephroprotective effect of coenzyme Q10 was investigated in mice with acute renal injury induced by a single i.p. injection of cisplatin (5 mg/kg). Coenzyme Q10 treatment (10 mg/kg/day, i.p.) was applied for 6 consecutive days,... more
The nephroprotective effect of coenzyme Q10 was investigated in mice with acute renal injury induced by a single i.p. injection of cisplatin (5 mg/kg). Coenzyme Q10 treatment (10 mg/kg/day, i.p.) was applied for 6 consecutive days, starting 1 day before cisplatin administration. Coenzyme Q10 significantly reduced blood urea nitrogen and serum creatinine levels which were increased by cisplatin. Coenzyme Q10 significantly compensated deficits in the antioxidant defense mechanisms (reduced glutathione level and superoxide dismutase activity), suppressed lipid peroxidation, decreased the elevations of tumor necrosis factor-alpha, nitric oxide and platinum ion concentration, and attenuated the reductions of selenium and zinc ions in renal tissue resulted from cisplatin administration. Also, histopathological renal tissue damage mediated by cisplatin was ameliorated by coenzyme Q10 treatment. Immunohistochemical analysis revealed that coenzyme Q10 significantly decreased the cisplatin-induced overexpression of inducible nitric oxide synthase, nuclear factor-kappaB, caspase-3 and p53 in renal tissue. It was concluded that coenzyme Q10 represents a potential therapeutic option to protect against acute cisplatin nephrotoxicity commonly encountered in clinical practice.
Research Interests:
The protective effect of telmisartan, the angiotensin II-receptor antagonist, against liver toxicity induced by sodium arsenite (5 mg/kg/day, p.o., for 30 days) was investigated in mice. Telmisartan treatment (10 mg/kg/day, p.o.) was... more
The protective effect of telmisartan, the angiotensin II-receptor antagonist, against liver toxicity induced by sodium arsenite (5 mg/kg/day, p.o., for 30 days) was investigated in mice. Telmisartan treatment (10 mg/kg/day, p.o.) was applied for 30 days, starting on the same day of arsenic administration. Telmisartan significantly reduced serum alanine aminotransferase level which was increased by sodium arsenite. Telmisartan significantly suppressed lipid peroxidation, and prevented the reduced glutathione depletion and nitric oxide elevation in the liver tissue resulted from arsenic administration. Also, the increase of arsenic ion, and the reductions of selenium and zinc ions in liver tissue were attenuated by telmisartan. Histopathological examination showed that liver tissue injury mediated by arsenic was ameliorated by telmisartan treatment. Immunohistochemical analysis revealed that telmisartan significantly decreased the arsenic-induced expression of inducible nitric oxide synthase, tumor necrosis factor-α, cyclooxygenase-2, nuclear factor-κB and caspase-3 in liver tissue. It was concluded that telmisartan may represent a potential option to protect the liver tissue from the detrimental effects of arsenic toxicity.
Research Interests:
Possible mechanisms underlying the gastroprotective effect of eugenol against indomethacin-induced ulcer in rats were investigated. Pyloric ligation was performed for collection of gastric juice, and gastric ulceration was induced by a... more
Possible mechanisms underlying the gastroprotective effect of eugenol against indomethacin-induced ulcer in rats were investigated. Pyloric ligation was performed for collection of gastric juice, and gastric ulceration was induced by a single intraperitoneal (i.p.) injection of indomethacin (30 mg/kg). Pretreatment with a single dose of eugenol (100 mg/kg, orally), 1 h before indomethacin administration caused significant reductions in gastric mucosal lesions, gastric acid outputs and pepsin activity associated with a significant increase in mucin concentration. Additionally, eugenol significantly attenuated the elevations in gastric mucosal malondialdehyde and total nitrite, and the decrease in reduced glutathione observed with indomethacin. The protective effect afforded by eugenol was significantly inhibited by prior administration of glibenclamide, the ATP-sensitive potassium (K(ATP)) channel blocker, but not by prior use of ruthenium red, the transient receptor potential vanilloid 1 (TRPV1) antagonist. The results indicate that the anti-ulcer effect of eugenol is mediated by opening of K(ATP) channels, scavenging free radicals, decreasing acid-pepsin secretion, increasing mucin production, and preventing the deleterious rise in nitric oxide level.
Research Interests:
We investigated the protective effect of telmisartan, an angiotensin II receptor antagonist, against ischemia/reperfusion renal injury in rats. Bilateral ischemia was induced by clamping both renal vascular pedicles for 45 min followed by... more
We investigated the protective effect of telmisartan, an angiotensin II receptor antagonist, against ischemia/reperfusion renal injury in rats. Bilateral ischemia was induced by clamping both renal vascular pedicles for 45 min followed by reperfusion for 3 h. Untreated rats exposed to ischemia/reperfusion showed significant elevations in blood urea nitrogen and serum creatinine levels, renal tissue levels of malondialdehyde, tumor necrosis factor-alpha and nitric oxide, and caspase-3 activity. This was associated with significant decreases in renal reduced glutathione level, catalase and superoxide dismutase activities. Also, significant increases in serum and renal tissue levels of homocysteine were detected following ischemia/reperfusion. Pre-ischemic treatment with telmisartan (0.3 mg/kg/day, i.p.) for 7 consecutive days significantly attenuated the increases in blood urea nitrogen, serum creatinine, renal malondialdehyde, tumor necrosis factor-alpha, nitric oxide, caspase-3 activity, and serum and renal homocysteine levels, and significantly restored the renal antioxidant defenses. In addition, light and electron microscopic examinations revealed that telmisartan pre-treatment markedly ameliorated ischemia/reperfusion-induced renal tissue damage. It was concluded that telmisartan, through its antioxidant, anti-inflammatory and antiapoptotic effects, can be considered a potential candidate to protect against acute ischemia/reperfusion renal injury.
Research Interests:
Research Interests: Life Sciences, Kidney diseases, Immunohistochemistry, Creatine, Kidney, and 13 moreMice, Nitric oxide, Animals, Glutathione, NF-kappa B, Catalase, Cadmium, Blood Urea Nitrogen, Lipid peroxidation, Tumor necrosis factor-alpha, Benzimidazoles, Biochemistry and cell biology, and Gene Expression Regulation
The protective effect of cannabidiol, the non-psychoactive component of Cannabis sativa, against liver toxicity induced by a single dose of cadmium chloride (6.5 mgkg(-1) i.p.) was investigated in rats. Cannabidiol treatment (5... more
The protective effect of cannabidiol, the non-psychoactive component of Cannabis sativa, against liver toxicity induced by a single dose of cadmium chloride (6.5 mgkg(-1) i.p.) was investigated in rats. Cannabidiol treatment (5 mgkg(-1)/day, i.p.) was applied for five days starting three days before cadmium administration. Cannabidiol significantly reduced serum alanine aminotransferase, and suppressed hepatic lipid peroxidation, prevented the depletion of reduced glutathione and nitric oxide, and catalase activity, and attenuated the elevation of cadmium level in the liver tissue resulted from cadmium administration. Histopathological examination showed that cadmium-induced liver tissue injury was ameliorated by cannabidiol treatment. Immunohistochemical analysis revealed that cannabidiol significantly decreased the cadmium-induced expression of tumor necrosis factor-α, cyclooxygenase-2, nuclear factor-κB, caspase-3, and caspase-9, and increased the expression of endothelial nitric oxide synthase in liver tissue. It was concluded that cannabidiol may represent a potential option to protect the liver tissue from the detrimental effects of cadmium toxicity.
Research Interests:
Research Interests: Kidney diseases, Hyperglycemia, Kidney, Insulin, Pharmacology and Clinical pharmacy, and 15 moreAldosterone, Nitric oxide, Animals, Male, Glutathione, Caspase, Rats, Reperfusion injury, Type 2 Diabetes Mellitus, Experimental Diabetes Mellitus Type 1 and 2, Angiotensin Converting Enzyme Inhibitors, Creatinine, Malondialdehyde, islets of Langerhans, and Captopril
Research Interests: Testosterone, Nitric oxide, Selenium, Animals, Male, and 15 moreGlutathione, NF-kappa B, Zinc, tESTIS, Cadmium, Lipid peroxidation, Caspase, Rats, Tumor necrosis factor-alpha, Benzimidazoles, Angiotensin Converting Enzyme Inhibitors, Cadmium Poisoning, Captopril, Random Allocation, and Testicular diseases
Research Interests:
The therapeutic potential of telmisartan was investigated in mice exposed to acute hepatotoxicity induced by a single dose of acetaminophen (500 mg/kg, p.o.). Telmisartan treatment (two i.p. injections, 10mg/kg, each) was given at 1 and... more
The therapeutic potential of telmisartan was investigated in mice exposed to acute hepatotoxicity induced by a single dose of acetaminophen (500 mg/kg, p.o.). Telmisartan treatment (two i.p. injections, 10mg/kg, each) was given at 1 and 12h following acetaminophen administration. Telmisartan significantly reduced the level of serum alanine aminotransferase, and suppressed lipid peroxidation, prevented the depletion of the antioxidant defenses (reduced glutathione level, and catalase and superoxide dismutase activities), and attenuated the elevation of nitric oxide resulted from acetaminophen administration. Also, telmisartan ameliorated the histopathological liver tissue damage induced by acetaminophen. Immunohistochemical analysis revealed that telmisartan significantly decreased the expression of inducible nitric oxide synthase, tumor necrosis factor-α, cyclooxygenase-2, nuclear factor-κB and caspase-3 in liver tissue of mice received acetaminophen overdose. In conclusion, telmisartan can be considered as a potential therapeutic option to protect against acute acetaminophen hepatotoxicity commonly encountered in clinical practice.
Research Interests:
Research Interests:
Research Interests: Apoptosis, Antioxidants, Liver, Ischemia, Animals, and 15 moreCell Death, Glutathione, Catalase, Glutathione Peroxidase, Lipid peroxidation, Caspase, European, Antioxidant Activity, Alanine Aminotransferase, Aspartate Aminotransferase, Aspartate Aminotransferases, Alanine Transaminase, Electron Microscope, Carnosine, and Liver injury
Research Interests:
Research Interests:
Research Interests: Immunohistochemistry, Oxidative Stress, Apoptosis, Antioxidants, Liver, and 15 moreNitric oxide, Selenium, Animals, Male, Glutathione, Catalase, Cytoprotection, Lipid peroxidation, Caspase, Rats, Biological markers, Acetaminophen, Drug Induced Liver Injury, Malondialdehyde, and ENVIRONMENTAL SCIENCE AND MANAGEMENT
The potential protective effect of cannabidiol, the major non-psychotropic Cannabis constituent, was investigated against doxorubicin cardiotoxicity in rats. Cardiotoxicity was induced by six equal doses of doxorubicin (2.5mgkg(-1) i.p.,... more
The potential protective effect of cannabidiol, the major non-psychotropic Cannabis constituent, was investigated against doxorubicin cardiotoxicity in rats. Cardiotoxicity was induced by six equal doses of doxorubicin (2.5mgkg(-1) i.p., each) given at 48h intervals over two weeks to achieve a total dose of 15mgkg(-1). Cannabidiol treatment (5mgkg(-1)/day, i.p.) was started on the same day of doxorubicin administration and continued for four weeks. Cannabidiol significantly reduced the elevations of serum creatine kinase-MB and troponin T, and cardiac malondialdehyde, tumor necrosis factor-α, nitric oxide and calcium ion levels, and attenuated the decreases in cardiac reduced glutathione, selenium and zinc ions. Histopathological examination showed that cannabidiol ameliorated doxorubicin-induced cardiac injury. Immunohistochemical analysis revealed that cannabidiol significantly reduced the expression of inducible nitric oxide synthase, nuclear factor-κB, Fas ligand and caspase-3, and increased the expression of survivin in cardiac tissue of doxorubicin-treated rats. These results indicate that cannabidiol represents a potential protective agent against doxorubicin cardiac injury.
Research Interests:
The therapeutic potential of coenzyme Q10 was investigated in rats with hepatocellular carcinoma induced by trichloroacetic acid (0.5g/kg/day, p.o., for five days). Coenzyme Q10 treatment (0.4mg/kg/day, i.p.) was applied for four weeks... more
The therapeutic potential of coenzyme Q10 was investigated in rats with hepatocellular carcinoma induced by trichloroacetic acid (0.5g/kg/day, p.o., for five days). Coenzyme Q10 treatment (0.4mg/kg/day, i.p.) was applied for four weeks following trichloroacetic acid administration. Coenzyme Q10 significantly suppressed lipid peroxidation, prevented the depletion of reduced glutathione and superoxide dismutase activity, and decreased the elevations of tumor necrosis factor-α and nitric oxide in liver tissue of rats with hepatocellular carcinoma. Also, the histopathological dysplastic changes induced by trichloroacetic acid in liver tissue were ameliorated by coenzyme Q10. Immunohistochemical analysis revealed that coenzyme Q10 significantly decreased the expression of hepPar-1, alpha-fetoprotein, inducible nitric oxide synthase, cyclooxygenase-2 and nuclear factor-κB in liver tissue of rats with hepatocellular carcinoma. It was concluded that coenzyme Q10 may represent a potential therapeutic option for liver carcinogenesis.
Research Interests: Antioxidants, Nitric oxide, Animals, Male, Hepatocellular Carcinoma, and 11 moreGlutathione, NF-kappa B, Anti-inflammatory agents, Superoxide Dismutase, Lipid peroxidation, Rats, Tumor necrosis factor-alpha, Antineoplastic Agents, Malondialdehyde, ENVIRONMENTAL SCIENCE AND MANAGEMENT, and Ubiquinone
Research Interests:
Research Interests:
Research Interests: Physiology, Type 2 Diabetes, Metformin, Nitric oxide, Animals, and 14 moreClinical, Male, Catalase, Medical Physiology, Rats, Oral Hypoglycemic Agents, Wistar Rats, Gastric Ulcer, Type 2 Diabetes Mellitus, Experimental Diabetes Mellitus Type 1 and 2, Mucins, Malondialdehyde, Indomethacin, and Gastric mucosa
The protective effect of eugenol and its possible mechanisms were investigated in rats with acute doxorubicin cardiotoxicity. Cardiac toxicity was induced by a single intraperitoneal injection of doxorubicin (20 mg/kg). Eugenol treatment... more
The protective effect of eugenol and its possible mechanisms were investigated in rats with acute doxorubicin cardiotoxicity. Cardiac toxicity was induced by a single intraperitoneal injection of doxorubicin (20 mg/kg). Eugenol treatment (5 mg/kg/day, orally) was started 2 days before doxorubicin administration and continued for five consecutive days. Eugenol significantly reduced the elevated serum creatine kinase and lactate dehydrogenase levels, and restored the electrocardiographic disturbances resulted from doxorubicin administration. Also, eugenol reversed doxorubicin-induced deficits in the antioxidant defense mechanisms, decreased lipid peroxidation and attenuated the elevations in cytosolic Ca(2+) and nitric oxide levels in cardiac tissue. In addition, doxorubicin-induced cardiac tissue damage observed by histopathological examination was markedly ameliorated with eugenol. Immunohistochemical analysis revealed that eugenol prevented the doxorubicin-induced activation of caspase-3 in cardiomyocytes. The cardioprotective effect afforded by eugenol was not significantly inhibited by prior administration of capsazepine, the transient potential vanilloid receptor-1 antagonist. It was concluded that eugenol, through its antioxidant activity and its ability to reduce cardiac Ca(2+) accumulation and nitric oxide levels, is a potential candidate to protect against acute doxorubicin cardiotoxicity, a major and dose-limiting clinical problem.