Egyptian Society for Physiological SciencesBulletin of Egyptian Society for Physiological Sciences1110-084239220191201Evaluating the therapeutic effect of Diallyl disulfide compared to that of Alderonate on Glucocorticoids induced osteoporosis in rats: Biochemical and histomorphometric analysis1291422898010.21608/besps.2019.6704.1011ENNohaBadaePhysiology,Faculty of medicine, Alexandria UniversityRasha AbdelmawlaGhazalaMedical Biochemistry department,
Faculty of Medicine,
Alexandria UniversityEiman IbrahimZakiHistology and Cell Biology department,
Faculty of Medicine,
Alexandria UniversitySuzan AwadAbdel-GhaniClinical pharmacology department,
Faculty of Medicine,
Alexandria UniversityJournal Article20181216Introduction: The prevalence of Glucocorticoids (GC) use made Glucocorticoid induced osteoporosis (GIO) an important form of secondary osteoporosis. Bisphosphonates (Alderonate) are considered as pharmacological agents in prevention and treatment of GIO. Garlic containing Diallyl disulfide (DAS) has received special attention for its beneficial effects as an antioxidant. The present study attempted to evaluate the Alendronate, DAS, and the combination of Alderonate and DAS effect on bone gene expression of RANKL and OPG, serum biochemical parameters [Ca, P, alkaline phosphatase (ALP)] and histological assessment of tibia in animal model of GIO.<br /> <br /> Material and Method: Fifty pathogen albino male rats were allocated in five groups:Control group(C), Methyl prednisolone group (M), methyl prednisolone Aldenronate group (A) Methyl prednisolone Diallyl disulfide (D), Diallyl disulfide Alendronate Methyl prednisolone (AD) group.Gene expression studies, biochemical parameters, histological and morphometric studies were assessed for all animals.<br /> <br /> Results: Among the study groups, Methyl prednisolone exposure provoked decrease in OPG (0.26±0.16) increase in RANKL (3.57±.39) gene expression, decrease in serum ALP(85.38±6.3),Ca(6.41±0.89), P(1.9 ±0.35) levels and decrease in trabecular thickness (57.01±23.22).Alderonate and Dially disulfide concomitant administration was shown to increase OPG(2.84 ±0.53)and decrease in RANKL (0.63 ± 0.27) gene expression, increase serum ALP(187.75±24.93),Ca(10.330 ±.69)and P(3.16 ±0.43) levels,increase trabecular thickness(154.7±31.7)(p < 0.001).<br /> <br /> Conclusion: Diallyl disulfide can add advantage to Alderonate in treatment of glucocorticoid induced osteoprosis.Egyptian Society for Physiological SciencesBulletin of Egyptian Society for Physiological Sciences1110-084239220191201Anti-adiposity impact of phosphodiesterase-5 inhibitor, Sildenafil is possibly through browning of white adipose tissue and FGF21 in obese rats1431572897910.21608/besps.2019.6747.1012ENMarwa HassanMuhammadMedical Physiology Department, Faculty of Medicine, Benha University, Qalubia, EgyptSaniaElwaiDepartment of Medical Biochemistry & Molecular Biology, Faculty of Medicine, Benha University, Qalubyia, Egypt.Shaymaa MohamedAbd El RahmanDepartment of Medical Biochemistry & Molecular Biology , Faculty of Medicine, Benha University, Qalubyia, EgyptJournal Article20181219Background & Aim: Fibroblast growth factor 21 (FGF21) plays an outstanding role in the metabolic homeostasis. It is recently discovered to be released from brown adipocytes. Induction of brown-like adipocytes termed beige/brite within the white adipose tissue (WAT) by means of browning agents is known as “browning process”. These beige/brite cells have plenty of mitochondria with a unique expression of uncoupling protein-1 (UCP1), essential for energy expenditure, and could release FGF21. Being the WAT is excessively expanded in adiposity, the browning agent has gained great interest to combat obesity. The available data on the browning effect of Sildenafil (Sild) in obese rats still a matter of debate. So, we aimed to illustrate this issue. Method & Results: 3 groups of rats were conducted; control group fed standard diet for 9 weeks, high-fat diet (HFD)-fed group for 9 weeks, and Sild-treated group fed HFD for 9 weeks and received Sild (20 mg /kg /each) twice daily, subcutaneously, in the last 3 weeks. Our findings revealed Sild reduced weight gain, fat depots weight, and adiposity index in spite of unchanged food intake in addition to reduced serum triglycerides, free fatty acids, glucose, insulin, and insulin resistance index. The subcutaneous WAT of Sild-treated rats exhibited augmented UCP1, citrate synthase activity, FGF21 and FGF21-Receptor1 expressions with the highest FGF21 serum levels. Conclusions: Our study suggested the protective impact of Sild against adiposity and insulin resistance is possibly through browning impact as well as enhanced FGF21 and FGF21-R1 levels in WAT of obese rats.Egyptian Society for Physiological SciencesBulletin of Egyptian Society for Physiological Sciences1110-084239220191201Mediating the cardiovascular and renal effects of hyperhomocysteinemia in rats: Role of angiotensin П type I receptor1581722898110.21608/besps.2019.6062.1009ENKarima ElsayedAhmedphysiology,faculty of Medicine, Suez Canal universitySalahKassabDepartment of Basic Sciences, College of Medicine, Qatar University, QatarAngie MohamedAminphysiology,Faculty of medicine, Suez Canal UniversityNoha MohsenAbogreshaphysiology,Faculty of Medicine, Suez Canal UniversityJournal Article20181204Hyperhomocysteinemia is usually associated with cardiovascular and renal disorders. Hyperhomocysteinemia is proved to be a cause of cell cytotoxicity, lipid peroxidation, platelet aggregation, increased activation of the coagulation system and stimulation of vascular smooth muscle cell proliferation. <br /> Aim: To identify whether the pathological changes on cardiovascular and renal systems induced by hyperhomocysteinemia could be mediated through the activation of angiotensin II type 1 receptors (AT1R) in rats.<br /> Methods: Animals were randomized into 3 groups. Each group contained 5 rats. Hyperhomocysteinemia was induced by methionine delivered in drinking water in a concentration of 1.5 g/kg/day per rat based on average water intake for 12 weeks in group II and group III. Valsartan was administered orally in drinking water at a concentration to deliver 30 mg/kg/day per rat in group III. Withdrawal of blood samples for chemical and spectral assay of antioxidant markers was done .Animals were sacrificed, heart, kidney and blood vessels were processed for histopathology .<br /> <br /> Results: There was a significant improvement in the serum levels of blood urea nitrogen in methionine-valsartan-treated group (GIII) rather than methionine-induction group (GII). In addition, there was marked improvement in methionine-valsartan treated group (GIII) than in methionine-induction group (GII) regarding interstitial edema, focal degeneration of myocytes and congestion. When comparing vacuolar degeneration of the medial layer, focal endothelial injury and wall thickness, we found marked improvement in methionine-valsartan-treated group (GIII) than in methionine-induction group (GII).<br /> <br /> Conclusion: Blocking Ang II AT1- receptors by valsartan reduces cardiovascular and renal changes in rats with hyperhomocysteinemia.Egyptian Society for Physiological SciencesBulletin of Egyptian Society for Physiological Sciences1110-084239220191201Possible role of angiogenesis suppression in rats model of non alcoholic fatty liver disease1731902897810.21608/besps.2019.4410.1004ENDalia MohammedAbdel Ghaffar Rezkphysiology department, faculty of medicine, mansoura university, talkha city, dakahlyia gov.0000-0002-0501-0676Mohammed El MahdySarhanphysiology depatment, Faculty of Medicine, Mansoura University, Masoura, Egypt.Hanaa AhmedAbdel Moniemphysiology department, faculty of medicine, mansoura university, mansoura, eygptAmr MedhatAbbasphysiology department, faculty of medicine, mansoura university, mansoura, eygptMohammad EldosokySalamaphysiology department, faculty of medicine, mansoura university, mansoura, eygpt.Journal Article20180717Objective:to evaluate development of angiogenesis in rats of NAFLD and to determine the protective effects of antiangiogenic therapy (sorafenib) in preventing the progression of NAFLD.<br /> Methods: 45 Albino rats (200-300 g) were divided into 3 groups (15 rats for each): Group I: Control group fed on an ordinary diet. Group II: rats received high fat, high fructose diet (HFD,HFr) with DEN ( twice weekly for 8 weeks, ip). Group III: rats received HFD, HFr + DEN + sorafenib orally for 8 weeks. Biochemical, histopathologial, and immunohistopathological examination were studied.<br /> Results: high fat, high fructose diet with DEN resulted in a significant elevation in the serum cholesterol, TG, LDL, and AST, and ALT, significantly lower levels of HDL and Albumin together with a significant decrease in hepatic GSH, Histopathological examination revealed that liver of untreated rats showed severe fatty infilteration (grade3). Immunohistochemical examination of liver of untreated NAFLD rats showed strong staining reactions against VEGF, α- SMA, CD31, and Caspase3 antibodies. Oral administration of sorafenib alleviated all these parameters.Egyptian Society for Physiological SciencesBulletin of Egyptian Society for Physiological Sciences1110-084239220191201Ameliorative potential of sitagliptin and/or calcipotriol on lipopolysaccharide-induced Alzheimer's disease1912033207510.21608/besps.2019.11331.1018ENAhmedKabelPharmacology Department, Faculty of Medicine, Tanta University, Tanta, EgyptHany MohammadBorgfaculty of medicine, kafrelsheikh universityMaalyAbd ElmaaboudPharmacology Department, Faculty of Medicine, Tanta University, Tanta, EgyptAhmedAshourBiomedical Dental Sciences Department, Faculty of Dentistry, Dammam University, Saudi Arabia
Anatomy and Embryology Department, Faculty of Medicine, Tanta University, Tanta, EgyptJournal Article20190330Background: Alzheimer's disease (AD) is a progressive neuropsychiatric disorder that causes dementia. It mostly affects people older than 65 years. The exact mechanisms of AD are not fully understood but affection of apoptosis, oxidative stress and neuroinflammation may be contributing factors. Aim: To evaluate the ability of sitagliptin and/or calcipotriol to attenuate lipopolysaccharide (LPS)-induced AD in mice and to elucidate their possible mechanisms of action. Methods: Sixty male Balb/c mice were divided into 6 equal groups: Control; LPS; LPS + carboxymethyl cellulose; LPS + Sitagliptin; LPS + Calcipotriol; and LPS + Sitagliptin + Calcipotriol group. Behavioral tests, tissue catalase (CAT), superoxide dismutse (SOD) and thiobarbituric acid derivatives (TBARS) were assessed. Also, tissue transforming growth factor beta-1 (TGF-β1), tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were determined. Parts of the hippocampus were subjected to histopathological, immunohistochemical and electron microscopic examination. Results: Administration of sitagliptin and/or calcipotriol prior to LPS injection induced significant increase in the recognition index, tissue CAT and SOD associated with significant decrease in tissue TBARS, TNF-α, IL-6 and TGF-β1 and significant improvement of the histopathological, immunohistochemical and electron microscopic picture compared to LPS group. These changes were significant in sitagliptin/calcipotriol combination group compared to the use of each of these drugs alone. Conclusion: Sitagliptin/calcipotriol combination might represent a new therapeutic modality for amelioration of Alzheimer’s disease.Egyptian Society for Physiological SciencesBulletin of Egyptian Society for Physiological Sciences1110-084239220191201AUDA as a modulator of lipid profile and endothelial function in diet induced hypercholesterolemia in rats2042153208210.21608/besps.2019.11996.1019ENKawkabRagabDepartment of medical physiology, faculty of medicine,Alexandria university, Alexandria, Egypt.LubnaBayoumiDepartment of medical physiology, faculty of medicine,Alexandria university, Alexandria, Egypt.Seham ZakariaNassarDepartment of medical physiology, faculty of medicine, Alexandria university, Alexandria, EgyptAmanyAbdelbaryDepartment of pathology, faculty of medicine,Alexandria university, Alexandria, Egypt.OlaBarghashDepartment of medical physiology, faculty of medicine,Alexandria university, Alexandria, Egypt.Journal Article20190416Background: Epoxyeicosatrienoic acids (EETs) are cytochrome P450 metabolites of arachidonic acid produced by the vascular endothelium and act as important regulators of vascular tone.<br /> Objectives: to study the effect of soluble epoxide hydrolase inhibition AUDA on endothelial function in hypercholesterolemic rats. <br /> Methods: Hypercholesterolemia was induced by using Matos diet for 8 weeks and it significantly increased TC, TG, and LDL-C and decreased HDL-C. AUDA, was used with a dose of 0.35 mg/ kg for 10 weeks via gastric gavage every other day. <br /> Results: AUDA treated group has significantly lower total-C, TG, LDL-C and higher HDL-C as compared to untreated group. AUDA also improved vascular reactivity and vasodilatory response to different doses of Acetyl choline. Histopathological examination of aortic rings showed reduced development of atherosclerotic changes in the vascular wall with no effect on e-NOS expression in vascular endothelial cells. <br /> Conclusions: We can conclude that AUDA treatment has improved lipid profile and protect against development of atherosclerotic histopathological changes.Egyptian Society for Physiological SciencesBulletin of Egyptian Society for Physiological Sciences1110-084239220191201Possible Neuroprotective Effects of Crocin Against Motor and Neurochemical Changes in Rotenone Induced Animal Model of Parkinson's Disease2162303322610.21608/besps.2019.7582.1015ENAhmed AlsayedAbdalfattahPhysiology department, Faculty of Medicine, Tanta UniversityAbeerAbo ZeidDepartment of Medical Physiology Faculty of Medicine, Tanta University, Tanta, EgyptJournal Article20190402Parkinson’s disease (PD) is considered the second most common neurodegenerative disease with subsequent motor and behavioral deficits. Oxidative stress plays a key role in the pathogenesis of PD. AIM: The aim of this study was to investigate the possible neuroprotective effects of crocin on rotenone-induced Parkinson- like behaviors. MATERIALS &METHODS: 70 male adult Wister Albino rats were randomly divided into 4 groups: (1) Control (10 rats); (2) Crocin 40 (10 rats); (3) Polyethylene glycol (PEG) (10 rats) ; (4) Rotenone (40 rats) injected I.P. of 1.5 mg/kg/48 hrs. for 2 weeks [11]; Preliminary behavioral tests and the rats that showed PD features were randomly subdivided into 4 equal groups of 10 rats per each. (4A) Rotenone-treated: (4B): Crocin 20 treated. (4C): Crocin 40 treated. (4D) L-DOPA treated- group. The neurobehavioral were done. In serum, the level of 8-hydroxydeoxyguanosine 8-OHdG was estimated. The level of malondialdehyde (MDA), reduced glutathione (GSH), tumor necrosis factor alpha TNF-α, dopamine, and nitrite/ nitrate levels were measured in the brain tissue. RESULTS: Rotenone induced neurobehavioral deficits with elevation of brain MDA, brain TNF- α, Nitrite/nitrate level and serum 8-OHdG and reduction of GSH, brain tissue dopamine. Crocin (20 or 40) improved these neurobehavioral deficits. Crocin (20 or 40) and L-DOPA decreased MDA, serum 8-OHdG, TNF- α and Nitrite/nitrate level and increased GSH and dopamine level. Crocin 40 had achieved potent effect compared with crocin 20. In summary, rotenone-induced Parkinson- like behavior in rats. Crocin achieved a protective effectEgyptian Society for Physiological SciencesBulletin of Egyptian Society for Physiological Sciences1110-084239220191201The Role of Erythropoietin , Vitamin C and L-NAME in Carboplatin- Induced Hematological and Renal Dysfunctions2312513542910.21608/besps.2019.12567.1021ENAhmed AbdulhakimElGendyDepartment of Medical Physiology,Faculty of Medicine,Mansoura University,Mansoura ,Egypt.0000-0002-3896-9023Wael MohamedElsaedDepartment of Anatomy & Embryology, Faculty of Medicine, Mansoura University, Mansoura, EgyptAbdel NaserBadawyDepartment of Medical Biochemistry, Faculty of Medicine, Mansoura University, EgyptJournal Article20190507Carboplatin is a neoplastic agent causing hematotoxicity, erythropoietin (EPO) resistance, increase oxidative stress and proinflammatory cytokines. Our study investigated the role of erythropoietin , vitamin C and L-NAME in carboplatin- induced hematological and renal dysfunctions.Seventy rats divided into seven groups; control, Carboplatin (100 mg/kg.), Carboplatin (250 mg/kg), Carboplatin (100 mg/kg.) pretreated by EPO , Carboplatin (250 mg/kg) pretreated by EPO, Carboplatin ( 250 mg/kg ) pretreated by EPO & Vitamin C and Carboplatin (250 mg/kg) pretreated by EPO & L-NAME. Hematological, plasma inflammatory cytokines, renal functions , oxidant, antioxidant parameters , serum EPO and vitamin C were measured with histopathology of liver tissue. Carboplatin decreased RBC count, hemoglobin concentration, packed cells volume, platelets count , superoxide dismutase , catalase and glutathione peroxidase, serum erythropoietin and vitamin C while WBCs count, interleukin 1, interleukin 6, tumor necrosis factor alpha, high-sensitivity C-reactive protein, serum blood urea nitrogen, serum creatinine, malondialdehyde and nitric oxide were increased. Vitamin C and L-NAME improved hematological derangement, EPO resistance, antioxidant parameters and histopathological findings while worsen plasma inflammatory markers, renal functions parameters and oxidative parameters. There was insignificant change in blood indices in all groups. We concluded that carboplatin had a hematological toxicity and oxidant stress effect in addition to increase proinflammatory cytokines and consequent renal insult. The development of EPO resistance was carboplatin – dose dependent . Vitamin C and L-NAME alleviate the hematological toxicity, oxidative stress, EPO resistance and decrease proinflammatory cytokines and in turn recovery of renal structure and functions.Egyptian Society for Physiological SciencesBulletin of Egyptian Society for Physiological Sciences1110-084239220191201Effect of Adrenomedullin and Omega-3 Polyunsaturated Fatty Acids on Celecoxib - Induced Acute Hepatic Injury in Experimental Rats2522704135910.21608/besps.2019.13769.1022ENAhmed AbdulhakimElGendyDepartment of Medical Physiology,Faculty of Medicine,Mansoura University,Mansoura ,Egypt.0000-0002-3896-9023Wael MohamedElsaedDepartment of Anatomy & Embryology, Faculty of Medicine, Mansoura University, Mansoura, EgyptHaussain AElazizDepartment of Medical Biochemistry-Faculty of Medicine-Mansoura UniversityAmrAhmedClinical Pharmacist -New Mansoura General Hospital-Mansoura-EgyptJournal Article20190617Celecoxib as a nonsteroidal anti-inflammatory agent has hepatotoxicity, increase both oxidative stress and proinflammatory cytokines. The present study investigated the effect of adrenomedullin and omega-3 polyunsaturated fatty acids in celecoxib - induced acute hepatic injury in experimental rats. Fifty Sprague-Dawley rats were divided into five groups; control, celecoxib treated group, celebrex and adrenomedullin treated group, celebrex and omega – 3 treated group, celebrex, adrenomedullin and omega – 3 treated group. Liver functions tests, hepatic oxidants and antioxidants parameters, plasma nitric oxide levels, serum proinflammatory cytokines, plasma PGE2 and adrenomedullin were measured and also histopathological examination was done. Celebrex significantly impaired liver functions, increase hepatic oxidants, decrease hepatic antioxidants, increase proinflammatory cytokines, decrease PGE2 and increase adrenomedullin ,moreover showing necrosis in histopathology. Adrenomedullin and omega-3 PUFAs improved liver functions, decrease oxidative stress, decrease cytokines and PGE2 but nitric oxide level was significantly increased by adrenomedullin whereas decreased by omega-3 PUFAs. There was insignificant change in serum albumin in all groups. Histopathological examination revealed that most of the hepatocytes appeared with normal colored esinophilic cytoplasm and vesicular basophilic nuclei. It could be concluded that celecoxib had an oxidant stress effect in addition to increase proinflammatory cytokines and consequent acute hepatic insult. The development of hepatic injury was celecoxib – dose dependent. Adrenomedullin and omega-3 polyunsaturated fatty acids could alleviate the acute hepatic injury, oxidative stress, decrease proinflammatory cytokines and by turn recovery of hepatic morphology and functions.Egyptian Society for Physiological SciencesBulletin of Egyptian Society for Physiological Sciences1110-084239220191201Role of Oxidative Stress, Apoptosis and Autophagy in Cadmium-induced Renal Injury in Rats: Renoprotective Effect of Ghrelin2712856739210.21608/besps.2019.14414.1025ENMohamed EldosokySalamaDepartment of Medical Physiology, Faculty of Medicine, Mansoura University, EgyptMohamedAdelDepartment of Medical Physiology, Faculty of Medicine, Mansoura University, EgyptGhadaHelalDepartment of Medical Biochemistry, Faculty of Medicine, Mansoura University, EgyptMohamedEl -ShafeyDepartment of Human anatomy and Embryology, Faculty of Medicine, Mansoura University, EgyptJournal Article20190705Background: Kidney diseases are one of the most common disorders of the modern life. Cadmium (Cd)-induced kidney damage is a common cause of chronic renal failure. Several mechanisms have been postulated to explain the mechanisms underlying Cd induced renal injury such as oxidative stress, apoptosis and autophagy. The aim of the present study was to examine the effect of ghrelin(AG) on renal damage induced by Cd and possible mechanisms Methods: Thirty male Sprague Dawley rats were subdivided into 3 equal groups; Group I (control) the vehicle control, Group II (Cd) group in which rats were subjected to 5 mg Cd/Kg/d via gastric gavage for 4 weeks, Group III (AG) as group II but rats were treated with 3 nmol of ghrelin/animal per day via subcutaneously route for 4 weeks. By the end of experiment, serum levels of creatinine ,Na+ and K, the levels of lipid peroxidations marker (MDA) and antioxidants (GSH) in kidney tissues, kidney injury molecule-1 (Kim-1) in urine and the expression of caspase-3 and LC3 in kidney tissues were measured. Results: Cd administration caused significant increase in serum creatinine and k, urine KIM1 with significant increase in kidney tissues LC3, caspase 3 and MDA that was concomitant with a significant decrease in GSH in (p< 0.05). Administration of AG with Cd caused significant improvement in the studied parameters. Conclusion: we concluded that AG attenuates the renal injury induced by cadmium, which might be due to attenuation of apoptosis, oxidative stress and autophagic process in kidney tissues.