Pub Date : 2020-06-01DOI: 10.21608/besps.2020.22519.1041
Magdi A. El-Damarawi, M. Abd-Elazeem
Background: Defects in glucose transporter-4 (GLUT-4) expression and function in the skeletal muscles and adipose tissue can be considered as the main cause of insulin resistance (IR) in type 2 diabetes mellitus (T2DM). Also, Oxidative stress and inflammation play a very important role in the development of IR and T2DM. Aim: Studying the effect of quercetin and metformin on GLUT-4 expression, oxidative stress, inflammation markers and IR in T2DM. Method: This study was carried out on 50 male Wistar rats which were divided into five groups; control, untreated diabetic rats, diabetic rats treated with metformin, diabetic rats treated with quercetin and diabetic rats treated with metformin and quercetin. Results: The use of metformin and quercetin separately produced significant decrease in plasma glucose, insulin, IL-6, TNF-α levels, HOMA-IR and TBARS level in skeletal muscle. Also, they caused significant elevation in the antioxidant enzyme activities in skeletal muscles with increased expression of GLUT-4 in the skeletal muscles and adipose tissue compared to the diabetic rats. Evidently, the quercetin effects were more significant than that of metformin on all the parameters except on HOMA-IR (similar significant improvement). Moreover, the combined use of quercetin and metformin produced highly significant improvement approaching control level in all the parameters than that observed by using either of them. Conclusion: The combined use of QC and MF improved hyperglycemia and IR by increasing the expression of GLUT-4 in skeletal muscles and adipose tissue together with the reversal of the oxidative stress and inflammatory states.
{"title":"Effect of Quercetin and Metformin on Glucose Transporter-4 Expression, Oxidative Stress, Inflammation Markers and Insulin Resistance in Type 2 Diabetes Mellitus","authors":"Magdi A. El-Damarawi, M. Abd-Elazeem","doi":"10.21608/besps.2020.22519.1041","DOIUrl":"https://doi.org/10.21608/besps.2020.22519.1041","url":null,"abstract":"Background: Defects in glucose transporter-4 (GLUT-4) expression and function in the skeletal muscles and adipose tissue can be considered as the main cause of insulin resistance (IR) in type 2 diabetes mellitus (T2DM). Also, Oxidative stress and inflammation play a very important role in the development of IR and T2DM. Aim: Studying the effect of quercetin and metformin on GLUT-4 expression, oxidative stress, inflammation markers and IR in T2DM. Method: This study was carried out on 50 male Wistar rats which were divided into five groups; control, untreated diabetic rats, diabetic rats treated with metformin, diabetic rats treated with quercetin and diabetic rats treated with metformin and quercetin. Results: The use of metformin and quercetin separately produced significant decrease in plasma glucose, insulin, IL-6, TNF-α levels, HOMA-IR and TBARS level in skeletal muscle. Also, they caused significant elevation in the antioxidant enzyme activities in skeletal muscles with increased expression of GLUT-4 in the skeletal muscles and adipose tissue compared to the diabetic rats. Evidently, the quercetin effects were more significant than that of metformin on all the parameters except on HOMA-IR (similar significant improvement). Moreover, the combined use of quercetin and metformin produced highly significant improvement approaching control level in all the parameters than that observed by using either of them. Conclusion: The combined use of QC and MF improved hyperglycemia and IR by increasing the expression of GLUT-4 in skeletal muscles and adipose tissue together with the reversal of the oxidative stress and inflammatory states.","PeriodicalId":9347,"journal":{"name":"Bulletin of Egyptian Society for Physiological Sciences","volume":"173 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86057341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-06-01DOI: 10.21608/besps.2019.16189.1032
M. Tohamy, M. Ghalwash, N. Abo-Elmaaty, Refka Messiha, Samah Fouad
The aim of this study was to investigate the possible protective role of Hydrogen sulfide on chronic unpredictable stress (CUS) -induced gastric lesions. Materials and methods: 40 rats were divided into 4 groups: control group, stressed rats group, stressed + Aminooxyacetic acid (AOAA) (inhibitor of H2S synthesis; 50mg/kg/48hour; IP), stressed + Sodium hydrosulfide (NaHS) (donor of H2S, 5mg/kg/48hour; IP). In all the groups exposed to CUS, a set of chronic unpredictable stressors was applied for 6 weeks in random order. At the end of experimental protocol blood samples, gastric content and gastric tissues samples were collected. Gastric tissues histopathological changes were evaluated by macroscopic and microscopic examination. Gastric content pH, serum MDA level, whole blood GSH level were estimated. Expression of Caspase-3 (apoptotic marker) and BCL-xl (anti-apoptotic marker) was assessed by immunohistochemistry. Results: In all the groups exposed to CUS, there was a significant reduction in gastric pH value and a range of gastric lesions ranging from superficial to deep ulceration as evident by macroscopic and microscopic examination. Also, there was significant elevation in MDA serum level and significant reduction in anti-oxidant GSH blood level. In all stressed rats, the expression of Caspase-3 was significantly higher whereas a significant decrease in expression of anti-apoptotic protein BCL-xl was observed. These findings were aggravated by AOAA while using NaHS improved them. Conclusion: it seems that increasing bioavailability of H2S could have a protective role against CUS induced gastric lesions. The results suggest that this protection could be through anti-oxidant and anti-apoptotic effects.
{"title":"The Role of Hydrogen Sulfide in Chronic Unpredictable Stress-Induced Gastric Lesions.","authors":"M. Tohamy, M. Ghalwash, N. Abo-Elmaaty, Refka Messiha, Samah Fouad","doi":"10.21608/besps.2019.16189.1032","DOIUrl":"https://doi.org/10.21608/besps.2019.16189.1032","url":null,"abstract":"The aim of this study was to investigate the possible protective role of Hydrogen sulfide on chronic unpredictable stress (CUS) -induced gastric lesions. Materials and methods: 40 rats were divided into 4 groups: control group, stressed rats group, stressed + Aminooxyacetic acid (AOAA) (inhibitor of H2S synthesis; 50mg/kg/48hour; IP), stressed + Sodium hydrosulfide (NaHS) (donor of H2S, 5mg/kg/48hour; IP). In all the groups exposed to CUS, a set of chronic unpredictable stressors was applied for 6 weeks in random order. At the end of experimental protocol blood samples, gastric content and gastric tissues samples were collected. Gastric tissues histopathological changes were evaluated by macroscopic and microscopic examination. Gastric content pH, serum MDA level, whole blood GSH level were estimated. Expression of Caspase-3 (apoptotic marker) and BCL-xl (anti-apoptotic marker) was assessed by immunohistochemistry. Results: In all the groups exposed to CUS, there was a significant reduction in gastric pH value and a range of gastric lesions ranging from superficial to deep ulceration as evident by macroscopic and microscopic examination. Also, there was significant elevation in MDA serum level and significant reduction in anti-oxidant GSH blood level. In all stressed rats, the expression of Caspase-3 was significantly higher whereas a significant decrease in expression of anti-apoptotic protein BCL-xl was observed. These findings were aggravated by AOAA while using NaHS improved them. Conclusion: it seems that increasing bioavailability of H2S could have a protective role against CUS induced gastric lesions. The results suggest that this protection could be through anti-oxidant and anti-apoptotic effects.","PeriodicalId":9347,"journal":{"name":"Bulletin of Egyptian Society for Physiological Sciences","volume":"34 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84064287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-12-01DOI: 10.21608/BESPS.2019.6704.1011
N. Badae, R. Ghazala, Eiman I Zaki, S. Abdel-Ghani
Introduction: 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. 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. 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). Conclusion: Diallyl disulfide can add advantage to Alderonate in treatment of glucocorticoid induced osteoprosis.
{"title":"Evaluating the therapeutic effect of Diallyl disulfide compared to that of Alderonate on Glucocorticoids induced osteoporosis in rats: Biochemical and histomorphometric analysis","authors":"N. Badae, R. Ghazala, Eiman I Zaki, S. Abdel-Ghani","doi":"10.21608/BESPS.2019.6704.1011","DOIUrl":"https://doi.org/10.21608/BESPS.2019.6704.1011","url":null,"abstract":"Introduction: 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. 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. 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). Conclusion: Diallyl disulfide can add advantage to Alderonate in treatment of glucocorticoid induced osteoprosis.","PeriodicalId":9347,"journal":{"name":"Bulletin of Egyptian Society for Physiological Sciences","volume":"91 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81586235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-12-01DOI: 10.21608/BESPS.2019.6747.1012
M. Muhammad, Sania Elwai, S. Rahman
Background & 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.
{"title":"Anti-adiposity impact of phosphodiesterase-5 inhibitor, Sildenafil is possibly through browning of white adipose tissue and FGF21 in obese rats","authors":"M. Muhammad, Sania Elwai, S. Rahman","doi":"10.21608/BESPS.2019.6747.1012","DOIUrl":"https://doi.org/10.21608/BESPS.2019.6747.1012","url":null,"abstract":"Background & 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.","PeriodicalId":9347,"journal":{"name":"Bulletin of Egyptian Society for Physiological Sciences","volume":"48 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73795103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-12-01DOI: 10.21608/BESPS.2019.4410.1004
D. M. A. G. Rezk, Mohammed E. Sarhan, hanaa ahmed abdel moniem, A. Abbas, M. E. Salama
Objective: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. 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. 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.
目的:观察NAFLD大鼠血管生成的情况，探讨抗血管生成治疗(索拉非尼)对NAFLD进展的保护作用。方法:将45只白化病大鼠(200 ~ 300 g)分为3组，每组15只:第一组:对照组，饲喂普通饲料。第二组:大鼠给予高脂肪、高果糖饮食(HFD、HFr)和DEN(每周2次，共8周，ip)。III组:大鼠口服HFD、HFr + DEN +索拉非尼8周。进行生化、组织病理学及免疫组织病理学检查。结果:高脂、高果糖饮食加DEN导致血清胆固醇、TG、LDL、AST、ALT显著升高，HDL、白蛋白水平显著降低，肝脏GSH显著降低，组织病理学检查显示，未经DEN治疗的大鼠肝脏出现严重的脂肪浸润(3级)。未经治疗的NAFLD大鼠肝脏免疫组化检查显示对VEGF、α- SMA、CD31和Caspase3抗体有较强的染色反应。口服索拉非尼可缓解上述症状。
{"title":"Possible role of angiogenesis suppression in rats model of non alcoholic fatty liver disease","authors":"D. M. A. G. Rezk, Mohammed E. Sarhan, hanaa ahmed abdel moniem, A. Abbas, M. E. Salama","doi":"10.21608/BESPS.2019.4410.1004","DOIUrl":"https://doi.org/10.21608/BESPS.2019.4410.1004","url":null,"abstract":"Objective: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. 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. 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.","PeriodicalId":9347,"journal":{"name":"Bulletin of Egyptian Society for Physiological Sciences","volume":"27 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84995198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-12-01DOI: 10.21608/BESPS.2019.13769.1022
A. Elgendy, Wael M Elsaed, H. A. Elaziz, Amr E Ahmed
Celecoxib 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.
{"title":"Effect of Adrenomedullin and Omega-3 Polyunsaturated Fatty Acids on Celecoxib - Induced Acute Hepatic Injury in Experimental Rats","authors":"A. Elgendy, Wael M Elsaed, H. A. Elaziz, Amr E Ahmed","doi":"10.21608/BESPS.2019.13769.1022","DOIUrl":"https://doi.org/10.21608/BESPS.2019.13769.1022","url":null,"abstract":"Celecoxib 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.","PeriodicalId":9347,"journal":{"name":"Bulletin of Egyptian Society for Physiological Sciences","volume":"13 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83430175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-08-21DOI: 10.21608/BESPS.2019.14913.1028
Fatma M. Lebda, Mona A. Ahmed, M. Shawky, W. Baher, Y. Sabry
Background: Type 2 diabetes mellitus (T2DM) is associated with obesity, insulin resistance, and hypertension. Exercise may play important role in combating obesity and diabetic complications. Irisin is a newly discovered exercise-induced myokine. Its role in mediating the beneficial effects of exercise is questionable. Aim: The present study was performed to reveal the beneficial effects of moderate-intensity exercise on diabetic-induced visceral obesity, and hypertension in a rat model of T2DM, as well as the potential role of irisin relative to exercise and the mechanisms-involved. Materials and methods: Rats were allocated into 4 groups; control, type 2 diabetes mellitus (T2DM), exercise-T2DM and irisin-T2DM groups. Body weight (BW), body mass index (BMI), perirenal fat (PF), systolic (SBP), diastolic (DBP), and mean blood pressures (MBP), fasting blood glucose (FBG), insulin, nitrite, and HOMA-insulin resistance (IR) and histology of adipose tissue were determined. Results: Exercise attenuated the adverse effects of T2DM, whereas PF, PF index, serum nitrite, plasma insulin, and HOMA-IR comparable to controls; however, FBG, SBP, DBP and MBP still significantly higher. Partial browning of white adipose tissue demonstrated. Irisin-T2DM rats showed a remarkable effect compared to exercise intervention documented by a reduction in BW, BMI, PF, PF index, DBP, FBG, and insulin, with increase in nitrite, and complete browning of adipose tissue. Conclusion It is concluded that exercise and irisin treatment can improve visceral adiposity and hypertension; however, the protective effect of irisin is more obvious. These data suggest irisin as a potential new strategy to combat obesity and hypertension in diabetic patients.
{"title":"Potential impact of exercise versus irisin on hypertension, and visceral adiposity in a rat model of type 2 diabetes mellitus","authors":"Fatma M. Lebda, Mona A. Ahmed, M. Shawky, W. Baher, Y. Sabry","doi":"10.21608/BESPS.2019.14913.1028","DOIUrl":"https://doi.org/10.21608/BESPS.2019.14913.1028","url":null,"abstract":"Background: Type 2 diabetes mellitus (T2DM) is associated with obesity, insulin resistance, and hypertension. Exercise may play important role in combating obesity and diabetic complications. Irisin is a newly discovered exercise-induced myokine. Its role in mediating the beneficial effects of exercise is questionable. Aim: The present study was performed to reveal the beneficial effects of moderate-intensity exercise on diabetic-induced visceral obesity, and hypertension in a rat model of T2DM, as well as the potential role of irisin relative to exercise and the mechanisms-involved. Materials and methods: Rats were allocated into 4 groups; control, type 2 diabetes mellitus (T2DM), exercise-T2DM and irisin-T2DM groups. Body weight (BW), body mass index (BMI), perirenal fat (PF), systolic (SBP), diastolic (DBP), and mean blood pressures (MBP), fasting blood glucose (FBG), insulin, nitrite, and HOMA-insulin resistance (IR) and histology of adipose tissue were determined. Results: Exercise attenuated the adverse effects of T2DM, whereas PF, PF index, serum nitrite, plasma insulin, and HOMA-IR comparable to controls; however, FBG, SBP, DBP and MBP still significantly higher. Partial browning of white adipose tissue demonstrated. Irisin-T2DM rats showed a remarkable effect compared to exercise intervention documented by a reduction in BW, BMI, PF, PF index, DBP, FBG, and insulin, with increase in nitrite, and complete browning of adipose tissue. Conclusion It is concluded that exercise and irisin treatment can improve visceral adiposity and hypertension; however, the protective effect of irisin is more obvious. These data suggest irisin as a potential new strategy to combat obesity and hypertension in diabetic patients.","PeriodicalId":9347,"journal":{"name":"Bulletin of Egyptian Society for Physiological Sciences","volume":"24 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78568278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-06-01DOI: 10.21608/BESPS.2019.11996.1019
K. Ragab, Lubna Bayoumi, S. Nassar, Amany Abdelbary, Ola Barghash
Background: Epoxyeicosatrienoic acids (EETs) are cytochrome P450 metabolites of arachidonic acid produced by the vascular endothelium and act as important regulators of vascular tone. Objectives: to study the effect of soluble epoxide hydrolase inhibition AUDA on endothelial function in hypercholesterolemic rats. 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. 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. Conclusions: We can conclude that AUDA treatment has improved lipid profile and protect against development of atherosclerotic histopathological changes.
{"title":"AUDA as a modulator of lipid profile and endothelial function in diet induced hypercholesterolemia in rats","authors":"K. Ragab, Lubna Bayoumi, S. Nassar, Amany Abdelbary, Ola Barghash","doi":"10.21608/BESPS.2019.11996.1019","DOIUrl":"https://doi.org/10.21608/BESPS.2019.11996.1019","url":null,"abstract":"Background: Epoxyeicosatrienoic acids (EETs) are cytochrome P450 metabolites of arachidonic acid produced by the vascular endothelium and act as important regulators of vascular tone. Objectives: to study the effect of soluble epoxide hydrolase inhibition AUDA on endothelial function in hypercholesterolemic rats. 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. 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. Conclusions: We can conclude that AUDA treatment has improved lipid profile and protect against development of atherosclerotic histopathological changes.","PeriodicalId":9347,"journal":{"name":"Bulletin of Egyptian Society for Physiological Sciences","volume":"15 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85322892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-06-01DOI: 10.21608/BESPS.2019.11331.1018
Ahmed M. Kabel, H. Borg, M. A. A. Elmaaboud, Ahmed S. Ashour
Background: 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.
{"title":"Ameliorative potential of sitagliptin and/or calcipotriol on lipopolysaccharide-induced Alzheimer's disease","authors":"Ahmed M. Kabel, H. Borg, M. A. A. Elmaaboud, Ahmed S. Ashour","doi":"10.21608/BESPS.2019.11331.1018","DOIUrl":"https://doi.org/10.21608/BESPS.2019.11331.1018","url":null,"abstract":"Background: 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.","PeriodicalId":9347,"journal":{"name":"Bulletin of Egyptian Society for Physiological Sciences","volume":"52 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74765173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-03-23DOI: 10.21608/besps.2019.6062.1009
K. E. Ahmed, S. Kassab, A. Amin, Noha M Abogresha
Hyperhomocysteinemia 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. 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. 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 . 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). Conclusion: Blocking Ang II AT1- receptors by valsartan reduces cardiovascular and renal changes in rats with hyperhomocysteinemia.
{"title":"Mediating the cardiovascular and renal effects of hyperhomocysteinemia in rats: Role of angiotensin П type I receptor","authors":"K. E. Ahmed, S. Kassab, A. Amin, Noha M Abogresha","doi":"10.21608/besps.2019.6062.1009","DOIUrl":"https://doi.org/10.21608/besps.2019.6062.1009","url":null,"abstract":"Hyperhomocysteinemia 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. 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. 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 . 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). Conclusion: Blocking Ang II AT1- receptors by valsartan reduces cardiovascular and renal changes in rats with hyperhomocysteinemia.","PeriodicalId":9347,"journal":{"name":"Bulletin of Egyptian Society for Physiological Sciences","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78642785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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