scholarly journals Beneficial Effect ofCissus quadrangularisLinn. on Osteopenia Associated with Streptozotocin-Induced Type 1 Diabetes Mellitus in Male Wistar Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Srinivasa Rao Sirasanagandla ◽  
Sreedhara Ranganath Pai Karkala ◽  
Bhagath Kumar Potu ◽  
Kumar M.R. Bhat
Keyword(s):  
Trabecular Bone ◽  
Bone Growth ◽  
Serum Alkaline Phosphatase ◽  
Serum Levels ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Tartrate Resistant Acid Phosphatase ◽  
Cissus Quadrangularis ◽  
Male Wistar Rats

Petroleum ether fraction ofCissus quadrangularis(PECQ) impact on the development of osteopenia in type 1 diabetic rat model has been evaluated. Diabetic rats were treated orally with two doses ofPECQ. Another group of diabetic rats were treated with subcutaneous injection of synthetic human insulin. The cortical and trabecular bone thickness and bone strength were significantly decreased in diabetic rats. Treatment with two doses ofPECQsignificantly prevented these changes in diabetic rats. However,PECQtreatment (two doses) did not alter the glycemic levels in these diabetic rats. Increased levels of serum alkaline phosphatase (ALP), tartrate-resistant acid phosphatase (TRAP), and hydroxyproline were noted in diabetic rats when compared to normal control rats. The two doses ofPECQtreatment further improved the serum ALP levels and significantly decreased the serum levels of TRAP and hydroxyproline. The effects ofPECQtreatment on histological, biomechanical, and biochemical parameters are comparable to those of insulin. SincePECQimproves the bone health in hyperglycemic conditions by enhancing the cortical and trabecular bone growth and altering the circulating bone markers, it could be used as an effective therapy against diabetes-associated bone disorders.

scholarly journals Nicotine Exposure Exacerbates Development of Cataracts in a Type 1 Diabetic Rat Model

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Nima Tirgan ◽  
Gabriela A. Kulp ◽  
Praveena Gupta ◽  
Adam Boretsky ◽  
Tomasz A. Wiraszka ◽  
...  
Keyword(s):  
Rat Model ◽  
Serum Levels ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Positive Trend ◽  
Sprague Dawley ◽  
Nicotine Treatment ◽  
Sprague Dawley Rats ◽  
Diabetic Rat Model

Diabetes and smoking are known risk factors for cataract development. In this study, we evaluated the effect of nicotine on the progression of cataracts in a type 1 diabetic rat model. Diabetes was induced in Sprague-Dawley rats by a single injection of 65 mg/kg streptozotocin. Daily nicotine injections were administered subcutaneously. Forty-five rats were divided into groups of diabetics with and without nicotine treatment and controls with and without nicotine treatment. Progression of lens opacity was monitored using a slit lamp biomicroscope and scores were assigned. To assess whether systemic inflammation played a role in mediating cataractogenesis, we studied serum levels of eotaxin, IL-6, and IL-4. The levels of the measured cytokines increased significantly in nicotine-treated and untreated diabetic animals versus controls and demonstrated a positive trend in the nicotine-treated diabetic rats. Our data suggest the presence of a synergistic relationship between nicotine and diabetes that accelerated cataract formation via inflammatory mediators.

Dietary Choline Deprivation Exacerbates Cardiomyopathy in Streptozotocin-Induced Diabetic Adult Rats

Diabetology ◽  
2021 ◽  
Vol 2 (4) ◽  
pp. 190-204
Author(s):  
Ahmed Al-Humadi ◽  
Athina Strilakou ◽  
Hussam Al-Humadi ◽  
Rafal Al-Saigh ◽  
Emmanouel Agapitos ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Dietary Intervention ◽  
Myocardial Dysfunction ◽  
Posterior Wall ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Myocardial Inflammation ◽  
Standard Diet ◽  
Adult Rats ◽  
Male Wistar Rats

Choline (Ch) is an essential molecule of substantial importance for the optimal development and function of several biological systems. Ch deprivation has been linked with abnormal fat metabolism, insulin resistance, and myocardial dysfunction. The current study provides evidence of an exacerbation of streptozotocin-induced cardiomyopathy in adult diabetic Wistar rats by dietary Ch deprivation through the administration of a Ch-deprived diet (CDD). Twenty-four adult male Wistar rats were randomly separated into four groups: control, diabetic (DM), choline-deprived through choline-deprived diet (CD), and diabetic choline-deprived (DM + CD). After five weeks of dietary intervention, myocardium echocardiographic and histological assessments were performed. Choline-deprived diabetic rats exhibited significantly slower heart rate, significantly higher myocardial ejection velocity and left ventricle wall tension index with a concomitant significant decreased LV posterior wall thickness as compared to diabetic rats fed on a standard diet. Moreover, histopathological evidence demonstrated an exacerbation of myocardial inflammation and fibrosis associated with significant up-regulation of VEGF expression in the diabetic rat myocardium as a result of Ch deprivation. The study’s findings are of particular significance since the examined experimental approach introduces a previously uncharacterised comorbidity simulation with regards to myocardial structure and functional profiling.

scholarly journals Curcumin attenuates oxidative stress in liver in Type 1 diabetic rats

2017 ◽  
Vol 12 (1) ◽  
pp. 452-459 ◽  
Author(s):  
Zhenglu Xie ◽  
Xinqi Zeng ◽  
Xiaqing Li ◽  
Binbin Wu ◽  
Guozhi Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Polyol Pathway ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Curcumin Treatment ◽  
Kinase C ◽  
Diabetic Model ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Plasma Malondialdehyde

AbstractWe investigated the effect of curcumin on liver anti-oxidative stress in the type 1 diabetic rat model induced by streptozotocin (STZ). Experimental diabetic rats were induced by STZ intraperitoneally. All rats were fed for 21 days including three groups of control (NC), diabetic model (DC) and curcumin-treated (Cur, 1.5 g/kg by gavage). The results showed that curcumin-treatment significantly decreased the blood glucose and plasma malondialdehyde levels, but significantly increased the plasma superoxide dismutase, glutathione peroxidase and reduced glutathione levels. Curcumin treatment decreased the activity of aldose reductase, but increased the plasma glucose-6-phosphate dehydrogenase, glucose synthetase and glucose-polymerizing activities. Curcumin treatment significantly decreased the protein of protein kinase C (PKC) and poly ADP ribose polymerase (PARP) expression in the Cur group compared with the DC group. Moreover, the sorbitol dehydrogenase activity was significantly decreased and deterred glucose enters into the polyol pathway leading to an increased NADPH content in the Cur group compared with the DC group. Our data provides evidence that oxidative stress in diabetic rats may be attenuated by curcumin by inhibiting polyol pathway associated with down-regulated expression of PKC and PARP, as evidenced by both an increase the antioxidant enzymes levels and glycogen biosynthesis enzymes activities.

scholarly journals Blockade of OGFr delays the onset and reduces the severity of diabetic ocular surface complications

2020 ◽  
pp. 153537022097206
Author(s):  
Ian S Zagon ◽  
Joseph W Sassani ◽  
Indira Purushothaman ◽  
Patricia J McLaughlin
Keyword(s):  
Growth Factor ◽  
Dry Eye ◽  
Ocular Surface ◽  
Serum Levels ◽  
Diabetic Rats ◽  
Sprague Dawley ◽  
Corneal Surface ◽  
Surface Sensitivity ◽  
Naltrexone Treatment

The opioid growth factor (OGF)–OGF receptor (OGFr) pathway is present in the ocular surface and functions to maintain homeostasis of the epithelium. The OGF–OGFr pathway has been reported to be dysregulated in diabetic individuals and animal models, and is reflected in elevations of the inhibitory growth factor, OGF, chemically termed [Met5]-enkephalin. Recently, our laboratory reported elevated levels of OGF and OGFr in the serum and corneal epithelium of type 1 diabetic rats, suggesting that dysregulation of the OGF–OGFr axis may lead to dry eye, abnormal corneal surface sensitivity, and delayed re-epithelialization. Blockade of OGF–OGFr pathway using naltrexone, a potent opioid receptor antagonist, reverses dry eye symptoms and restores corneal surface sensitivity in diabetic rats when used as a therapy. Based on the evidence that both OGF and OGFr are elevated in type 1 diabetic rats, this study examined whether systemic or topical naltrexone treatment initiated at the time of induction of hyperglycemia could protect against the development of diabetic ocular surface complications. Diabetic male Sprague-Dawley rats treated systemically or topically with naltrexone had a delayed onset of dry eye and altered corneal surface sensitivity, and an improved healing rate for corneal wounds, that were comparable to non-diabetic rats. Serum levels of OGF were normal for rats receiving systemic naltrexone, and OGF tissue levels were normal for type 1 diabetic rats receiving twice daily naltrexone drops. OGFr levels remained elevated. These data support the role of the OGF–OGFr axis in regulation of ocular surface complications, and suggest that naltrexone therapy may be beneficial for pre-diabetic and early diabetic individuals.

scholarly journals Can troxerutin pretreatment prevent testicular complications in prepubertal diabetic male rats?

2020 ◽  
Vol 54 (2) ◽  
pp. 85-95
Author(s):  
Afsaneh Ghadiri ◽  
Fariba Mirzaei Bavil ◽  
Gholam Reza Hamidian ◽  
Hajar Oghbaei ◽  
Zohreh Zavvari Oskuye ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Blood Glucose ◽  
Serum Insulin ◽  
Insulin Level ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Male Rats ◽  
Male Wistar Rats ◽  
Apoptosis Process

AbstractObjective. The vast majority of type 1 diabetes leads to a higher prevalence of reproductive system’s impairments. Troxerutin has attracted much attention owing to its favorable properties, including antihyperglycemic, anti-inflammatory, and antiapoptotic effects. This investigation was proposed to evaluate whether pretreatment with troxerutin could prevent apoptosis-induced testicular disorders in prepubertal diabetic rats.Methods. Fifty prepubertal male Wistar rats were randomly allocated into five groups: control (C), troxerutin (TX), diabetic (D), diabetic+troxerutin (DTX), and diabetic+insulin (DI). Diabetes was induced by 55 mg/kg of streptozotocin applied intraperitoneally. In TX and DTX groups, 150 mg/kg troxerutin was administered by oral gavage. Diabetic rats in DI group received 2–4 U NPH insulin subcutaneously. Troxerutin and insulin treatments were begun immediately on the day of diabetes confirmation. After 30 days, the testicular lipid peroxidation and antioxidant activity, apoptosis process, and stereology as well as serum glucose and insulin levels were assessed.Results. The results showed that diabetes caused a significant increase in the blood glucose, the number of TUNEL positive cells and tubules, and the malondialdehyde level as well as a significant decrease in serum insulin level compared to controls. The stereological analysis also revealed various alterations in diabetic rats compared to controls. Troxerutin treatment improved these alterations compared to the diabetic group.Conclusion. Troxerutin-pretreatment may play an essential role in the management of the type-1 diabetes-induced testicular disorders by decreasing blood glucose and modulating apoptosis.

scholarly journals Dalteparin as a Novel Therapeutic Agent to Prevent Diabetic Encephalopathy by Targeting Oxidative Stress and Inflammation

2020 ◽  
Vol 11 (6) ◽  
pp. 795-804
Author(s):  
Motahareh Zeinivand ◽  
◽  
Arezo Nahavandi ◽  
Tourandokht Baluchnejadmojarad ◽  
Mehrdad Roghani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Therapeutic Agent ◽  
Diabetic Rats ◽  
Brain Inflammation ◽  
Iron Level ◽  
Hepcidin Expression ◽  
Iron Load ◽  
Y Maze ◽  
Male Wistar Rats

Introduction: Hepcidin is the main modulator of systemic iron metabolism, and its role in the brain has been clarified recently. Studies have shown that hepcidin plays an important role in neuronal iron load and inflammation. This issue is of significance because neuronal iron load and inflammation are pathophysiological processes that are highly linked to neurodegeneration. Moreover, the activity of hepcidin has recently been manipulated to recover the neuronal impairment caused by brain inflammation in animal models. Methods: Streptozotocin (STZ) was used to induce type 1 diabetes. Male Wistar rats (n = 40) with a weight range of 200–250 g were divided into control, diabetic, diabetic + insulin, and diabetic + dalteparin groups. Dalteparin (100 mg/kg IP) and insulin (100 mg/kg SC) were administered for 8 weeks. At the end of the experiment, Y-maze and passive avoidance tasks were carried out. The animals were perfused randomly and their hippocampal tissue was isolated for the analysis of markers such as lipid peroxidation like Malondialdehyde (MDA), hepcidin expression, iron, and ferritin. Blood samples were taken for the measurement of serum inflammatory cytokine Interleukin (IL)-6. Results: The findings indicated that treatment with dalteparin reduced IL-6, MDA, ferritin, and hepcidin expression in diabetic rats compared to treatment with insulin (P<0.05). Moreover, treatment with dalteparin did not decrease the iron level or prevented its decline. Conclusion: Treatment with dalteparin improved the cognitive dysfunctions and symptoms of Alzheimer disease in STZ-induced diabetic rats by appropriately modulating and reducing oxidative stress and neuroinflammation. This may enhance the existing knowledge of therapeutics to reduce cognitive impairment in diabetes and is suggested to be a potential therapeutic agent in diabetes.

scholarly journals Hungry bone syndrome after thyroidectomy for thyroid storm

2019 ◽  
Vol 12 (10) ◽  
pp. e231411
Author(s):  
Kazuhisa Kusuki ◽  
Yuzo Mizuno
Keyword(s):  
Vitamin D ◽  
Serum Alkaline Phosphatase ◽  
High Serum ◽  
Thyroid Storm ◽  
Graves Disease ◽  
Tartrate Resistant Acid Phosphatase ◽  
Procollagen Type ◽  
Hungry Bone Syndrome ◽  
Hungry Bone

A 39-year-old man was admitted to our hospital with the diagnosis of thyroid storm due to Graves’ disease. Near-total thyroidectomy was performed after 1 month’s pharmacological treatment, and he presented with tetany next morning. Serum corrected calcium value was 5.7 mg/dL. Procollagen type 1 N-terminal propeptide increased considerably, while tartrate-resistant acid phosphatase 5b decreased. These changes indicated that bone formation exceeded bone resorption in reverse after thyroidectomy. Calcium gluconate was administered intravenously for 14 days, before the patient was discharged. Oral administration of calcium and active forms of vitamin D was continued for 4 months. Rapid skeletal uptake of calcium from blood caused severe and persistent hypocalcaemia, which is called hungry bone syndrome. When patients with Graves’ disease have severe thyrotoxicosis, high serum alkaline phosphatase levels and low bone mineral densities, they are at high risk for hungry bone syndrome after thyroidectomy, and should be educated for the symptoms of hypocalcaemia.

Atorvastatin inhibits brain oxidative stress of Streptozotocininduced diabetic rat

2013 ◽  
Vol 1 (1) ◽  
pp. 35
Author(s):  
Mohammad Taghi Mohammadi ◽  
Mojtaba Gaedniaye Jahromi ◽  
Mohammad Hossein Mirjalili ◽  
Mehdi Ramezani Binabaj ◽  
Mahvash Jafari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Atorvastatin Treatment ◽  
Increase Blood Glucose ◽  
Increase Blood Glucose Level ◽  
Male Wistar Rats ◽  
Brain Oxidative Stress ◽  
The Brain

It is well known that production of ROS compounds and generation of oxidative stress during diabetes are the most important mechanisms of tissue damage. The aim of this study was to examine the effects of atorvastatin treatment, as an antioxidant, to prevent the brain tissue oxidative stress in streptozotocin-induced diabetic rats. Male Wistar rats were randomly divided into four groups (five rats in each group) as followed: normal, normal treated was orally received 20 mg/kg/day atorvastatin for 30 days, diabetic group was given 40 mg/kg streptozotocin by intravenous injection and diabetic treated similar to normal treated rats. After 30 days of treatment, rats were sacrificed under deep anesthesia to remove the brain. After tissue homogenization, superoxide dismutase (SOD) and catalase (CAT) activities, as well as glutathione (GSH) and malondialdehyde (MDA) levels were determined by biochemical methods. In addition to increase blood glucose level in diabetic rats (78%), brain SOD and CAT activities were significantly increased compared with normal rats. Also, diabetes significantly decreased the GSH content of brain tissue by 57%, and increased the brain MDA level by 35%. Finally treatment with atorvastatin significantly decreased the augmented brain CAT activity and the MDA level during diabetes. Based on the finding of this study, diabetes-induced hyperglycemia provoked the production of free radicals in the brain tissue that leading to oxidative stress. Also, treatment with atorvastatin may have prevented from hyperglycemia-induced oxidative stress in the brain of diabetic rat.

scholarly journals Anti-Diabetic Effects of the Ethyl-Acetate Fraction of Trichilia catigua in Streptozo-tocin-Induced Type 1 Diabetic Rats

2017 ◽  
Vol 42 (3) ◽  
pp. 1087-1097 ◽  
Author(s):  
Rodrigo Mello Gomes ◽  
Luis Fernando de Paulo ◽  
Cynthia Priscilla do Nascimento Bonato Panizzon ◽  
Camila Quaglio Neves ◽  
Bruna Colombo Cordeiro ◽  
...  
Keyword(s):  
Ethyl Acetate ◽  
Kidney Tissue ◽  
Ethyl Acetate Fraction ◽  
Diabetic Rats ◽  
Diabetic Group ◽  
Male Wistar Rats ◽  
Food And Water Intake ◽  
Pancreas Morphology ◽  
Group D

Background/Aims: Trichilia catigua A. Juss., known as “catuaba” in Brazil, has been popularly used as a tonic for fatigue, impotence and memory deficits. Previously, our group demonstrated that the ethyl-acetate fraction (EAF) of T. catigua has antioxidant and anti-inflammatory effects. The present study evaluated the anti-diabetic activity of EAF in type 1 diabetic rats. Methods: Male Wistar rats were divided into four groups (N: non-diabetic group, D: type 1 diabetic group, NC: non-diabetic + EAF group and DC: type 1 diabetic + EAF group). The latter two groups were treated with 200 mg/kg EAF. Type 1 diabetes was induced by intravenous streptozotocin (STZ) injection (35 mg/kg). Starting two days after STZ injection, EAF was administered daily by gavage for 8 weeks. Results: EAF attenuated body mass loss and reduced food and water intake. EAF improved hyperglycaemia and other biochemical parameters, such as alkaline phosphatase (ALP), alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Furthermore, the number of pancreatic β-cells and the size of the islets had increased by β-cell proliferation in the DC group. EAF promoted reduction in kidney tissue damage in STZ-induced diabetic rats by reduction of renal fibrosis. Conclusion: The present study showed that EAF improves glucose homeostasis and endocrine pancreas morphology and inhibits the development of diabetic nephropathy in STZ-induced diabetic rats.

Kupffer cell-initiated remote hepatic injury following bilateral hindlimb ischemia is complement dependent

2001 ◽  
Vol 280 (2) ◽  
pp. G279-G284 ◽  
Author(s):  
Robert W. Brock ◽  
Robert G. Nie ◽  
Kenneth A. Harris ◽  
Richard F. Potter
Keyword(s):  
Kupffer Cell ◽  
Kupffer Cells ◽  
Hepatic Injury ◽  
Cell Function ◽  
Ischemia Reperfusion ◽  
Serum Levels ◽  
Hindlimb Ischemia ◽  
Male Wistar Rats ◽  
Stimulation Of

Intravital fluorescence microscopy was applied to the livers of male Wistar rats to test the hypothesis that complement mobilization stimulates Kupffer cells and subsequently initiates hepatic injury after hindlimb ischemia/reperfusion (I/R). Following 3 h of limb reperfusion, hepatocellular viability (serum levels of alanine transaminase and cell death via propidium iodide labeling) decreased significantly from levels in sham-operated animals. Inhibition of complement mobilization with soluble complement receptor type 1 (20 mg/kg body wt) and interruption of Kupffer cell function with GdCl3 (1 mg/100g body wt) resulted in significant hepatocellular protection. Although the effects of hindlimb I/R on hepatic microvascular perfusion were manifest as increased heterogeneity, both complement inhibition and suppression of Kupffer cell function resulted in marked improvements. No additional hepatocellular protection and microvascular improvements were provided by combining the interventions. Furthermore, inhibition of complement mobilization significantly depressed Kupffer cell phagocytosis by 42% following limb reperfusion. These results suggest that the stimulation of Kupffer cells via complement mobilization is necessary but is not the only factor contributing to the early pathogenesis of hepatic injury following hindlimb I/R.

Sign in / Sign up

Export Citation Format

Share Document