ABSTRACT
Insulin resistance predicts development of type 2 diabetes mellitus [DM]. Adipocytes release tumor Necrosis factor-alpha [TNF-alpha], and adiponectin. They modulate whole-body insulin sensitivity. The disturbance in the relationship between good and bad adipokines may cause insulin resistance. The renin-angiotensin aldosteron system [RAAS] plays a role in DM and the consequence of cardiovascular complications development. It is considered as a target for therapy. The present objective examined the relationship between renin angiotensin system and DM. There were, Group [1]: Normal non obese rats, Group [2]: Obese diabetic rats, Group [3]: Obese diabetic rats with telmisartan, Group [4]: Obese diabetic rats with enalapril, Group [5]: Obese diabetic rats with aliskiren. There was a significant increase in serum glucose, lipid profile [triglycerides [TGs], low-density lipoprotein cholesterol [LDL], total serum cholesterol [TC]], tumor Necrosis factor-alpha [TNF-alpha], malondialdehyde [MDA] and a significant decrease in adiponectin associated with minor changes in superoxide dismutase [SOD] activity in the obese diabetic rats. Administration of telmisartan, enalapril and or aliskiren caused a significant improvement in serum lipid profile and adiponectin, a minor improvement in SOD activity, a decrease in TNF- alpha and or MDA. Conclusion: Renin angiotensin blockers significantly improve the metabolism and oxidative dysfunctions in Type 2 DM and aliskiren may show a promising powerful therapy
ABSTRACT
Cardiovascular disease is responsible for 80% of deaths among diabetic patients. Diabetic patients may suffer from cardiac insult termed 'diabetic cardiomyopathy. Investigation of biochemical structural and ultastructural changes of the diabetic hearts and effect of supplementation with alpha-lipoic acid [ALA]. Thirty adult male albino rats were divided into: group I control rats, group II diabetic rats and group III diabetic rats receiving ALA. Diabetes was induced in rats of groups II and III by streptozotocin drug. The animals were sacrificed after 16 weeks. The hearts and sera were prepared for biochemical and microscopical studies. Diabetic [Group-II] animals showed significant increase in levels of serum; glucose, malondialdehyde [MDA], cholesterol and hepatic glucose -6-phosphatase enzyme [G-6-Pase] activity in addition to a significant decrease in tissue glutathione [GSH]. Structurally, cardiac muscle fibers appeared swollen with areas devoid of fibers, with collagen deposition among them. Ultrastructurally, diabetic hearts showed poorly organized myofibrils and sarcomeres, disrupted Z lines, dilated sarcoplasmic reticulum, abnormal mitochondria with heterogonous electron dense matrix and disrupted mitochondrial membranes. Some mitochondria showed vacuoles and thsion with each other. The wall of blood vessels was irregular. Secondary lysosomes and myelin bodies in between myofibrils were detected. In diabetic [Group-Ill] animals, ALA partially prevented biochemical structural and ultrastructural changes. Different structural, ultrastructural and biochemical changes were evident in diabetic rats after 16 weeks. The supplementation of ALA in diabetic rats partially prevented such changes, suggesting its possible protective effect against the risk of the progression of cardiovascular diseases during diabetes
ABSTRACT
Background: Peptic ulcers mainly are etiologically related to infection' with Helicobacter pylori or use of nonsteroidal anti-inflammatory drugs [NSAIDs]. The cytoprotective role of antioxidants in the prevention and healing of gastric lesions has been widely investigated. Trimetazidine [TMZ], a metabolic agent with a cytoprotective properties through many actions. The aim of this work is to investigate the beneficial effect of trimetazidine in preventing indomethacin-induced gastric damage and compare it with traditionally used lansoprazol regarding its role in controlling oxidative damage
Methods: The present study was done on 40 rats. They were divided into 2 main groups. Group I: 10 rats as control group, received distilled water. Group II: consists of 30 animals; subdivided into 3 equal subgroups as the following: Subgroup II A: Indomethacin-induced ulceration group. Rats were treated with indomethacin in a single of 45mg/kg intragastrically. Subgroup II B: Rats were treated with lansoprazole in a dose of 4mg/kg for 7 days before induction of ulceration by indomethacin. Subgroup II C: Rats were treated with trimetazidine in a dose of 20mg/ kg for 7 days before induction of ulceration by indomethacin. Blood and stomach were obtained for biochemical analysis and macroscopic examination respectively
Results: Indomethacin-treated rats showed a significant increase in MDA and a significant decrease in GSH and SOD. Tnimetazidine and lansoprazole restored tissue GSH and SOD with a fall in tissues TBARS. Also, both drugs decreased macroscopic gross lesion score of gastric mucosa
Conclusion: The present work demonstrated that tnimetazidine has a protective effect in preventing indomethacin-induced peptic ulcer. It is as effective as lansoprazole, however, it is safe without side effects
Subject(s)
Animals, Laboratory , Rats , Protective Agents , Trimetazidine/therapeutic use , Treatment OutcomeABSTRACT
Diabetic cardiomyopathy can be considered as one of the most common complications of diabetes. Oxidative stress and the production of reactive oxygen species [ROS] were considered to play a key role in the pathogenesis of this cardiomyopathy. Accordingly, this study was planned to detect the biochemical disorders and structural changes in the cardiac muscle in experimentally-induced diabetic rats and to emphasize the role of vitamin C, which could be considered to have an antioxidant effect, in the correction of these abnormalities. Thirty adult male albino rats were classified into three equal groups; group A served as Sham-injected control, while group B rats were turned diabetic by a single intraperitoneal injection of streptozotocin in a dose of 50 mg / kg body weight / rat and left under observation for 16 weeks. The animals of group C were turned diabetic by the same method, but they received vitamin C by stomach tubes for one week before and 16 weeks after induction of diabetes in a single daily dose of 200 mg /kg body weight / rat. Biochemically, significant hyperglycemia and an increase in serum malondialdehyde [MDA] levels with a significant decrease in myocardial glutathione [GSH] were noticed in the animals of group 6 [16 weeks after induction of diabetes]. This was accompanied with extensive microscopic changes in the cardiac muscle in the form of depletion of glycogen content, increased collagen deposition and decreased ATPase activity. Ultrastructurally, myofibrillar disarray in the form of discontinuous, irregular and fragmented Z lines, loss of microfilaments and disorganization of sarcomeres was noticed. The mitochondria appeared irregular in shape with heterogeneous electron dense matrix and disrupted or absent cristae. In addition, appearance of secondary lysosomes and absence of glycogen granules were encountered. The intercalated discs showed a large area having no cellular junctions. These biochemical and morphological abnormalities were apparently reduced in the diabetic rats that received vitamin C. Accordingly, the daily use of vitamin C might play an essential role in the protection against diabetes-induced cardiomyopathy with a more positive impact on management