Effects of Melatonin in Prevention of Neuropathy in STZ-Induced Diabetic Rats

Zangiabadi, Nasser; Sheibani, Vahid; Asadi-Shekaari, Majid; Shabani, Mohammad; Jafari, Mandana; Asadi, Ali; Tajadini, Haleh; Jarahi, M

doi:10.3844/ajptsp.2011.59.67

Cited by 25 publications

(26 citation statements)

References 37 publications

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“…Untreated or poorly controlled hyperglycemia of diabetes can cause long-term damage, dysfunction, and failure of various organs (1). Hyperglycemia enhances biochemical abnormalities such as formation of advanced glycation end products (AGE), antioxidant enzyme inactivation, over activity of polyol pathway and protein kinase C activation and cytokine production, leading to increase of oxidative stress induced injury and development of diabetic complications (2,3).…”

Section: Introductionmentioning

confidence: 99%

Hepato-renal protective effects of gallic acid and p-coumaric acid in nicotinamide/streptozotocin-induced diabetic rats

Abdel-Moneim

El‐Twab

Ashour

et al. 2016

IJB

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The goal of diabetes treatment is primarily to save life and alleviate symptoms and secondary to prevent long-term diabetic complications resulting from hyperglycemia. Thus, our present investigation was designed to evaluate the hepato-renal protective effects of gallic acid and p-coumaric acid in nicotinamide/streptozotocin (NA/STZ)-induced diabetic rats. Experimental type 2 diabetes was induced by a single intraperitoneal (i.p.) injection of STZ (65 mg/kg b.wt.), after 15 min of i.p. injection of NA (120 mg/kg b.wt.). Gallic acid and p-coumaric acid were orally administered to diabetic rats at a dose of 20, 40 mg/kg b.wt./day, respectively, for 6 weeks. Body weight, serum glucose, protein profile, liver function enzymes and kidney function indicators was assayed. Treatment with either gallic acid or p-coumaric acid significantly ameliorated the elevated levels of glucose, alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea and uric acid. Both compounds were also found to restore total protein, albumin, and globulin as well as body weight of diabetic rats to near normal values. It can conclude that both gallic acid and p-coumaric acid have potent hypoglycemic and hepato-renal protective effects in diabetic rats. Therefore, our results suggest promising hypoglycemic agents that can attenuate the progression of diabetic hepatopathy and nephropathy.

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Section: Introductionmentioning

confidence: 99%

Hepato-renal protective effects of gallic acid and p-coumaric acid in nicotinamide/streptozotocin-induced diabetic rats

Abdel-Moneim

El‐Twab

Ashour

et al. 2016

IJB

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“…Elevated production of Reactive Oxygen Species (ROS) and/or depletion of antioxidants have been observed in a variety of pathological conditions, including inflammatory joint diseases. ROS catalyzelipid per oxidation and tissue injury (Zangiabadi et al, 2011). It is possible though that reactive species may be involved in the path physiological process of OA.…”

Section: Introductionmentioning

confidence: 99%

The Impact of Antioxidants on Inflammation and Oxidative Stress Markers in Osteoarthritis Rat Model: Scanning Electron Microscope Insights

Heidar¹,

Faya²,

Hassan³

et al. 2014

American Journal of Pharmacology and Toxicology

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Osteoarthritis (OA) is characterized by degradation of matrix and destruction of articular cartilage. Articular chondrocytes are solely responsible for the production and maintenance of the extracellular matrix. Therefore, chondrocyte disruption is implicated in cartilage degeneration. Numerous studies have shown that antioxidant treatments are promising therapeutics in cases of OA. This study was designedto examine whether vitamin E protects rat articular chondrocytes against increased inflammatory markers and oxidative stress and prevents cartilage destruction in mono-iodoacetateinduced osteoarthritis rat model. Data showed that osteoarthritis group showed a significant increase in inflammatory markers, Tumor Necrosis Factor-α (TNF-α) (38±1 ng/mL), Interlukin-6 (IL-6) (253±15 ng/mL) and oxidative stress marker, Super Oxide Dismutase (SOD) (14±1 ng/mL) compared to control (18±1 ng/mL), (121+/-23 ng/mL) and (8±1 ng/mL) respectively. Opposite trend was found when animals were treated with vitamin E where TNF-α (27±2 ng/mL) and SOD (10±1 ng/mL) declined significantly. Electro-microscopic examination documented the above results and showed improvement of knee joint after administration of vitamin E. This study supported the notion that OA is a multi factorial complication, caused by inflammation and increased oxidative stress. Administration of vitamin E decreased the markers of inflammation and oxidative stress as well asimproved ultra-structure of the knee jointin acute OA animal model. However, further work id needed to validate reliability in human patients suffering from osteoarthritis.

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“…Oxidative stress results from an imbalance between radical-generating and radical scavenging systems, that is, increased free radical production or reduced activity of antioxidant defense or both. In diabetes, protein glycation and glucose autoxidation may generate free radicals, which in turn catalyse lipid peroxidation and tissue injury (Zangiabadi et al, 2011). Moreover, disturbances of antioxidant defence systems in diabetes were shown to cause decreases in antioxidant enzymes (El-Nabarawy et al, 2010), impaired glutathione metabolism (El-Nabarawy et al, 2010) and decreased antioxidants levels, i.e., Ascorbic acid (Ambali et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

“…The prevalence rate is 8.9%-12.3% in human population (Zangiabadi et al, 2011). It leads to various complications in long term.…”

Section: Introductionmentioning

confidence: 99%

“…Evidences suggest that oxidative stress and free radicals play an important role in the pathogenesis of diabetes mellitus and diabetic complications including tissue damage and injury (Zangiabadi et al, 2011). Oxidative stress results from an imbalance between radical-generating and radical scavenging systems, that is, increased free radical production or reduced activity of antioxidant defense or both.…”

Section: Introductionmentioning

confidence: 99%

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Remedial Effects of Vitamin E and L-Arginine on Peripheral Neuropathy in Streptozotocin-Induced Diabetic Rats

Bin-Jaliah¹

2014

American Journal of Pharmacology and Toxicology

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It was shown that hyperglycemia in diabetic patients is the main factor of diabetic peripheral neuropathies. Various pathways related to oxidative stress, vascular defect and defective endothelium dependent relaxation have been implicated in the development of diabetic peripheral neuropathy. A substantial number of studies have shown that antioxidant treatment are promising therapeutics that can prevent or correct reduced motor nerve conduction in diabetic rats by acting on these mechanisms. This study was designed to investigate the possible role of insulin treatment along with or without vitamin E or L-arginine on diabetic neuropathy. This goal was accessed by examining nerve conduction, parameters of oxidative stress and lipid peroxidation as well as the expression level of endothelial nitric oxide synthase in the sciatic nerve of control and streptozotocine-induced diabetic rats. Data showed that diabetic rats showed increased levels of serum glucose (382.5%) and sciatic nerve lipid peroxidation Marker (MDA, 261.6%) with a concomitant decrease in the expression of sciatic nerve eNOS mRNA as compared to control rats. The nerve conduction studies of the sciatic nerves of these rats showed decrease conduction as evident by delayed NCV (63.6%) and low Amplitude of Muscle Contraction (AMC, 36.4%). Solitary insulin treatment (but not vitamin-E or L-arginine) corrected serum glucose to control values and corrected nerve conduction parameters in the sciatic nerve. However, treating diabetic rats with different doses of vitamin E (300 mg kg −1 and 600 mg kg −1 ) significantly reduced oxidative stress by decreasing MDA and increasing GPx activity, corrected NCV by reducing the latency and improving AMC and increased eNOS mRNA expression in sciatic nerve with a more profound effect to seen with the high dose (600 mg kg −1 ). However, the maximum potent ameliorating effect of the vitamin E on these parameters was seen when administered in combination with insulin. On the other hand, L-arginine treatment alone or in combination with insulin had no effect on the oxidative stress markers nor eNOS expression but significantly and maximally improved NCV through reducing the conduction latency and increasing AMC. This study supported the notion that diabetic peripheral neuropathy is a multifactorial complication, caused by hyperglycemia, oxidative stress and vascular impairment. It is concluded that conjugate treatment with vitamin-E, especially in higher doses, with insulin could be of great value. Moreover correction of impaired nerve blood flow by drugs that induce nitric oxide has proved to be efficient in the protection against and correction of experimental diabetic peripheral neuropathy.

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Effects of Melatonin in Prevention of Neuropathy in STZ-Induced Diabetic Rats

Cited by 25 publications

References 37 publications

Hepato-renal protective effects of gallic acid and p-coumaric acid in nicotinamide/streptozotocin-induced diabetic rats

Hepato-renal protective effects of gallic acid and p-coumaric acid in nicotinamide/streptozotocin-induced diabetic rats

The Impact of Antioxidants on Inflammation and Oxidative Stress Markers in Osteoarthritis Rat Model: Scanning Electron Microscope Insights

Remedial Effects of Vitamin E and L-Arginine on Peripheral Neuropathy in Streptozotocin-Induced Diabetic Rats

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