Neuroprotection by  -Lipoic Acid in Streptozotocin-Induced Diabetes

Baydaş, Gıyasettin; Dönder, Emir; Kiliboz, M.; Sonkaya, Ertuğrul; Tuzcu, Mehmet; Yasar, Abdullah; Недзвецкий, В. С.

doi:10.1023/b:biry.0000043542.39691.95

Cited by 39 publications

(33 citation statements)

References 16 publications

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“…Manda et al [23] observed a significant decrease in peroxidation products in X-irradiated mouse cerebellar tissue following treatment with α-lipoic acid. Baydas et al [1] demonstrated an α-lipoic acid-mediated protective effect against lipid peroxidation in the glial cells of diabetic rats.…”

Section: Discussionmentioning

confidence: 99%

The COMBINATION OF Α-Lipoic ACID INTAKE WITH ECCENTRIC EXERCISE MODULATES ERYTHROPOIETIN RELEASE

Morawin¹,

Turowski²,

Naczk³

et al. 2014

Biol Sport

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The generation of reactive nitrogen/oxygen species (RN/OS) represents an important mechanism in erythropoietin (EPO) expression and skeletal muscle adaptation to physical and metabolic stress. RN/OS generation can be modulated by intense exercise and nutrition supplements such as α-lipoic acid, which demonstrates both anti- and pro-oxidative action. The study was designed to show the changes in the haematological response through the combination of α-lipoic acid intake with running eccentric exercise. Sixteen healthy young males participated in the randomised and placebo-controlled study. The exercise trial involved a 90-min run followed by a 15-min eccentric phase at 65% VO2max (-10% gradient). It significantly increased serum concentrations of nitric oxide (NO), hydrogen peroxide (H2O2) and pro-oxidative products such as 8-isoprostanes (8-iso), lipid peroxides (LPO) and protein carbonyls (PC). α-Lipoic acid intake (Thiogamma: 1200 mg daily for 10 days prior to exercise) resulted in a 2-fold elevation of serum H2O2 concentration before exercise, but it prevented the generation of NO, 8-iso, LPO and PC at 20 min, 24 h, and 48 h after exercise. α-Lipoic acid also elevated serum EPO level, which highly correlated with NO/H2O2 ratio (r = 0.718, P < 0.01). Serum total creatine kinase (CK) activity, as a marker of muscle damage, reached a peak at 24 h after exercise (placebo 732 ± 207 IU · L-1, α-lipoic acid 481 ± 103 IU · L-1), and correlated with EPO (r = 0.478, P < 0.01) in the α-lipoic acid group. In conclusion, the intake of high α-lipoic acid modulates RN/OS generation, enhances EPO release and reduces muscle damage after running eccentric exercise.

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Section: Discussionmentioning

confidence: 99%

The COMBINATION OF Α-Lipoic ACID INTAKE WITH ECCENTRIC EXERCISE MODULATES ERYTHROPOIETIN RELEASE

Morawin¹,

Turowski²,

Naczk³

et al. 2014

Biol Sport

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“…Therefore, DHLA may act as a strong chain-breaking antioxidant and may enhance the antioxidant potency of other antioxidants like vitamin C in both the aqueous and in hydrophobic membrane phase 98. In addition to its antioxidant properties, LA can be neuroprotective in vivo through suppression of glial reactivity 99. Since chronic reactive gliosis exacerbates diabetic neuropathy, the administration of LA can prevent neuropathy by reducing both oxidative stress and glial hyperactivity 99.…”

Section: Nomenclature and Classification Of Antioxidantsmentioning

confidence: 99%

Structural, Chemical and Biological Aspects of Antioxidants for Strategies Against Metal and Metalloid Exposure

Flora

2009

Oxidative Medicine and Cellular Longevity

516

226

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Oxidative stress contributes to the pathophysiology of exposure to heavy metals/metalloid. Beneficial renal effects of some medications, such as chelation therapy depend at least partially on the ability to alleviate oxidative stress. The administration of various natural or synthetic antioxidants has been shown to be of benefit in the prevention and attenuation of metal induced biochemical alterations. These include vitamins, N-acetylcysteine, α-lipoic acid, melatonin, dietary flavonoids and many others. Human studies are limited in this regard. Under certain conditions, surprisingly, the antioxidant supplements may exhibit pro-oxidant properties and even worsen metal induced toxic damage. To date, the evidence is insufficient to recommend antioxidant supplements in subject with exposure to metals. Prospective, controlled clinical trials on safety and effectiveness of different therapeutic antioxidant strategies either individually or in combination with chelating agent are indispensable. The present review focuses on structural, chemical and biological aspects of antioxidants particularly related to their chelating properties.

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“…Additionally, excessive production of oxygen-free radicals and/or antioxidant deficiency to various brain regions were reported to cause morphological abnormalities and memory deficits during aging [14]. Treatment with antioxidants has been shown to protect neurons against diabetes-induced excitotoxicity and neurodegenerative conditions [15]. Additionally, diabetes is also accompanied with the marked release of inflammatory cytokines [13,16].…”

Section: Introductionmentioning

confidence: 99%

Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats

Mao

Cao

et al. 2014

IJMS

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The present study was designed to probe the effects of Huperzine A (HupA) on diabetes-associated cognitive decline (DACD) using a streptozotocin (STZ)-injected rat model. Diabetic rats were treated with HupA (0.05 and 0.1 mg/kg) for seven weeks. Memory functions were evaluated by the water maze test. Nissl staining was selected for detecting neuronal loss. Protein and mRNA levels of brain-derived neurotrophic factor (BDNF) were analyzed by ELISA and real-time PCR, respectively. The activities of choline acetylase (ChAT), Acetylcholinesterase (AChE), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), NF-κB p65 unit, TNF-α, IL-1β, IL-6 and caspase-3 were measured using corresponding kits. After seven weeks, diabetic rats exhibited remarkable reductions in: body weight, percentage of time spent in target quadrant, number of times crossing the platform, ChAT and BDNF levels, SOD, GSH-Px and CAT accompanied with increases in neuronal damage, plasma glucose levels, escape latency, mean path length, AChE, MDA level as well as CAT, NF-κB p65 unit, TNF-α, IL-1β, IL-6 and caspase-3 in cerebral cortex and hippocampus. Supplementation with HupA significantly and dose-dependently reversed the corresponding values in diabetes. It is concluded that HupA ameliorates DACD via modulating BDNF, oxidative stress, inflammation and apoptosis.

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Neuroprotection by -Lipoic Acid in Streptozotocin-Induced Diabetes

Cited by 39 publications

References 16 publications

The COMBINATION OF Α-Lipoic ACID INTAKE WITH ECCENTRIC EXERCISE MODULATES ERYTHROPOIETIN RELEASE

The COMBINATION OF Α-Lipoic ACID INTAKE WITH ECCENTRIC EXERCISE MODULATES ERYTHROPOIETIN RELEASE

Structural, Chemical and Biological Aspects of Antioxidants for Strategies Against Metal and Metalloid Exposure

Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats

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