Alpha-lipoic acid provides neuroprotection from ischemia-reperfusion injury of peripheral nerve

Mitsui, Yosuke; Schmelzer, James D.; Zollman, Paula J.; Mitsui, Manami; Tritschler, Hans; Low, Phillip A.

doi:10.1016/s0022-510x(99)00017-9

Cited by 84 publications

(64 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Терапия данной патологии включает применение препаратов, оптимизирующих метаболизм головного мозга, проявляющих антиоксидантное действие, препятствующих агрегации тромбоцитов, что позволяет обеспечить защиту нейронов от действия повреждающих факторов, лежащих в основе большинства клинических форм заболеваний центральной нервной системы (ЦНС) [3,4]. Одним из наиболее универсальных и перспективных антиоксидантов в комплексной терапии ишемии головного мозга в настоящее время является a-липоевая кислота [5][6][7]. В условиях экспериментальной ишемии препараты, содержащие ЛК, подавляют агрегацию Тц и снижают концентрацию малонового диальдегида (МДА) -основного биохимического маркера ишемического повреждения, являющегося вторичным продуктом перекисного окисления липидов (ПОЛ) [8,9].…”

Section: Introductionunclassified

Liposomal form of lipoic acid: preparation and determination of antiplatelet and antioxidant activity

et al. 2016

View full text Add to dashboard Cite

Подобраны условия для получения липосом из фосфатидилхолина (ФХ), содержащих a-липоевую кислоту (ЛК). Полученные ФХ липосомы, представляют собой частицы размером 175¸284 нм, характеризующиеся эффективностью включения субстанции равной 85% и медленным высвобождением ЛК из них. Установлено влияние как "пустых" липосом, так и липосомальной формы ЛК на агрегацию тромбоцитов (Тц) крови человека, индуцированную арахидоновой кислотой (АК). Обнаружено, что "пустые" липосомы на 30% уменьшают агрегацию Тц, вызванную АК, а липосомы с ЛК подавляют её на 80%. Определено содержание тиобарбитурат продуктов (ТБКП), в образцах плазмы крови человека, обогащенной тромбоцитами, инкубированными с липосомальной ЛК. При этом показано, что ЛК в составе липосом сохраняет свои антиоксидантные свойства и содержание продуктов окисления в исследуемых образцах плазмы крови человека, дозозависимо уменьшается при использовании в качестве индуктора агрегации Тц арахидоновой кислоты.Ключевые слова: липосомы, липоевая кислота, тромбоциты, арахидоновая кислота

show abstract

Section: Introductionunclassified

Liposomal form of lipoic acid: preparation and determination of antiplatelet and antioxidant activity

et al. 2016

View full text Add to dashboard Cite

show abstract

“…It is an ROS scavenger, which is able to stimulate the insulin signaling pathway, chelate metal and regenerate endogenous natural antioxidants (6). In previous decades, using several different experimental models of I/R, studies have demonstrated the protective effects of LA against I/R-induced injury, including myocardial injury (7), peripheral nerve injury (8), testicular injury (9) and retinal injury (10). In addition, it has been reported that LA can activate phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt and extracellular signal-regulated kinase 1/2 (ERK1/2) pathways to induce protection against I/R injury in other organs (11)(12)(13) to the best of our knowledge, few studies were reported to address whether LA has neuroprotective effects against cerebral I/R-induced injury and its potential mechanisms.…”

Section: Introductionmentioning

confidence: 99%

α-lipoic acid protects against cerebral ischemia/reperfusion-induced injury in rats

Deng

Zuo

Zhang

et al. 2015

Molecular Medicine Reports

View full text Add to dashboard Cite

Abstract. It is well established that the brain is sensitive to ischemia/reperfusion (I/R)-induced injury. α-lipoic acid (LA), a free radical scavenger and antioxidant, has a neuroprotective effect against cerebral I/R-induced injury, however, the underlying mechanisms remain to be elucidated. Therefore, the present study was undertaken to evaluate whether LA was able to protect against cerebral I/R-induced injury and to examine the potential mechanisms. The neuroprotective effects of LA were investigated in a rat model of transient focal ischemia induced by middle cerebral artery occlusion (MCAO) followed by reperfusion. Adult male Sprague-Dawley rats were randomly assigned into the sham, cerebral I/R injury model and model plus LA groups. Cerebral I/R injury was induced by 90 min MCAO followed by reperfusion for 24 h. Cerebral infarct size was detected by 2,3,5-triphenyltetrazolium chloride staining. Neurological deficit score (NDS), brain water content and oxidative parameters, including malondialdehyde (MDA), nitric oxide (NO), total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) were measured. The expression of cleaved caspase-3, brain-derived neurotrophic factor (BDNF), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), p-Akt and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) were also analyzed using western blotting. The present study demonstrated that pretreatment with LA significantly decreased the infarction size, brain water content and improved NDS. LA reversed the levels of oxidative parameters, including MDA, NO, T-AOC and SOD to their normal state in rat brains following cerebral I/R. Furthermore, the expression of cleaved caspase-3 markedly decreased and the expression of BDNF, PI3K, p-Akt and p-ERK1/2 significantly increased following administration of LA. On the basis of these findings, it was concluded that LA protected the brain from cerebral I/R damage by attenuation of oxidative stress and caspase-dependent apoptosis. Furthermore, LA exerts its neuroprotective effects potentially through activation of the BDNF-PI3K/Akt-ERK1/2 pathway. IntroductionCerebral ischemic injury is one of the leading causes of human mortality and disability worldwide (1). Restoration of blood flow to the ischemic brain is often used to treat patients in clinical experiments. However, reperfusion itself also has the potential to produce additional injuries in the ischemic brain due to overproduction of reactive oxygen species (ROS). The potential pathological mechanisms of ischemia/reperfusion (I/R) injury include glutamate excitotoxicity, calcium overload, nitric oxide (NO) production, oxidative stress, inflammation and apoptosis, which eventually lead to cell death (2). Oxidative stress and apoptosis following cerebral I/R are the two major processes that induce neuronal injury (3,4). For this reason, multifunctional molecules with anti-oxidative and anti-apoptotic properties are ideal neuroprotective agents.α-lipoic acid (LA), an endogenous short-chain fatty acid, is a cofact...

show abstract

“…The mechanism of the improvement in neuropathic symptoms with a-lipoic acid (ALA) may be related to an improvement in nerve blood flow mediated by the antioxidant action (3,4,5,6,7). ALA can also reduce levels of interleukin 6 and plasminogen activator 1 in plasma, suggesting that it may improve endothelial dysfunction through anti-inflammatory and anti-thrombotic mechanisms (8).…”

Section: Introductionmentioning

confidence: 99%

THERAPY OF ENDOCRINE DISEASE: A systematic review and meta-analysis of α-lipoic acid in the treatment of diabetic peripheral neuropathy

Han

Bai

Liu

et al. 2012

European Journal of Endocrinology

142

View full text Add to dashboard Cite

Objective: To evaluate the effects and safety of 300-600 mg a-lipoic acid (ALA) given i.v. for diabetic peripheral neuropathy (DPN). Methods: We searched the databases of Medline, Embase, and Cochrane central register of Controlled Trials and Chinese biological medicine for clinical trials of ALA in the treatment of DPN. Data were extracted to examine methodological quality and describe characteristics of studies. The primary outcomes were efficacy, median motor nerve conduction velocity (MNCV), median sensory nerve conduction velocity (SNCV), peroneal MNCV, and peroneal SNCV. Secondary outcomes were adverse events. Results: Fifteen randomized controlled trials met the inclusion criteria. The treatment group involved the administration of ALA 300-600 mg i.v. per day. And the control group used the same interventions except for ALA. Compared with the control group, nerve conduction velocities increased significantly in the treatment group. The weighted mean differences in nerve conduction velocities were 4.63 (95% confidence interval 3.58-5.67) for median MNCV, 3.17 (1.75-4.59) for median SNCV, 4.25 (2.78-5.72) for peroneal MNCV, and 3.65 (1.50-5.80) for peroneal SNCV in favor of the treatment group. The odds ratio in terms of efficacy was 4.03 (2.73-5.94) for ALA. Furthermore, no serious adverse events were observed during the treatment period. Conclusions:The results of this meta-analysis provide evidence that treatment with ALA (300-600 mg/day i.v. for 2-4 weeks) is safe and that the treatment can significantly improve both nerve conduction velocity and positive neuropathic symptoms. However, the evidence may not be strong because most of the studies included in this meta-analysis have poor methodological quality.

show abstract

Alpha-lipoic acid provides neuroprotection from ischemia-reperfusion injury of peripheral nerve

Cited by 84 publications

References 24 publications

Liposomal form of lipoic acid: preparation and determination of antiplatelet and antioxidant activity

Liposomal form of lipoic acid: preparation and determination of antiplatelet and antioxidant activity

α-lipoic acid protects against cerebral ischemia/reperfusion-induced injury in rats

THERAPY OF ENDOCRINE DISEASE: A systematic review and meta-analysis of α-lipoic acid in the treatment of diabetic peripheral neuropathy

Contact Info

Product

Resources

About