Beneficial effects of α-lipoic acid plus vitamin E on neurological deficit, reactive gliosis and neuronal remodeling in the penumbra of the ischemic rat brain

González-Pérez, Óscar; González-Castañeda, Rocío E.; Huerta, Miguel; Luquı́n, Sonia; Gómez‐Pinedo, Ulises; Sanchez-Almaraz, E.; Navarro-Ruíz, A.; Garcı́a-Estrada, Joaquı́n

doi:10.1016/s0304-3940(02)00056-3

Cited by 60 publications

(38 citation statements)

References 19 publications

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“…The research showed that ALA-VE mixtures reduce glial scar and increase the expression of remodelling proteins when both antioxidants were administrated pre-and post-ischemia. In addition, the authors reported important functional recovery as a consequence of the prophylactic administration of these antioxidants [42]. Additional findings indicate that a prophylactic treatment with an ALA-VE mixture can reduce infarct volume and lipid peroxidation after cerebral ischemia [43].…”

Section: Synergism Between Lipoate and Tocopherolmentioning

confidence: 80%

Therapeutic perspectives on the combination of α-lipoic acid and vitamin E

González-Pérez

González-Castañeda

2006

Nutrition Research

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Alpha-lipoic acid and vitamin E have synergistic effects, as determined in models of oxidant radical lesions. This review summarizes recent findings showing that the combination of alpha-lipoic acid plus vitamin E has beneficial effects in reducing oxidative damage in ischemic or other oxidationrelated pathological events. Both antioxidants are common in the normal human diet and side effects are very rare. Therefore, alpha-lipoic acid and vitamin E can counteract oxidative processes and could have an important role in clinical medicine.

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Section: Synergism Between Lipoate and Tocopherolmentioning

confidence: 80%

Therapeutic perspectives on the combination of α-lipoic acid and vitamin E

González-Pérez

González-Castañeda

2006

Nutrition Research

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“…Co-administration of ALA with other medications (vitamin E, apocynin, acetyl-l-carnitine, resveratrol, etc.) enhances its neuroprotective effects in a rat model of I/RI [23,24,33]. Moreover, ischaemic preconditioning and ALA preconditioning provide stronger protective effects against hepatic I/RI-induced toxicity in rats [30].…”

Section: Discussionmentioning

confidence: 98%

Alpha-Lipoic Acid Preconditioning and Ischaemic Postconditioning Synergistically Protect Rats from Cerebral Injury Induced by Ischemia and Reperfusion Partly via Inhibition TLR4/MyD88/ NF-κB Signaling Pathway

Zhang

Fan

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: A combination of alpha-lipoic acid preconditioning (ALAP) and ischaemic preconditioning (IPC) has not been tested in an in vivo rat cerebral ischaemia/reperfusion injury (I/RI) model, and the potential protective mechanisms have not been well elucidated. The aim of this study was to investigate the role of the TLR4/ MyD88/ NF-κB signaling pathway in the synergistically neuroprotective and anti-inflammatory effects of ALAP and IPC. Methods: One hundred and fifty male Sprague-Dawley rats, weighing 180-230 g, were randomly divided into the following 5 groups: 1) sham-operated control; 2) I/R; 3) I/R+ALAP; 4) I/R+IPC; 5) I/R+IPC+ALAP. After 2 h of reperfusion, the infarct size, neurological deficit scores, brain oedema, oxidative stress, and inflammatory and apoptotic biomarkers were assessed. In addition, reactive oxygen species (ROS) and cell apoptosis were detected by DHE staining and TUNEL staining, respectively. Results: Both ALAP and IPC treatment attenuated the I/RI-induced neuronal injury, reflected by reductions in the infarct size, neurological deficit scores, brain oedema, lactate dehydrogenase (LDH) release and the inflammatory response, as well as decreased HMGB1, TLR4, MyD88, p65, C-Caspase 3 and Bax expression and increased IKB-α, HO-1, SOD-2 and Bcl-2 expression compared to that in the I/R group. Furthermore, the combination of the two strategies had synergistic anti-inflammatory effects and antioxidant benefits, ultimately limiting neuronal apoptosis. Conclusion: The ‘cocktail’ strategy exhibited a significant neuroprotection against I/RI by attenuating neuroinflammation via inhibition of the TLR4/MyD88/NF-κB signaling pathway.

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“…There exists support in the literature for the potential neurotrophic role of vitamin E in ischemic animal models. Gonzalez-Perez et al 48 have shown a beneficial effect of vitamin E on neural remodeling in an ischemic rat model. Additionally, vitamin E has been shown to Erectile function in a diabetic animal model L De Young et al reduce oxidative stress in congestive heart failure, the mechanism is not yet known, but may have in our work contributed to the improved intracorporal pressure rises.…”

Section: Vitamin E Vit E + Sildenafilmentioning

confidence: 99%

Effect of PDE5 inhibition combined with free oxygen radical scavenger therapy on erectile function in a diabetic animal model

Young

Freeman

et al. 2003

Int J Impot Res

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Phosphodiesterase (PDE) inhibitors represent an important advance in the treatment of erectile dysfunction (ED). In spite of widespread use and generally good efficacy, as a class they remain ineffective in 15-57% of men. Specific cohorts of patients with severe vascular or neurogenic basis to their ED, such as diabetic men or those who have undergone radical pelvic surgery, demonstrate lower response rates with PDE inhibition treatment. We believe that circulating levels of nitric oxide (NO) may be enhanced through delivery of adequate concentrations of free oxygen radical scavenger molecules such as vitamin E. Higher levels of NO, theoretically, should produce increased penile blood flow with the potential for a synergistic effect when combined with a PDE5 inhibitor. With this hypothesis in mind, 20 adult male Sprague-Dawley streptozotocin-induced (60 mg/kg i.p.) diabetic rats were divided into four therapeutic groups (n ¼ 5). Group IFcontrol animals received peanut oil, group IIFvitamin E 20 IU/day, group IIIFsildenafil 5 mg/kg/day and group IVFvitamin E 20 IU/day plus sildenafil 5 mg/kg/day, by oral gavage daily for 3 weeks. Erectile function was assessed as a rise in intracavernous pressure following cavernous nerve electrostimulation. Penile tissue was harvested to determine the changes in tissue morphology including neuronal nitric oxide synthase, smooth muscle a-actin and endothelial cell integrity. PDE5 protein content and activity were measured. Significant increases in intracavernous pressure were measured in the animals receiving combined vitamin E plus sildenafil treatment. Immunohistochemical staining showed increases of neuronal nitric oxide synthase, endothelial cell and smooth muscle cell staining. Western blot analysis did not show significant differences of PDE5 protein between the groups. However, higher PDE5 activity was measured in the sildenafil group and lower activity of PDE5 was recorded in the cohort receiving vitamin E with sildenafil. Vitamin E enhanced the therapeutic effect of the PDE5 inhibitor in a meaningful way in this animal model of diabetes. This study indicates a potential means of salvaging erectile function among patients who are refractory to sildenafil.

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Beneficial effects of α-lipoic acid plus vitamin E on neurological deficit, reactive gliosis and neuronal remodeling in the penumbra of the ischemic rat brain

Cited by 60 publications

References 19 publications

Therapeutic perspectives on the combination of α-lipoic acid and vitamin E

Therapeutic perspectives on the combination of α-lipoic acid and vitamin E

Alpha-Lipoic Acid Preconditioning and Ischaemic Postconditioning Synergistically Protect Rats from Cerebral Injury Induced by Ischemia and Reperfusion Partly via Inhibition TLR4/MyD88/ NF-κB Signaling Pathway

Effect of PDE5 inhibition combined with free oxygen radical scavenger therapy on erectile function in a diabetic animal model

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