scholarly journals 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

2018 ◽  
Vol 51 (3) ◽  
pp. 1448-1460 ◽  
Author(s):  
Jing Zhang ◽  
Fan Xiao ◽  
Lieliang Zhang ◽  
Xifeng Wang ◽  
Xiaoyang Lai ◽  
...  
Keyword(s):  
Infarct Size ◽  
Signaling Pathway ◽  
Lipoic Acid ◽  
Neurological Deficit ◽  
Brain Oedema ◽  
Cerebral Injury ◽  
Tunel Staining ◽  
Alpha Lipoic Acid ◽  
Sprague Dawley ◽  
Anti Inflammatory

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.

scholarly journals Protective effect of alpha lipoic acid on diabetic nephropathy in rats

2019 ◽  
Vol 20 (3) ◽  
pp. 19-23
Author(s):  
Samar Yabes ◽  
Mohamed EL-Adl ◽  
Mohamed Hamed ◽  
Gehad El-Sayed
Keyword(s):  
Diabetic Nephropathy ◽  
Lipoic Acid ◽  
Nitrosative Stress ◽  
Acid Group ◽  
Controlled Study ◽  
Alpha Lipoic Acid ◽  
Sprague Dawley ◽  
Glycemic Status ◽  
Oxidative And Nitrosative Stress ◽  
Tissue Samples

Objective: To evaluate the protective role of alpha lipoic acid in rats affected with experimentally-induced diabetes and secondarily complicated with nephropathy. Design: Randomized controlled study. Animals: Forty-eight Sprague Dawley rats. Procedures: Rats were allocated randomly into four groups (12 each); Control rats (Group 1); alpha lipoic acid (ALA) supplemented rats (Group 2); rats with induced diabetic nephropathy (Group 3), and rats with diabetic nephropathy and supplemented with alpha lipoic acid (Group 4). After one month of experimental induction, serum, plasma and renal tissue samples were harvested to determine glycemic status, renal damage markers, antioxidant status, oxidative and nitrosative stress markers, apoptotic marker and histopathology of kidney tissues. Results: In comparison with non-supplemented diabetic rats, alpha lipoic acid reduced renal malondialdehyde (5.74± 0.26 vs 11.3± 1.96 nmol/g. tissue) and renal nitric oxide (30.06± 2.07 vs 36.6± 1.07 nmol/g. tissue). ALA significantly improved the antioxidant enzyme activity (catalase and reduced glutathione), glycemic status, and decreased caspase 3 concentration (P<0.05). Conclusion and clinical relevance: Alpha lipoic acid may be an alternative intervention to alleviate nephropathy as a complication of diabetes. Further studies need to be done in naturally occurring cases.

Evaluation of alpha-lipoic acid anti-inflammatory properties using zebrafish as in vivo model

2019 ◽  
Vol 91 ◽  
pp. 389-390
Author(s):  
G. Camiolo ◽  
L. Rodríguez-Ruiz ◽  
Irene Pardo-Sanchez ◽  
G. Li Volti ◽  
R. Avola ◽  
...  
Keyword(s):  
Lipoic Acid ◽  
In Vivo Model ◽  
Alpha Lipoic Acid ◽  
Anti Inflammatory

scholarly journals Alpha-lipoic acid activates eNOS through activation of PI3-kinase/Akt signaling pathway

2015 ◽  
Vol 64 ◽  
pp. 28-35 ◽  
Author(s):  
Zhekang Ying ◽  
Xiaoyun Xie ◽  
Minjie Chen ◽  
Kevin Yi ◽  
Sanjay Rajagopalan
Keyword(s):  
Signaling Pathway ◽  
Lipoic Acid ◽  
Akt Signaling ◽  
Pi3 Kinase ◽  
Alpha Lipoic Acid ◽  
Akt Signaling Pathway

scholarly journals The anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on acrylamide-induced neurotoxicity in rats

2019 ◽  
Author(s):  
Jie Guo ◽  
Xiaolu Cao ◽  
Xianmin Hu ◽  
Shulan Li ◽  
Jun Wang
Keyword(s):  
Oxidative Stress ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Tunel Staining ◽  
High Dose ◽  
Sprague Dawley ◽  
Curcumin Treatment ◽  
Concurrent Administration ◽  
Tnf Α ◽  
Anti Inflammatory

Abstract Background: As a chemical extensively used in industrial areas as well as formed during heating of carbohydrate-rich food and tobacco, acrylamide (ACR) has been known as well-established neurotoxic pollutant. Although the precise mechanism is unclear, enhanced apoptosis, oxidative stress and inflammation have been demonstrated to contribute to the ACR-induced neurotoxicity. In this study, we assessed the possible anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin, the most active component in a popular spice known as turmeric, on the neurotoxicity caused by ACR in rats. Methods: Curcumin at the dose of 50 and 100 mg/kg was orally given to ACR- intoxicated Sprague-Dawley rats exposed by ACR at 40mg/kg for 4 weeks. All rats were subjected to behavioral analysis. The HE staining and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) staining were used to detect histopathological changes and apoptotic cells, respectively. The mRNA and protein expressions of apoptosis-related molecule telomerase reverse transcriptase (TERT) were detected using real-time PCR and immunohistochemistry, respectively. The contents of malondialdehyde (MDA) and glutathione (GSH) as well as the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured as the indicators for evaluating the level of oxidative stress in brain. The levels of pro-inflammatory cytokinestumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in cerebral homogenates were detected using ELISA assay. Results: Concurrent administration of curcumin at the oral doses of 50 and 100 mg/kg with ACR significantly protected the rats from ACR-induced weigh loss and motor function deficits, and improved the pathological alterations in the ACR-intoxicated brains. Curcumin treatment especially at a high dose enhanced the TERT mRNA expression level and increased the number of TERT-positive nerve cells in cortex tissues of ACR intoxicated rats. The levels of MDA, TNF-α and IL-1β in the cerebral homogenates were reduced, the contents of GSH as well as the activities of SOD and GSH-Px were increased by curcumin treatment, compared to ACR control group. Conclusions: These data suggested the anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on ACR-induced neurotoxicity in rats. And maintaining TERT-related anti-apoptotic function might be one mechanism underlying the protective effect of curcumin on ACR-intoxicated brains.

An alpha-lipoic acid–vitamin E mixture reduces post-embolism lipid peroxidation, cerebral infarction, and neurological deficit in rats

2003 ◽  
Vol 47 (2) ◽  
pp. 219-224 ◽  
Author(s):  
Joaquin Garcia-Estrada ◽  
Oscar Gonzalez-Perez ◽  
Rocio Elizabeth Gonzalez-Castaneda ◽  
Alicia Martinez-Contreras ◽  
Sonia Luquin ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Cerebral Infarction ◽  
Lipoic Acid ◽  
Neurological Deficit ◽  
Alpha Lipoic Acid

scholarly journals The Combination of N-Acetyl Cysteine, Alpha-Lipoic Acid, and Bromelain Shows High Anti-Inflammatory Properties in NovelIn VivoandIn VitroModels of Endometriosis

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
C. Agostinis ◽  
S. Zorzet ◽  
R. De Leo ◽  
G. Zauli ◽  
F. De Seta ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Lipoic Acid ◽  
Inflammatory Diseases ◽  
Inflammatory Marker ◽  
The Novel ◽  
Alpha Lipoic Acid ◽  
Therapeutic Uses ◽  
Anti Inflammatory ◽  
Set Up

To evaluate the efficacy of an association of N-acetyl cystein, alpha-lipoic acid, and bromelain (NAC/LA/Br) in the treatment of endometriosis we set up a newin vivomurine model. We explored the anti-inflammatory and proapoptotic effect of this combination on human endometriotic endothelial cells (EECs) and on endothelial cells isolated from normal uterus (UtMECs). We implanted fragments of human endometriotic cysts intraperitoneally into SCID mice to evaluate the efficacy of NAC/LA/Br treatment. UtMECs and EECs, untreated or treated with NAC/LA/Br, were activated with the proinflammatory stimulus TNF-αand their response in terms of VCAM1 expression was evaluated. The proapoptotic effect of higher doses of NAC/LA/Br on UtMECs and EECs was measured with a fluorogenic substrate for activated caspases 3 and 7. The preincubation of EECs with NAC/LA/Br prior to cell stimulation with TNF-αprevents the upregulation of the expression of the inflammatory “marker” VCAM1. Furthermore NAC/LA/Br were able to induce EEC, but not UtMEC, apoptosis. Finally, the novel mouse model allowed us to demonstrate that mice treated with NAC/LA/Br presented a lower number of cysts, smaller in size, compared to untreated mice. Our findings suggest that these dietary supplements may have potential therapeutic uses in the treatment of chronic inflammatory diseases like endometriosis.

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