Neuroprotective effect of alpha-lipoic acid on hydrostatic pressure-induced damage of retinal ganglion cells in vitro

Liu, Bing; Ma, Xiaojuan; Guo, Dadong; Guo, Yuanyuan; Chen, Ninghong; Bi, Hongsheng

doi:10.1016/j.neulet.2012.08.016

Cited by 20 publications

(20 citation statements)

References 26 publications

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“…α -LA is a powerful antioxidant that quenches various intracellular ROS [35]. Thus, α -LA has been introduced to prevent or treat oxidative stress-associated diseases, such as diabetes [36, 37], ischemia-reperfusion injury [38, 39], fibrosis [40, 41], and neurodegenerative processes [42, 43]. …”

Section: Discussionmentioning

confidence: 99%

α-Lipoic Acid InhibitsHelicobacter pylori-Induced Oncogene Expression and Hyperproliferation by Suppressing the Activation of NADPH Oxidase in Gastric Epithelial Cells

Byun

Lim

Kim

et al. 2014

Mediators of Inflammation

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Hyperproliferation and oncogene expression are observed in the mucosa of Helicobacter pylori- (H. pylori-) infected patients with gastritis or adenocarcinoma. Expression of oncogenes such as β-catenin and c-myc is related to oxidative stress. α-Lipoic acid (α-LA), a naturally occurring thiol compound, acts as an antioxidant and has an anticancer effect. The aim of this study is to investigate the effect of α-LA on H. pylori-induced hyperproliferation and oncogene expression in gastric epithelial AGS cells by determining cell proliferation (viable cell numbers, thymidine incorporation), levels of reactive oxygen species (ROS), NADPH oxidase activation (enzyme activity, subcellular levels of NADPH oxidase subunits), activation of redox-sensitive transcription factors (NF-κB, AP-1), expression of oncogenes (β-catenin, c-myc), and nuclear localization of β-catenin. Furthermore, we examined whether NADPH oxidase mediates oncogene expression and hyperproliferation in H. pylori-infected AGS cells using treatment of diphenyleneiodonium (DPI), an inhibitor of NADPH oxidase. As a result, α-LA inhibited the activation of NADPH oxidase and, thus, reduced ROS production, resulting in inhibition on activation of NF-κB and AP-1, induction of oncogenes, nuclear translocation of β-catenin, and hyperproliferation in H. pylori-infected AGS cells. DPI inhibited H. pylori-induced activation of NF-κB and AP-1, oncogene expression and hyperproliferation by reducing ROS levels in AGS cells. In conclusion, we propose that inhibiting NADPH oxidase by α-LA could prevent oncogene expression and hyperproliferation occurring in H. pylori-infected gastric epithelial cells.

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Section: Discussionmentioning

confidence: 99%

α-Lipoic Acid InhibitsHelicobacter pylori-Induced Oncogene Expression and Hyperproliferation by Suppressing the Activation of NADPH Oxidase in Gastric Epithelial Cells

Byun

Lim

Kim

et al. 2014

Mediators of Inflammation

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“…Recently, ALA has been recognized as a powerful anti‐oxidant that eliminates oxidative stress by quenching various intracellular reactive oxygen species (ROS) . Furthermore, ALA has been shown to prevent or treat many oxidative stress‐associated diseases, such as diabetes, ischaemia–reperfusion injury, fibrosis and neurodegenerative processes . In particular, Cadirci et al .…”

Section: Introductionmentioning

confidence: 99%

“…8 Furthermore, ALA has been shown to prevent or treat many oxidative stress-associated diseases, such as diabetes, 9,10 ischaemia-reperfusion injury, [11][12][13] fibrosis [14][15][16] and neurodegenerative processes. 17,18 In particular, Cadirci et al 19 reported that ALA attenuates acute lung injury and reduces mortality in caecal puncture and ligation (CPL)-induced septic rats. However, whether ALA can protect against septic acute kidney injury has not yet been investigated.…”

Section: Introductionmentioning

confidence: 99%

α‐Lipoic acid prolongs survival and attenuates acute kidney injury in a rat model of sepsis

Gao

Jia

et al. 2014

Clin Exp Pharma Physio

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Acute kidney injury is a frequent and serious complication in patients with severe sepsis. α-Lipoic acid (ALA), a naturally occurring dithiol compound, has been shown to possess anti-inflammatory and anti-oxidative properties. In the present study we investigated whether ALA could attenuate acute kidney injury and improve survival in a rat model of sepsis. Rats were subjected to caecal ligation and puncture (CLP) to induce sepsis. α-Lipoic acid (200 mg/kg) was administered by oral gavage either immediately (early treatment) or 12 h after the surgical procedure (delayed treatment). Both early and delayed ALA treatment effectively prolonged survival, improved pathological damage in kidney tissues and reduced serum blood urea nitrogen and creatinine levels in CLP-induced septic rats. Furthermore, early treatment with ALA markedly inhibited the release of tumour necrosis factor-α, interleukin (IL)-6 and IL-1β into the serum and reduced mRNA and protein expression of inducible nitric oxide synthase and high mobility group box 1 in kidney tissues from CLP-induced rats. Finally, CLP-induced nuclear factor-κB activation in kidney tissues was significantly suppressed by early ALA treatment. Together, the results indicate that ALA is able to reduce mortality and attenuate acute kidney injury associated with sepsis, possibly by anti-inflammatory actions. α-Lipoic acid may be a promising novel agent for the treatment of conditions associated with septic shock.

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“…2 h at 60 or 100 mm Hg and 6 h at 50 mm Hg, increase oxidative stress markers in RGC-5 cells and induce cell apoptosis [25,47] mediated by calpain activation via apoptosis-inducing factor [34] . These findings further support the role of oxidative stress as an initial event in glaucomatous neuronal damage [25,47] . Exposure of RGC-5 cells to 30 mm Hg for 72 h leads to mitochondrial fission, abnormal cristae depletion, alteration of the optic atrophy type 1 (OPA1) gene expression, and the release of OPA1 and cytochrome C into the cytoplasm, triggering apoptotic cell death [40] .…”

Section: Pressurized Chambermentioning

confidence: 99%

“…In fact, relatively short exposures, i.e. 2 h at 60 or 100 mm Hg and 6 h at 50 mm Hg, increase oxidative stress markers in RGC-5 cells and induce cell apoptosis [25,47] mediated by calpain activation via apoptosis-inducing factor [34] . These findings further support the role of oxidative stress as an initial event in glaucomatous neuronal damage [25,47] .…”

Section: Pressurized Chambermentioning

confidence: 99%

Modeling Human Glaucoma: Lessons from the in vitro Models

Aires

Ambrósio²,

Santiago³

2016

Ophthalmic Res

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Glaucoma, a leading cause of blindness worldwide, is a degenerative disease characterized by retinal ganglion cell (RGC) loss and optic nerve atrophy. Elevated intraocular pressure (IOP) is a main risk factor for onset and progression of the disease. Since increased IOP is the only modifiable risk factor, relevant models for glaucoma would comprise RGC and optic nerve damage triggered by ocular hypertension. Animal models of glaucoma have greatly contributed to the understanding of the molecular mechanisms of this pathology, and they have also facilitated the development of new pharmacological interventions. Although animal models of glaucoma have provided valuable information about the disease, there is still no ideal model for studying glaucoma due to its complexity. There is a recognized demand for in vitro models that can replace or reduce the need for animal experiments. Several in vitro models have emerged as a great opportunity in the field of glaucoma research, helping to clarify the mechanisms involved in disease progression. Several types of equipment have been developed to expose cells and tissue cultures to elevated pressures. Herein, we discuss the methodology used to increase pressure, the main findings, and the relevance of in vitro models for the study of the pathophysiology of glaucoma.

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Neuroprotective effect of alpha-lipoic acid on hydrostatic pressure-induced damage of retinal ganglion cells in vitro

Cited by 20 publications

References 26 publications

α-Lipoic Acid InhibitsHelicobacter pylori-Induced Oncogene Expression and Hyperproliferation by Suppressing the Activation of NADPH Oxidase in Gastric Epithelial Cells

α-Lipoic Acid InhibitsHelicobacter pylori-Induced Oncogene Expression and Hyperproliferation by Suppressing the Activation of NADPH Oxidase in Gastric Epithelial Cells

α‐Lipoic acid prolongs survival and attenuates acute kidney injury in a rat model of sepsis

Modeling Human Glaucoma: Lessons from the in vitro Models

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