Role of α-lipoic acid in LPS/d-GalN induced fulminant hepatic failure in mice: Studies on oxidative stress, inflammation and apoptosis

Xia, Xiaomin; Su, Chuanyang; Fu, Juanli; Zhang, Pu; Jiang, Xiaoji; Xu, Dan; Hu, Lihua; Song, Erqun; Song, Yang

doi:10.1016/j.intimp.2014.07.008

Cited by 76 publications

(48 citation statements)

References 36 publications

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“…In addition, ALA has both hydrophilic and lipophilic characteristics, so it is able to reduce oxidized antioxidants at the lipid-water interface (Islam 2009;Packer et al 2001;Park et al 2014). Studies performed using in vivo and in vitro showed that ALA can prevent stress oxidative by inducing of enzymatic antioxidant activity (SOD, catalase and GSH) as well as enhancing the capacity of free radical scavenging and by blocking lipid peroxidation (Abdou and Abdel-Daim 2014;Castro et al 2014;Gorąca et al 2013;Xia et al 2014). Because of its antioxidant activity, ALA acts as a neuroprotective agent in various neurodegenerative diseases related to stress oxidative stress (Boyaci et al 2014;Dalazen et al 2014;Demir et al 2014;Jalali-Nadoushan and Roghani 2013;Li et al 2013;Veskovic et al 2014).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of alpha lipoic acid on high glucose-induced neurotoxicity in PC12 cells

2014

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Hyperglycemia plays an important role in the development of diabetic neuropathy. In this study, we investigated the protective effects of alpha lipoic acid (ALA) against high glucose-induced neurotoxicity in PC12 cells as a suitable in vitro model for studying neuronal functions. PC12 cells were treated with high glucose (25 mg/ml for 24 h) in the absence and presence of ALA (100 μM for 24 h). The viability of PC12 cells was estimated by using MTT assay. The expression of pro- apoptotic Bax, anti- apoptotic Bcl-2 and caspase 3 protein were evaluated by western blotting. The reactive oxygen species (ROS) levels were determined with 2,7-dichlorodihydro- fluorescein diacetate (H2DCFDA). Biochemical markers of oxidative stress were assessed by using the total antioxidant power (TAP), lipid peroxidation (LPO), ADP/ATP ratio, activity of antioxidant enzymes catalase (CAT) and superoxide dismutase (SOD). Pretreatment of PC12 cells with ALA, significantly improved high glucose-induced toxicity by increasing activity of antioxidant enzymes CAT and SOD in the PC12 cell. It also increased the concentrations of TAP. An elevated level of cell death and ROS in high glucose conditions, diminished with ALA treatment. Over expression of Bax and caspase 3 protein, elevation of ADP/ATP ratio and LPO level in high glucose- treated PC12 cells, were significantly reduced by ALA. It was concluded that ALA attenuates neurotoxicity induced by high glucose in PC12 cells.

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Section: Discussionmentioning

confidence: 99%

Protective effects of alpha lipoic acid on high glucose-induced neurotoxicity in PC12 cells

2014

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“…Compound 10b inhibits apoptosis following cerebral ischemia/ reperfusion The proto-oncoproteins (Bcl-2 and Bax) are key regulators of the mitochondrial apoptotic pathway initiated by a variety of extracellular and intracellular stressors [27][28][29] . As shown in Figure 6B, NBP treatment, Eda treatment, NBP+Eda treatment and 10b (70 or 140 mg/kg) treatment significantly increased the expression of Bcl-2 in mitochondria and inhibited the translocation of Bax to the mitochondria.…”

Section: Attenuation Of Cerebral Damagementioning

confidence: 99%

The edaravone and 3-n-butylphthalide ring-opening derivative 10b effectively attenuates cerebral ischemia injury in rats

Hua

Sheng

et al. 2015

Acta Pharmacol Sin

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“…Thioctic acid has known anti-inflammatory effects: 29,30 it significantly reduces interleukin-1b and TNF-a levels in experimental acute pancreatitis (in rats) and inhibits the increase in inducible NO synthase expression and activity in morphine-dependent rat brain. 31,32 These anti-inflammatory actions may be responsible for the antiallodynic effects of thioctic acid in neuropathy.…”

Section: Timepointmentioning

confidence: 99%

The effect of thioctic acid on allodynia in a rat vincristine-induced neuropathy model

et al. 2015

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Objective: To investigate the antiallodynic effects of thioctic acid in vincristine-induced neuropathy in rats. Methods: Neuropathy was induced in Sprague-Dawley rats via vincristine intraperitoneal injection. After 15 days, rats were investigated for the presence of mechanical and cold allodynia, and those with allodynia received intraperitoneal injection with normal saline or 1, 5, or 10 mg/kg thioctic acid. Mechanical and cold allodynia were assessed before treatment and at 15, 30, 60, 90, 150 and 180 min after treatment. Results: Mechanical and cold allodynia were reduced by thioctic acid injection. The duration of effect increased with thioctic acid dose. Conclusion: Thioctic acid may be an effective treatment for vincristine-induced neuropathy.

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Role of α-lipoic acid in LPS/d-GalN induced fulminant hepatic failure in mice: Studies on oxidative stress, inflammation and apoptosis

Cited by 76 publications

References 36 publications

Protective effects of alpha lipoic acid on high glucose-induced neurotoxicity in PC12 cells

Protective effects of alpha lipoic acid on high glucose-induced neurotoxicity in PC12 cells

The edaravone and 3-n-butylphthalide ring-opening derivative 10b effectively attenuates cerebral ischemia injury in rats

The effect of thioctic acid on allodynia in a rat vincristine-induced neuropathy model

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