Allicin alleviates acrylamide-induced oxidative stress in BRL-3A cells

Yuan, Hong; Nan, Bo; Wu, Xuan; Yan, Haiyang; Yuan, Yuan

doi:10.1016/j.lfs.2019.116550

Cited by 44 publications

(38 citation statements)

References 42 publications

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“…In addition, by measuring MTP, we showed that AOPP-induced mitochondrial damage in NP cells was attenuated in the allicin-pretreated groups. Overall, our results showed that allicin could mitigate AOPP-induced oxidative stress and activation of the mitochondrial apoptosis pathway through its antioxidative properties in human NP cells, consistent with the results of Hong et al [ 66 ] who discovered that allicin abated acrylamide-induced oxidative stress in BRL-3A cells. However, it is possible that these results do not represent the intracorporal effect of allicin, whose elucidation requires further experiments.…”

Section: Discussionsupporting

confidence: 92%

Allicin Attenuated Advanced Oxidation Protein Product-Induced Oxidative Stress and Mitochondrial Apoptosis in Human Nucleus Pulposus Cells

Xiang

Cheng

Wang

et al. 2020

Oxidative Medicine and Cellular Longevity

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Intervertebral disc degeneration (IDD) is one of the most common chronic degenerative musculoskeletal disorders. Oxidative stress-induced apoptosis of the nucleus pulposus (NP) cells plays a key role during IDD progression. Advanced oxidation protein products (AOPP), novel biomarkers of oxidative stress, have been reported to function in various diseases due to their potential for disrupting the redox balance. The current study is aimed at investigating the function of AOPP in the oxidative stress-induced apoptosis of human NP cells and the alleviative effects of allicin during this process which was known for its antioxidant properties. AOPP were demonstrated to hamper the viability and proliferation of NP cells in a time- and concentration-dependent manner and cause cell apoptosis markedly. High levels of reactive oxygen species (ROS) and lipid peroxidation product malondialdehyde (MDA) were detected in NP cells after AOPP stimulation, which resulted in depolarized mitochondrial transmembrane potential (MTP). Correspondingly, higher levels of AOPP were discovered in the human degenerative intervertebral discs (IVD). It was also found that allicin could protect NP cells against AOPP-mediated oxidative stress and mitochondrial dysfunction via suppressing the p38-MAPK pathway. These results disclosed a significant role of AOPP in the oxidative stress-induced apoptosis of NP cells, which could be involved in the primary pathogenesis of IDD. It was also revealed that allicin could be a promising therapeutic approach against AOPP-mediated oxidative stress during IDD progression.

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Section: Discussionsupporting

confidence: 92%

Allicin Attenuated Advanced Oxidation Protein Product-Induced Oxidative Stress and Mitochondrial Apoptosis in Human Nucleus Pulposus Cells

Xiang

Cheng

Wang

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Allicin is modified by alliinase and has strong hydrophobicity. It can quickly reach the intracellular space through the cell membrane [ 112 , 113 ]. Allicin can exert an antioxidant effect by scavenging free radicals, reducing reactive oxygen species, inducing glutathione production, and regulating NOS.…”

Section: Application Of Antioxidant Natural Drugs For Cardiovasculmentioning

confidence: 99%

Natural Drugs as a Treatment Strategy for Cardiovascular Disease through the Regulation of Oxidative Stress

Chang

Zhang

et al. 2020

Oxidative Medicine and Cellular Longevity

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Oxidative stress (OS) refers to the physiological imbalance between oxidative and antioxidative processes leading to increased oxidation, which then results in the inflammatory infiltration of neutrophils, increased protease secretion, and the production of a large number of oxidative intermediates. Oxidative stress is considered an important factor in the pathogenesis of cardiovascular disease (CVD). At present, active components of Chinese herbal medicines (CHMs) have been widely used for the treatment of CVD, including coronary heart disease and hypertension. Since the discovery of artemisinin for the treatment of malaria by Nobel laureate Youyou Tu, the therapeutic effects of active components of CHM on various diseases have been widely investigated by the medical community. It has been found that various active CHM components can regulate oxidative stress and the circulatory system, including ginsenoside, astragaloside, and resveratrol. This paper reviews advances in the use of active CHM components that modulate oxidative stress, suggesting potential drugs for the treatment of various CVDs.

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“…An in vitro study was undertaken, to explore the mechanism of action of ACR and NR1 on PC12 cells. Hong et al proved in their study that ACR induced ROS in BRL-3A cells ( Hong et al, 2019 ). Recent studies have also found that Panax notoginseng saponins decreased the level of ROS.…”

Section: Resultsmentioning

confidence: 98%

Notoginsenoside R1 Protects Against the Acrylamide-Induced Neurotoxicity via Upregulating Trx-1-Mediated ITGAV Expression: Involvement of Autophagy

Wang

Thomas

et al. 2020

Front. Pharmacol.

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Acrylamide (ACR) is a common chemical used in various industries and it said to have chronic neurotoxic effects. It is produced during tobacco smoking and is also generated in high-starch foods during heat processing. Notoginsenoside R1 (NR1) is a traditional Chinese medicine, which is used to improve the blood circulation and clotting. The objective of this study was to investigate the mechanism of ACR-triggered neurotoxicity and to identify the protective role of NR1 by upregulating thioredoxin-1 (Trx-1). Our results have shown that NR1 could block the spatial and cognitive impairment caused by ACR administration. Bioinformatics analysis revealed that Trx-1 regulated autophagy via Integrin alpha V (ITGAV). NR1 could resist the ACR-induced neurotoxicity by upregulating thioredoxin-1 in PC12 cells and mice. The autophagy-related proteins like autophagy-related gene (ATG) 4B, Cathepsin D, LC3 II, lysosomal-associated membrane protein 2a (LAMP2a), and ITGAV were restored to normal levels by NR1 treatment in both PC12 cells and mice. Besides, we also found that overexpression of Trx-1 resisted ACR-induced autophagy in PC12 cells and downregulation of Trx-1 triggered autophagy induced by ACR in PC12 cells. Therefore, it could be concluded that Trx-1 was involved in the autophagy pathway. Besides, we also found that ITGAV was an intermediate node linking Trx-1 and the autophagy pathway.

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Allicin alleviates acrylamide-induced oxidative stress in BRL-3A cells

Cited by 44 publications

References 42 publications

Allicin Attenuated Advanced Oxidation Protein Product-Induced Oxidative Stress and Mitochondrial Apoptosis in Human Nucleus Pulposus Cells

Allicin Attenuated Advanced Oxidation Protein Product-Induced Oxidative Stress and Mitochondrial Apoptosis in Human Nucleus Pulposus Cells

Natural Drugs as a Treatment Strategy for Cardiovascular Disease through the Regulation of Oxidative Stress

Notoginsenoside R1 Protects Against the Acrylamide-Induced Neurotoxicity via Upregulating Trx-1-Mediated ITGAV Expression: Involvement of Autophagy

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